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Fastest race boat? Meet Wally’s new TP52 beater, the wallyrocket51

• Toby Hodges
• October 4, 2023

Wally Yachts has unveiled a new one-design racing yacht, the wallyrocket51. Toby Hodges takes a look at what Wally hopes to be the fastest race boat

Product Overview

“This will be the fastest boat in the world on corrected time,” Wally founder Luca Bassani announced at Ferretti Yachts’ global unveiling of the wallyrocket51 in September. On paper, the one-design racer should be faster than the top racing yachts in IRC and ORC classes, yet rates lower. Its potential for prizes (and fun) therefore looks highly promising.

‘Faster and less expensive’ is the slogan.

It’s a surprise move from the iconic Italian brand, which has latterly been focussed on large power yachts and performance cruising superyachts . This is its smallest new Wally since the 37ft Wally Nano daysailer 15 years ago, and by far the most race oriented.

And it’s deliberately pitted in this size range to line up against the most competitive class, the TP52s . “The benchmark boat to beat is the TP52,” Bassani confirms, “but Wally will always be faster.” He calculates that in a one hour race the wallyrocket51 will be 20-30 seconds quicker in real time and 40-50 seconds quicker on corrected time. That’s not bad over a typical two hour race!

The wallyrocket51’s sleek deck lines

Wallyrocket51, TP52 killer?

The 1ft less length is critical in allowing the design team to optimise the hull and appendages to get a rating bonus in other areas, such as the wallyrocket’s very light displacement, water ballast and a trim tab on the keel.

What really sets this new project apart from just marketing hyperbole, is that the naval architecture is by Botin Partners, the same designers behind some of the most successful TP52s. This studio’s designs have won 12 consecutive season titles, so it knows all the secrets of the class and design rules.

“It’s designed by Botin against a Botin. In light winds it will be faster in any condition,” says Bassani with a knowing smile.

The ultralight displacement of 6,250kg will be key to achieving such a promise. It compares with the TP52’s minimum displacement (governed by its box rule) of 6,975kg or the 8,250kg of the ClubSwan 50 . While there will be less crew aboard too…

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The water ballast system has a 550-litre capacity, the equivalent of five crewmembers on the rail. It takes 80 seconds to fill, 60 seconds to ditch, and just 10 seconds to transfer from side to side.

Meanwhile, an adjustable trim tab on the trailing edge of the keel will help it go faster and higher, and crucially, not sideways, says Bassani. The aim of the trim tab is to produce lift upwind for a smaller keel stem profile to help produce neutral leeway. Aligning water flow with the boat also means less drag, hence Wally’s claims that it will sail higher and faster than the competition.

While it’s’ designed for 11 crew (935kg), the wallyrocket51 can actually be crewed with 8 or 9 aboard with the addition of a fully electric winch package, says Bassani. Nevertheless they have gone with twin grinding pedestals to avoid a higher rating penalty (the aft pedestal can be replaced by an electric motor for more shorthanded racing ).

Vasco Vascotto, one of the world’s most successful regatta sailors, and Argentinian Olympic sailor Guillermo Parada, are project developers, who have helped shape the one-design series as well as make the design easier to handle and fun. Vascotto believes the wallyrocket51 is something everyone is looking for and wants: “A yacht able to perform in all regatta fields, but at the same time that maintains the design and that is fun.”

The aft grinding pedestal can be replaced if electric winches are fitted for shorthanded sailing

Carrau expands further on this: “We looked at everything, from windward-leeward courses in 6 to 25 knots of wind, to the classic offshore 600-milers such as the Rolex Middle Sea , Rolex Giraglia, RORC Caribbean 600 or Fastnet Race … Indeed, our simulations show that she can beat her competition under IRC or ORC in any of those inshore or offshore scenarios.”

“The wallyrocket51 is very close to our hearts and has eluded us for years as we sought to develop a design that could win any regatta in the world,” continues Wally’s managing director Stefano de Vivo. “We have cracked it at last.”

The first wallyrocket51 is in build at Wally’s new carbon fibre specialist facility within Ferretti’s gargantuan 70,000m2 yard in Ravenna. This includes two new ovens to cook yachts up to 50m. “No one else has this facility,” says Bassani.

Hulls will be built in pre-preg carbon with Corecell foam, while Nomex is used as the core for the deck. Wallyrockets will sport high modulus Southern Spars masts, Future Fibres AeroSix rigging, and carry 164m2 of upwind sail and over 360m2 downwind.

So what about the cost – the ‘less expensive’ part of the slogan? ”It costs around €2m to run a TP52,” Bassani estimates, “but you will be able to run this for less than a third of that.” He puts this largely down to TPs needing those extra crew numbers over a full season of events. And that Wally will have strict rules on expenditure, which a one-design format helps control.

They will offer their staff to look after the boats, so he sees some clients doing long charters too.

Wally has prided itself on being a market innovator, claiming it is ‘30 years old but 20 years ahead’. As an example, it cites the beach terrace concept Bassani came up with in the late 1990s and which is used by many new designs today.

So why now? Why try to top a class which is already 20 years old? Bassani says that there is a need for a new racing class, something exciting but smart and reasonable. While secondly, he adds that: “fast and easy was always Wally… and we need to go back to fast!”

Wally has a network of owners and knows what they are looking for. With its new WallyWhy power range as potential motherships, Bassani believes the wallyrocket51 will be the perfect complement for racing. “It’s more fun and much less expensive than a 40m performance cruising sailing yacht,” he says, adding that such a superyacht is three to four times the price of a 90ft WallyWhy 200.

The first two wallyrocket51s are slated to launch in the summer of 2024.

Wallyrocket51 specifications

LOA: 15.5m LWL: 14.68m Beam: 4.32m Light Displacement: 6,250kg Draught: 3.50m Water ballast: 550kg

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Theses & Dissertations: Cancer Research

Theses/dissertations from 2023 2023.

Development of Combination Therapy Strategies to Treat Cancer Using Dihydroorotate Dehydrogenase Inhibitors , Nicholas Mullen

Overcoming Resistance Mechanisms to CDK4/6 Inhibitor Treatment Using CDK6-Selective PROTAC , Sarah Truong

Theses/Dissertations from 2022 2022

Omics Analysis in Cancer and Development , Emalie J. Clement

Investigating the Role of Splenic Macrophages in Pancreatic Cancer , Daisy V. Gonzalez

Polymeric Chloroquine in Metastatic Pancreatic Cancer Therapy , Rubayat Islam Khan

Evaluating Targets and Therapeutics for the Treatment of Pancreatic Cancer , Shelby M. Knoche

Characterization of 1,1-Diarylethylene FOXM1 Inhibitors Against High-Grade Serous Ovarian Carcinoma Cells , Cassie Liu

Novel Mechanisms of Protein Kinase C α Regulation and Function , Xinyue Li

SOX2 Dosage Governs Tumor Cell Identity and Proliferation , Ethan P. Metz

Post-Transcriptional Control of the Epithelial-to-Mesenchymal Transition (EMT) in Ras-Driven Colorectal Cancers , Chaitra Rao

Use of Machine Learning Algorithms and Highly Multiplexed Immunohistochemistry to Perform In-Depth Characterization of Primary Pancreatic Tumors and Metastatic Sites , Krysten Vance

Characterization of Metastatic Cutaneous Squamous Cell Carcinoma in the Immunosuppressed Patient , Megan E. Wackel

Visceral adipose tissue remodeling in pancreatic ductal adenocarcinoma cachexia: the role of activin A signaling , Pauline Xu

Phos-Tag-Based Screens Identify Novel Therapeutic Targets in Ovarian Cancer and Pancreatic Cancer , Renya Zeng

Theses/Dissertations from 2021 2021

Functional Characterization of Cancer-Associated DNA Polymerase ε Variants , Stephanie R. Barbari

Pancreatic Cancer: Novel Therapy, Research Tools, and Educational Outreach , Ayrianne J. Crawford

Apixaban to Prevent Thrombosis in Adult Patients Treated With Asparaginase , Krishna Gundabolu

Molecular Investigation into the Biologic and Prognostic Elements of Peripheral T-cell Lymphoma with Regulators of Tumor Microenvironment Signaling Explored in Model Systems , Tyler Herek

Utilizing Proteolysis-Targeting Chimeras to Target the Transcriptional Cyclin-Dependent Kinases 9 and 12 , Hannah King

Insights into Cutaneous Squamous Cell Carcinoma Pathogenesis and Metastasis Using a Bedside-to-Bench Approach , Marissa Lobl

Development of a MUC16-Targeted Near-Infrared Antibody Probe for Fluorescence-Guided Surgery of Pancreatic Cancer , Madeline T. Olson

FGFR4 glycosylation and processing in cholangiocarcinoma promote cancer signaling , Andrew J. Phillips

Theses/Dissertations from 2020 2020

Cooperativity of CCNE1 and FOXM1 in High-Grade Serous Ovarian Cancer , Lucy Elge

Characterizing the critical role of metabolic and redox homeostasis in colorectal cancer , Danielle Frodyma

Genomic and Transcriptomic Alterations in Metabolic Regulators and Implications for Anti-tumoral Immune Response , Ryan J. King

Dimers of Isatin Derived Spirocyclic NF-κB Inhibitor Exhibit Potent Anticancer Activity by Inducing UPR Mediated Apoptosis , Smit Kour

From Development to Therapy: A Panoramic Approach to Further Our Understanding of Cancer , Brittany Poelaert

The Cellular Origin and Molecular Drivers of Claudin-Low Mammary Cancer , Patrick D. Raedler

Mitochondrial Metabolism as a Therapeutic Target for Pancreatic Cancer , Simon Shin

Development of Fluorescent Hyaluronic Acid Nanoparticles for Intraoperative Tumor Detection , Nicholas E. Wojtynek

Theses/Dissertations from 2019 2019

The role of E3 ubiquitin ligase FBXO9 in normal and malignant hematopoiesis , R. Willow Hynes-Smith

BRCA1 & CTDP1 BRCT Domainomics in the DNA Damage Response , Kimiko L. Krieger

Targeted Inhibition of Histone Deacetyltransferases for Pancreatic Cancer Therapy , Richard Laschanzky

Human Leukocyte Antigen (HLA) Class I Molecule Components and Amyloid Precursor-Like Protein 2 (APLP2): Roles in Pancreatic Cancer Cell Migration , Bailee Sliker

Theses/Dissertations from 2018 2018

FOXM1 Expression and Contribution to Genomic Instability and Chemoresistance in High-Grade Serous Ovarian Cancer , Carter J. Barger

Overcoming TCF4-Driven BCR Signaling in Diffuse Large B-Cell Lymphoma , Keenan Hartert

Functional Role of Protein Kinase C Alpha in Endometrial Carcinogenesis , Alice Hsu

Functional Signature Ontology-Based Identification and Validation of Novel Therapeutic Targets and Natural Products for the Treatment of Cancer , Beth Neilsen

Elucidating the Roles of Lunatic Fringe in Pancreatic Ductal Adenocarcinoma , Prathamesh Patil

Theses/Dissertations from 2017 2017

Metabolic Reprogramming of Pancreatic Ductal Adenocarcinoma Cells in Response to Chronic Low pH Stress , Jaime Abrego

Understanding the Relationship between TGF-Beta and IGF-1R Signaling in Colorectal Cancer , Katie L. Bailey

The Role of EHD2 in Triple-Negative Breast Cancer Tumorigenesis and Progression , Timothy A. Bielecki

Perturbing anti-apoptotic proteins to develop novel cancer therapies , Jacob Contreras

Role of Ezrin in Colorectal Cancer Cell Survival Regulation , Premila Leiphrakpam

Evaluation of Aminopyrazole Analogs as Cyclin-Dependent Kinase Inhibitors for Colorectal Cancer Therapy , Caroline Robb

Identifying the Role of Janus Kinase 1 in Mammary Gland Development and Breast Cancer , Barbara Swenson

DNMT3A Haploinsufficiency Provokes Hematologic Malignancy of B-Lymphoid, T-Lymphoid, and Myeloid Lineage in Mice , Garland Michael Upchurch

Theses/Dissertations from 2016 2016

EHD1 As a Positive Regulator of Macrophage Colony-Stimulating Factor-1 Receptor , Luke R. Cypher

Inflammation- and Cancer-Associated Neurolymphatic Remodeling and Cachexia in Pancreatic Ductal Adenocarcinoma , Darci M. Fink

Role of CBL-family Ubiquitin Ligases as Critical Negative Regulators of T Cell Activation and Functions , Benjamin Goetz

Exploration into the Functional Impact of MUC1 on the Formation and Regulation of Transcriptional Complexes Containing AP-1 and p53 , Ryan L. Hanson

DNA Polymerase Zeta-Dependent Mutagenesis: Molecular Specificity, Extent of Error-Prone Synthesis, and the Role of dNTP Pools , Olga V. Kochenova

Defining the Role of Phosphorylation and Dephosphorylation in the Regulation of Gap Junction Proteins , Hanjun Li

Molecular Mechanisms Regulating MYC and PGC1β Expression in Colon Cancer , Jamie L. McCall

Pancreatic Cancer Invasion of the Lymphatic Vasculature and Contributions of the Tumor Microenvironment: Roles for E-selectin and CXCR4 , Maria M. Steele

Altered Levels of SOX2, and Its Associated Protein Musashi2, Disrupt Critical Cell Functions in Cancer and Embryonic Stem Cells , Erin L. Wuebben

Theses/Dissertations from 2015 2015

Characterization and target identification of non-toxic IKKβ inhibitors for anticancer therapy , Elizabeth Blowers

Effectors of Ras and KSR1 dependent colon tumorigenesis , Binita Das

Characterization of cancer-associated DNA polymerase delta variants , Tony M. Mertz

A Role for EHD Family Endocytic Regulators in Endothelial Biology , Alexandra E. J. Moffitt

Biochemical pathways regulating mammary epithelial cell homeostasis and differentiation , Chandrani Mukhopadhyay

EPACs: epigenetic regulators that affect cell survival in cancer. , Catherine Murari

Role of the C-terminus of the Catalytic Subunit of Translesion Synthesis Polymerase ζ (Zeta) in UV-induced Mutagensis , Hollie M. Siebler

LGR5 Activates TGFbeta Signaling and Suppresses Metastasis in Colon Cancer , Xiaolin Zhou

LGR5 Activates TGFβ Signaling and Suppresses Metastasis in Colon Cancer , Xiaolin Zhou

Theses/Dissertations from 2014 2014

Genetic dissection of the role of CBL-family ubiquitin ligases and their associated adapters in epidermal growth factor receptor endocytosis , Gulzar Ahmad

Strategies for the identification of chemical probes to study signaling pathways , Jamie Leigh Arnst

Defining the mechanism of signaling through the C-terminus of MUC1 , Roger B. Brown

Targeting telomerase in human pancreatic cancer cells , Katrina Burchett

The identification of KSR1-like molecules in ras-addicted colorectal cancer cells , Drew Gehring

Mechanisms of regulation of AID APOBEC deaminases activity and protection of the genome from promiscuous deamination , Artem Georgievich Lada

Characterization of the DNA-biding properties of human telomeric proteins , Amanda Lakamp-Hawley

Studies on MUC1, p120-catenin, Kaiso: coordinate role of mucins, cell adhesion molecules and cell cycle players in pancreatic cancer , Xiang Liu

Epac interaction with the TGFbeta PKA pathway to regulate cell survival in colon cancer , Meghan Lynn Mendick

Theses/Dissertations from 2013 2013

Deconvolution of the phosphorylation patterns of replication protein A by the DNA damage response to breaks , Kerry D. Brader

Modeling malignant breast cancer occurrence and survival in black and white women , Michael Gleason

The role of dna methyltransferases in myc-induced lymphomagenesis , Ryan A. Hlady

Design and development of inhibitors of CBL (TKB)-protein interactions , Eric A. Kumar

Pancreatic cancer-associated miRNAs : expression, regulation and function , Ashley M. Mohr

Mechanistic studies of mitochondrial outer membrane permeabilization (MOMP) , Xiaming Pang

Novel roles for JAK2/STAT5 signaling in mammary gland development, cancer, and immune dysregulation , Jeffrey Wayne Schmidt

Optimization of therapeutics against lethal pancreatic cancer , Joshua J. Souchek

Theses/Dissertations from 2012 2012

Immune-based novel diagnostic mechanisms for pancreatic cancer , Michael J. Baine

Sox2 associated proteins are essential for cell fate , Jesse Lee Cox

KSR2 regulates cellular proliferation, transformation, and metabolism , Mario R. Fernandez

Discovery of a novel signaling cross-talk between TPX2 and the aurora kinases during mitosis , Jyoti Iyer

Regulation of metabolism by KSR proteins , Paula Jean Klutho

The role of ERK 1/2 signaling in the dna damage-induced G2 , Ryan Kolb

Regulation of the Bcl-2 family network during apoptosis induced by different stimuli , Hernando Lopez

Studies on the role of cullin3 in mitosis , Saili Moghe

Characteristics of amyloid precursor-like protein 2 (APLP2) in pancreatic cancer and Ewing's sarcoma , Haley Louise Capek Peters

Structural and biophysical analysis of a human inosine triphosphate pyrophosphatase polymorphism , Peter David Simone

Functions and regulation of Ron receptor tyrosine kinase in human pancreatic cancer and its therapeutic applications , Yi Zou

Theses/Dissertations from 2011 2011

Coordinate detection of new targets and small molecules for cancer therapy , Kurt Fisher

The role of c-Myc in pancreatic cancer initiation and progression , Wan-Chi Lin

The role of inosine triphosphate pyrophosphatase (ITPA) in maintanence [sic] of genomic stability in human cells , Miriam-Rose Menezes

Molecular insights into major histocompatibility complex class I folding and assembly , Laura Christina Simone

The role of bcl-2 in colon cancer metastatic progression , Wang Wang

A rational peptidomimetic approach towards generation of high affinity BRCT (BRCA1) inhibitors , Ziyan Yuan

D-type cyclins and breast cancer , Quian Zhang

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Ovarian Cancer: An Integrated Review

Affiliations.

• 1 Carolina's Medical Center, Charlotte, NC. Electronic address: [email protected] .
• 2 Assistant Vice President Patient Care Services, Carolina's Medical Center, Rock Hill, SC.
• 3 Interim Dean, Harris College of Nursing & Health Sciences, Associate Dean for Nursing & Professor, Texas Christian University, Ft Worth, TX.
• PMID: 30867104
• DOI: 10.1016/j.soncn.2019.02.001

Objective: To provide an overview of the risk factors, modifiable and non-modifiable, for ovarian cancer as well as prevention, diagnostic, treatment, and long-term survivorship concerns. This article will also examine current and future clinical trials surrounding ovarian cancer.

Data sources: A review of articles dated 2006-2018 from CINAHL, UpToDate, and National Comprehensive Cancer Network guidelines.

Conclusion: There is no screening test for ovarian cancer and with diagnosis often in the late stages, recurrence is high in this population. Early identification can range from knowing the vague symptoms associated with the cancer to prophylactic surgical removal of at-risk tissue. Standard treatment for ovarian cancer is surgery followed by combination chemotherapy. Although advances are being made, ovarian cancer remains the most fatal female gynecologic cancer.

Implications for nursing practice: Becoming familiar with and educating women about risk factors and the elusive symptoms of ovarian cancer can increase patient autonomy and advocacy, as well as potentially improve patient outcomes for those affected by ovarian cancer.

Keywords: BRCA; gynecologic; oncology; ovarian cancer; prevention; risk factors.

Copyright © 2019 Elsevier Inc. All rights reserved.

Publication types

• Ovarian Neoplasms / diagnosis
• Ovarian Neoplasms / epidemiology*
• Ovarian Neoplasms / prevention & control
• Ovarian Neoplasms / therapy
• Risk Factors

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• Long Course Article
• Published: 17 February 2005

Origins and molecular pathology of ovarian cancer

• Debra A Bell 1  

Modern Pathology volume  18 ,  pages S19–S32 ( 2005 ) Cite this article

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Epithelial ovarian cancer comprises the majority of malignant ovarian tumors in adult women. These neoplasms are classified into distinct morphologic categories based on the appearance of the epithelium into tumors of serous, mucinous, endometrioid, clear cell, transitional, squamous, mixed and undifferentiated type. Current data indicate that each of these histologic subtypes is associated with distinct morphologic and molecular genetic alterations: high-grade serous and possibly endometrioid carcinomas most probably arise from surface epithelial inclusion glands with TP53 mutations and dysfunction of BRCA1 and/or BRCA2 ; low-grade serous carcinomas probably arise in a stepwise fashion in an adenoma–borderline tumor–carcinoma sequence from typical to micropapillary borderline tumors to low-grade invasive serous carcinoma via activation of the RAS–RAF signaling pathway secondary to mutations in KRAS and BRAF ; mucinous carcinomas arise via an adenoma–borderline tumor–carcinoma sequence with mutations in KRAS ; low-grade endometrioid carcinomas arise from endometriosis via mutations in CTNNB1 (the gene encoding β -catenin) and PTEN . Although the morphologic data strongly support an origin of clear cell carcinoma from endometriosis, there is limited data on the genetic alterations in these uncommon tumors. Thus it is likely that most low-grade, relatively indolent ovarian carcinomas of serous, mucinous and endometrioid type arise from pre-existing cystadenomas or endometriosis whereas most high-grade serous carcinomas arise without an easily identifiable precursor lesion.

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Epithelial ovarian cancer comprises the majority of malignant ovarian tumors in adult women. These neoplasms are classified into distinct morphologic categories based on the appearance of the epithelium into tumors of serous, mucinous, endometrioid, clear cell, transitional, squamous, mixed and undifferentiated type. 1 , 2 Two types of ovarian surface epithelial lesions have been described as possible precursors of these carcinomas: lesions that appear in situ in surface epithelium or surface epithelial inclusion glands (SEIG); and pre-existing benign epithelial ovarian tumors and endometriosis. The morphologic and genetic data implicating each as a precursor lesion of the major histologic subtypes of ovarian carcinoma are discussed.

Surface epithelium and surface epithelial inclusion glands as precursor lesions

Morphologic data.

Two types of morphologic data are available regarding the malignant potential of ovarian surface epithelium and inclusion glands, alterations in these structures and studies on microscopic ovarian carcinoma.

Surface epithelium and surface epithelial inclusion glands

Despite the widespread acceptance of the origin of surface epithelial cancers from the ovarian surface epithelium and its inclusion glands, only rarely have putative precursor lesions been described at these sites. Two types of lesions have been suggested as possible precursors: proliferative–metaplastic changes and cytologic atypia. Ovaries have been examined for such lesions in four settings: (1) prophylactic oophorectomy specimens from patients with a strong family history of ovarian cancer or breast cancer or both, or with known BRCA1 or BRCA2 gene mutations; (2) uninvolved ovaries contralateral to ovarian carcinomas or benign or borderline epithelial tumors or a combination of these tumors; (3) surface epithelium and epithelial inclusion glands adjacent to invasive ovarian carcinomas; (4) ovaries removed after positive or suspicious cul-de-sac aspirates performed to screen for ovarian cancer.

Unfortunately, most studies of the surface epithelium are limited by its fragility; it is usually denuded by allowing the surface to dry intraoperatively or by touching or rubbing it during removal or gross pathologic examination. 3 , 4 As a result, often all that remains for microscopic examination is residual intact epithelium either in crevasses below a gyriform surface or under the protection of fibrous adhesions.

Only rare examples of lesions showing significant epithelial atypia (severe dysplasia or carcinoma in situ ) of the ovary have been reported. 5 , 6 , 7 , 8 , 9 , 10 , 11 These lesions are characterized by stratification of cells lining the ovarian surface or epithelial inclusion glands with loss of nuclear polarity and marked nuclear pleomorphism, hyperchromasia and chromatin clumping ( Figure 1 ). In their study of cul-de-sac aspirates obtained for ovarian cancer screening, Graham et al 9 identified these changes adjacent to a microscopic serous carcinoma in one patient and in the surface epithelium of 20 additional patients with malignant cells in their aspirates. 7 , 8 Bell and Scully 6 noted severe cytologic atypia adjacent to or near incidentally detected microscopic invasive ovarian carcinomas in three of 14 women, and Gusberg and Deligdisch 5 noted such changes in two of three women whose ovaries had been removed prophylactically because of the finding of ovarian carcinoma in an identical twin. Mild-to-moderate atypia was noted in the third twin, and has also been reported in surface epithelium adjacent to grossly visible or microscopic ovarian carcinomas. 6 , 12 , 13 , 14 Ovarian carcinoma- in situ has been reported in only a single prophylactic oophorectomy specimen. This patient underwent a hysterectomy and bilateral salpingo-ooporectomy for persistent bleeding on Tamoxifen. 11 Sherman et al 4 identified mild atypia of the surface epithelium more frequently in the ovaries of women at increased risk for ovarian carcinoma (prophylactically removed ovaries from women with a strong family history of ovarian cancer or known BRCA mutations, or ovaries contralateral to ovarian cancer) than controls. Although this difference was statistically significant, the number of cases was small. Werness et al 15 were unable to identify a difference in the frequency of atypia in prophylactically removed ovaries and controls on light microscopic examination, but demonstrated a statistically significant increase in nuclear enlargement and chromatin heterogeneity in prophylactically removed ovaries morphometrically. Several other groups have failed to demonstrate epithelial atypia in the prophylactic oophorectomy specimens from women with a strong family history of ovarian cancer 16 or with known BRCA1 or 2 mutations. 17 , 18 Two groups of investigators have noted mild atypia of the surface epithelium in uninvolved ovaries contralateral to ovarian carcinomas or borderline tumors; 4 , 19 the latter group, however, failed to detect atypia in epithelial inclusion glands. Several other investigators were unable to demonstrate a statistically significant increase in atypia in ovaries contralateral to ovarian tumors over control ovaries. 20 , 21 Deligdisch et al 22 have noted ‘ovarian dysplasia’ as detected by a morphometric method utilizing discriminant analysis based on nuclear area and texture in both prophylactic oophorectomy specimens and in epithelium adjacent to carcinomas.

Ovarian carcinoma in situ . The epithelium is thickened by stratified cells showing loss of nuclear polarity and marked nuclear pleomorphism, hyperchromasia and chromatin clumping.

Although early studies had suggested that proliferative or metaplastic changes of the ovarian surface epithelium such as papillae, epithelial stratification and tufting, and metaplasia are precursors of ovarian carcinoma, 23 similar findings have been reported to be increased in frequency in only one more recent large series of prophylactic oophorectomy specimens from women with a strong family history of ovarian cancer. 16 The remainder of the recent studies 4 , 15 , 17 , 18 , 24 have failed to demonstrate any differences in the frequency of these histologic features between cases and controls. A few such studies have shown an increase in the number of inclusion cysts in prophylactic oophorectomy specimens 15 and in ovaries contralateral to ovarian carcinoma, 25 others have failed to confirm these findings. 16 , 19 , 20 , 21

Microscopic surface-epithelial carcinomas

A very small number of microscopic or tiny gross carcinomas have been reported, usually as incidental findings at operations for other gynecologic disorders or, more recently, in prophylactic oophorectomy specimens from patients at high risk for the development of ovarian carcinoma. 6 , 8 , 9 , 16 , 22 , 26 , 27 , 28 The largest study of such cases and the only one to include meaningful follow-up data was reported prior to widespread BRCA mutation testing and comprised 14 cases of ovarian carcinomas that had not been recognized preoperatively, intraoperatively or even on gross examination of the ovaries but were discovered only on microscopic examination. 6 The patients ranged in age from 27 to 65 (mean 50) years. Three women had a family history of ovarian cancer, six did not, and the family history was unknown or unreliable in the remaining cases. All of the tumors were incidental findings in patients operated on because of a gynecologic indication that did not include a suspicion of ovarian cancer. The tumors ranged in diameter from less than 1 to 7 mm. All of them were unilateral and four appeared to be multifocal. Surface involvement was found in five of the 13 cases in which this feature could be evaluated. The tumors had the typical microscopic features of larger clinically apparent tumors of the same cell type and were classified as serous in 10 cases, endometrioid in one, clear cell in one and undifferentiated in two. In all, 12 of the 14 tumors were grade 2 or 3 ( Figure 2 ). Follow-up data of 2 or more years duration were available for 10 of the 14 patients. Five of the seven whose diagnoses had been made prospectively at the time of oophorectomy were alive without recurrence 2–12 years postoperatively. At the time of publication of the series one patient was alive with recurrent tumor and one had died of tumor. Subsequently, at least one patient originally categorized as alive without recurrence had died of tumor. Two of the three women whose ovarian tumors had been diagnosed for the first time on retrospective microscopic examination of previously removed ovaries after the development of peritoneal carcinomatosis 6, 7 and 10 years subsequently died and the third was alive with recurrent tumor.

High-grade serous microcarcinoma. The tumor is present on the ovarian surface and in the superficial cortex.

Recent studies on prophylactic oophorectomy specimens from women with BRCA 1 or 2 mutations have revealed surprisingly few cases of early ovarian carcinoma (three at the date of this review). 22 , 28 , 29 , 30 One of these patients died of tumor. 29

Clearly, although the data are limited, the prognosis of patients with minute ovarian epithelial cancers is guarded. It is unclear, however, whether the subsequent peritoneal tumor in these women reflect late metastasis from the ovarian carcinoma or the development of a second primary tumor of the peritoneum. Further studies are necessary to answer this question.

Fallopian tube as the primary site of origin of epithelial ovarian carcinoma

Although very few cases of ovarian carcinoma- in situ or severe cytologic atypia or minute carcinomas have been identified in prophylactic salpingo-oophorectomy specimens, each such study that has included careful sampling of the fallopian tubes has reported examples of tubal carcinoma- in situ or severe atypia or small tubal carcinomas, especially in women with BRCA1 mutations. 30 , 31 , 32 , 33 , 34 These findings have engendered speculation that ‘ovarian’ carcinomas in women with BRCA1 mutations may originate from undetected exfoliated tubal carcinomas 30 , 33 , 35 and have led to the suggestion that ovarian and fallopian tube carcinomas in women with BRCA mutations should be termed ‘female adnexal carcinoma’. 24 , 35

Molecular Genetic Data

Surface epithelial inclusion glands.

Only a small number of studies have examined the molecular genetic features of surface epithelium, its inclusion cysts or early carcinomas. Several small studies have examined the immunohistochemical expression of proliferation and differentiation-related proteins in nonatypical ovarian surface epithelium and SEIG in prophylactic oophorectomy specimens compared to controls. 15 , 18 , 24 , 36 , 37 Most of these studies failed to document differences in expression of p53, c-erbB2, and Ki67 in surface epithelium or SEIG. Additionally, Piek et al 24 also failed to note differences in expression of p21, p27, cyclin A, cyclin D, and estrogen receptor in surface epithelium or SEIG in prophylactic oophorectomy specimens vs controls. They did note increased expression of bcl-2 and progesterone receptor in SEIG epithelium in prophylactic oophorectomy specimens, however. In contrast, one study (36,37) found p53 overexpression in cortical clefts or inclusion cysts in 10 of 37 patients with BRCA mutations, and TP53 mutations in three of these, two of which showed loss of heterozygosity (LOH) of wild-type BRCA 1 or 2 alleles. Nnene et al 38 have noted that an increased level of morphologic abnormalities of ovarian surface epithelium and SEIG is associated with expression of p53 in normal ovaries, suggesting that abnormalities of p53 are an early event.

High-grade serous carcinomas

It has been well established that TP53 mutations are frequent in both hereditary and sporadic high-grade serous carcinoma. 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 It has also been demonstrated that loss of BRCA1 or BRCA2 function by a variety of mechanisms is present in the majority of both sporadic and hereditary high-grade serous and endometrioid carcinomas. 48 , 49 Boyd and co-workers 36 , 37 and Mok and Bell (unpublished data) demonstrated TP53 mutations in microcarcinomas and Werness et al 11 demonstrated loss of heterozygosity at BRCA1 and TP53 and overexpression of p53 in one microscopic ovarian surface carcinoma- in situ . A few studies have examined genetic abnormalities in surface epithelium or SEIG adjacent to coexisting conventional serous carcinoma. Hutson et al 10 demonstrated overexpression of p53 in SEIG associated with coexisting carcinoma. and Boyd and coworkers 36 , 37 demonstrated the same mutation in the carcinoma and the adjacent normal or atypical epithelium in a small number of cases. These data suggest that mutation of TP53 is an early event in the development of ovarian carcinoma and is present prior to stromal invasion. Additionally, Shridhar et al 50 found that early (Stage I) compared to advanced (Stage III) carcinomas (that were mostly high-grade serous carcinomas) have similar patterns of gene expression.

Conclusions

These data demonstrating increasing atypia and common and accumulating genetic alterations in surface epithelial inclusion glands, ovarian ‘carcinoma in situ ’, microcarcinomas and typical high-grade serous carcinoma suggest that high-grade serous and perhaps endometrioid ovarian adenocarcinomas arise from these structures. Additionally, the data from a small number of cases indicates that TP53 mutation occurs in preinvasive epithelium with loss of BRCA1 or BRCA2 function in the majority of tumors, findings compatible with the high degree of genetic instability of these tumors. The suggestion that ovarian carcinomas are surface implants of occult fallopian tube carcinomas is deserving of further study.

Benign and borderline serous tumors as precursor lesions

Whether surface epithelial cancers arise in pre-existing benign or borderline epithelial tumors of the same cell type and, if so, how often, has been specifically studied only recently. Benign ovarian neoplasms are almost always removed as soon as they are detected, and therefore their natural history is largely unknown. Evidence of a benign to malignant transformation is largely circumstantial and includes: (1) a generally observed older-age incidence of carcinomas than benign tumors of the same cell type; in that most investigators have reported progressively higher mean ages for benign, borderline, and invasive tumors in both the serous and mucinous categories, with average ages for the combined categories 44, 48 and 56 years, respectively; 51 (2) a reported five-fold increase in the frequency of benign epithelial tumors in first- and second-degree relatives of women with ovarian carcinoma; 52 (3) the presence of enlarging ovarian cysts on ultrasound prior to the development of carcinoma, 53 and (4) the frequent observation of various combinations of benign, borderline, and invasive neoplasia within the same specimen; 54 , 55

Benign serous tumors

Several studies have shown a relatively low frequency of coexisting benign serous epithelium and serous carcinomas (the great majority of which were high grade) of 15–56%, and it is unusual to encounter a high-grade serous carcinoma as an incidental finding in a serous cystadenoma or borderline tumor, although such cases are rarely encountered. 54 , 55 , 56

Serous borderline tumors

It is rare to see high-grade serous carcinoma arising in a serous borderline ovarian tumor of either typical or micropapillary type. It has been shown recently, however, that the majority of low-grade invasive serous ovarian carcinomas arise in association with serous borderline ovarian tumors of micropapillary type, 57 which in turn usually coexist with serous borderline tumors of the typical type ( Figure 3a–d ). 57 , 58 , 59 , 60 , 61

Probable progression of serous borderline tumor to invasive low-grade serous carcinoma. ( a ) Typical serous borderline tumor. ( b ) Typical serous borderline tumor (lower portion of field) coexisting with micropapillary serous borderline tumor. ( c ) Micropapillary serous borderline tumor. ( d ) Micropapillary serous borderline tumor with stromal invasion by low-grade serous carcinoma (right).

Most studies have not detected p53 overexpression or TP53 mutations (which are common in high-grade serous carcinomas) in serous cystadenomas. 62 , 63 , 64 , 65 However, a recent study utilizing microdissection 66 found TP53 mutations in 6% (2/24) of benign serous tumors. Zheng et al 67 and Wolf et al 68 found that benign cysts in continuity with serous carcinomas have similar cytogenetic and mutational changes, suggesting that such cysts already have genetic abnormalities that predispose them to malignant transformation. An alternative interpretation is that such benign-appearing epithelium represents morphologic maturation of malignant epithelium and does not indicate a benign precursor lesion. Thomas et al 66 noted a surprisingly high frequency of LOH of 73% on at least one chromosome arm in benign serous tumors when 56 microsatellite markers on chromosomes 6, 7, 9, 11 and 17 (chromosomes that exhibit frequent LOH in typical ovarian carcinomas) were analyzed. The specific frequencies of LOH were 8, 23, 7, 10 and 7% for chromosomes 6, 7, 9, 11 and 17, respectively. In contrast, Tapper et al 69 found significant differences in gene expression between benign and malignant serous ovarian tumors.

Serous borderline tumors compared to high- and low-grade serous carcinoma

Most studies of serous neoplasms have shown different molecular changes in serous cystadenomas, borderline tumors and high-grade carcinomas, indicating that in most cases these tumor types develop via different genetic pathways. 42 , 70 , 71 , 72 , 73 , 74 TP53 mutations and p53 immunohistochemical overexpression are uncommon in borderline serous tumors, whereas approximately 60% of high-grade serous carcinomas have detectable mutations or overexpression of TP53 . 38 , 39 , 40 , 41 , 42 , 44 , 45 Serous borderline tumors have a higher rate of KRAS mutations (27–36%) than high-grade serous carcinomas (0–12%). 40 , 46 , 47 , 75 , 76 , 77 , 78 BRAF mutations, which are seen in 33–50% of serous borderline tumors of typical or micropapillary type, have not been identified in high-grade serous carcinoma. 74 , 76 , 78

A few studies analyzing and comparing serous borderline tumors and low-grade serous carcinomas have been performed only recently. These studies have found a similar frequency of KRAS mutations in approximately one-third of typical or micropapillary serous borderline tumors and invasive low-grade serous carcinomas (invasive micropapillary serous carcinoma), and BRAF mutations in an additional similar proportion. Interestingly, KRAS and BRAF mutations are present only very rarely in the same neoplasm; thus, in aggregate these mutations are present in 60% of serous borderline ovarian tumors and 68% of low-grade serous carcinomas. 74 , 76 , 78 In contrast, BRAF mutations have not as yet been reported in high-grade conventional serous carcinoma and KRAS mutations have been reported only rarely (0–12%). 46 , 74 , 76 , 78

Studies utilizing other techniques have also demonstrated substantial differences between borderline tumors and/or low-grade serous carcinomas and high-grade serous carcinomas. One study has demonstrated that the allelic imbalance index gradually increases from typical to micropapillary serous borderline tumor to invasive low-grade serous carcinoma in contrast to the finding of high levels of allelic imbalance in even tiny high-grade ovarian serous carcinomas, 73 (Mok, Bell unpublished data). Comparative genomic hybridization (CGH) studies have also demonstrated differences between low- and high-grade serous carcinomas in that high-grade serous carcinomas showed significantly higher CNA frequencies than low-grade tumors. 79 , 80 , 81 Differences between low- and high-grade tumors were also demonstrated genetically. High-grade carcinomas showed under-representation of 11p and 13q, and over-representation of 8q and 7p, while 12p under-representation and 18p over-representation were present significantly more frequently in well and moderately differentiated tumors. 82

These findings suggest that invasive low-grade serous carcinomas (or invasive micropapillary serous carcinomas) and high-grade serous carcinomas arise via different pathways, with low-grade carcinomas most probably arising in an adenoma–carcinoma sequence, with a progression from typical to micropapillary borderline tumors to invasive low-grade carcinoma via alteration of the RAS–RAF signaling pathway by mutations in either KRAS or BRAF . 73 , 74 , 75 , 76 , 77 , 78 , 79

These data indicate that low- and high-grade serous carcinomas, in the great majority of cases, arise via different genetic pathways. Low-grade serous carcinomas most probably arise via an ‘adenoma–borderline tumor-carcinoma’ progression from typical to micropapillary serous borderline tumor to low-grade serous carcinoma via alteration of the RAS–RAF signaling pathway secondary to mutations in KRAS and BRAF . As noted in the previous section, high-grade serous carcinomas most probably arise from SEIG in the great majority of cases with TP53 mutations and BRCA1 or BRCA2 dysfunction.

Benign and borderline mucinous tumors as precursor lesions

The studies of Scully et al 54 and Puls et al 55 showed coexisting benign mucinous epithelium in primary ovarian mucinous carcinomas in 74–90% of cases. Several recent detailed studies of invasive primary mucinous ovarian carcinomas of gastrointestional type showed coexisting mucinous borderline tumor in 67–69% of cases ( Figure 4a, b ). 83 , 84 The two studies describing endocervical-like mucinous carcinomas reported coexisting Mullerian mucinous or mixed cell type borderline tumors in 75–100% of cases. 85 , 86 These morphologic findings are highly suggestive that mucinous carcinomas arise from pre-existing benign and borderline mucinous tumors.

Probable progression of mucinous cystadenoma to mucinous carcinoma. ( a ) Mucinous cystadenoma (left) with a transition to mucinous borderline tumor (right). ( b ) Mucinous borderline tumor (right) in continuity with mucinous carcinoma (left).

Greater similarities in mutation rates and overexpression of oncogenes and tumor suppressor genes have been reported in benign, borderline and malignant mucinous tumors than serous tumors. Most studies have shown a high and increasing frequency of KRAS mutations in mucinous cystadenomas, borderline tumors and carcinomas, ranging from 33 to 86%. 47 , 70 , 72 , 75 , 87 , 88 Several groups 75 , 87 , 88 have noted similar KRAS mutation patterns in benign, borderline and malignant mucinous areas within the same neoplasm, which suggests that KRAS mutation is an early event in mucinous tumorigenesis. It has also been noted that the rate of TP53 mutations is lower in mucinous borderline tumors than mucinous carcinomas (13 vs 40%). 38 , 70 , 77 In contrast to serous borderline tumors, mucinous borderline tumors have not shown BRAF mutations. 78 , 89 These data suggest that ovarian mucinous carcinomas arise via an adenoma–borderline tumor–carcinoma sequence with activation of the RAS–RAF signaling pathway by KRAS mutations. 78 , 89

The majority of mucinous ovarian carcinomas arise via an adenoma–borderline tumor–carcinoma sequence with activation of the RAS–RAF signaling pathway secondary to KRAS mutations.

Endometriosis as a precursor lesion

Endometriosis, particularly cystic ovarian endometriosis, has been shown to be related to an increased risk of developing ovarian endometrioid and clear cell carcinoma in several epidemiologic studies. 90 , 91 , 92 , 93 , 94 Endometriosis-associated ovarian carcinomas are more frequently low-grade and low stage and have a more favorable prognosis than carcinomas not associated with endometriosis. 90 It has also been noted in one clinical study that 20% of endometrioid and 88% of clear cell carcinomas were preceeded by an ultrasonographically detected endometriotic cyst. 53

Many types of neoplasms have been documented to arise in endometriosis morphologically, particularly endometrioid and clear cell carcinomas, and rarely, other types of surface epithelial carcinomas and even mesenchymal tumors such as endometrioid stromal sarcoma. 1 , 95 , 96 , 97 , 98 Endometrioid carcinoma has been reported to originate directly from endometriotic tissue in up to 24% of the cases in various series ( Figure 5 ). Ipsilateral ovarian endometriosis has been detected in 11–31%, ovarian endometriosis of unspecified laterality in 9–20%, and pelvic endometriosis in 11–28% of cases of ovarian endometrioid carcinoma. 96 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 Well-differentiated or low-grade endometrioid ovarian carcinomas are associated with an especially high frequency of associated endometriosis (63%) or endometrioid adenofibromas (47%). 108

Endometrioid adenocarcinoma arising in endometriosis.

Russell 104 reported a 47% frequency of pelvic endometriosis in 30 cases of clear cell carcinoma of the ovary, and Aure et al 99 demonstrated a 24% frequency of ovarian endometriosis in 59 cases of the same type of tumor; both of those figures were surprisingly higher than the figures given by the same authors for the association of endometriosis with endometrioid carcinoma (28 and 9%, respectively). Although isolated examples of serous and mucinous carcinoma have been reported to originate in endometriosis, the association of these tumors in general with that disorder is not significant. Russell 104 found only a 2.5% frequency of pelvic endometriosis in 163 cases of serous carcinoma and a 6% frequency in 17 cases of mucinous carcinoma; and Aure et al 99 detected no ovarian endometriosis in 283 cases of serous carcinoma and only an 0.8% frequency, in 203 cases of mucinous carcinoma. Rutgers and Scully, 109 however, reported the finding of ovarian endometriosis in 30% of cases of mucinous borderline tumors of endocervical-like (Müllerian) type, which accounted for 15% of the mucinous borderline tumors in their series; in contrast, there was no significant association of ovarian endometriosis and the more common mucinous borderline tumor of intestinal type. Borderline tumors of mixed Müllerian epithelial cell types also have a frequent association with ovarian endometriosis. 110

Hyperplasia in endometrosis as a precursor lesion

Because carcinoma of the endometrium often arises on a background of hyperplasia with cytologic and architectural atypicality, one might expect that a proportion of carcinomas arising in endometriosis would have similar precursors. Hyperplasia with varying degrees of architectural and cytologic atypia resembling that seen in the endometrium occurs in 2–7% of cases of ovarian endometriosis or ovarian endometriotic cysts without coexisting carcinoma and in 67–100% of endometriosis associated with coexisting carcinoma ( Figure 6 ). 1 , 95 , 111 , 112 , 113 , 114 , 115 , 116 The prognostic significance of such changes is unclear because follow-up data have been limited to only a small number of women. Seidman 113 reported follow-up information on 13 women with complex atypical hyperplasia and seven women with ‘early carcinoma’, arising in ovarian endometriosis. All the women with complex atypical hyperplasia were followed for a mean of 8.5 years and survived without the development of carcinoma, however, most of the lesions were completely excised. Similarly, the four women with ‘adenomatous hyperplasia’ in ovarian endometriosis in the report of Czernobilsky and Morris 111 were followed for 3–5 years without recurrence or the development of carcinoma, although 10 of their 11 patients with ‘adenomatous hyperplasia’ or severe atypia of cyst lining epithelium were treated by oophorectomy, presumably excising completely the atypical lesion. We have observed one case, however, in which the left ovary of a 55-year-old woman, which contained severely atypical endometriotic tissue, was dissected away from the pelvic wall; she received estrogen therapy for 3 years, and subsequently returned with an endometrioid adenocarcinoma that had arisen in the area where ovarian tissue had presumably been left behind. The outcome in this case is interesting in light of epidemiologic studies that have demonstrated a significant increase in the incidence of endometrioid carcinoma of the ovary in women on estrogen therapy 117 , 118 and in view of the number of reported cases of carcinoma developing in endometriosis in women receiving replacement therapy with estrogens unopposed by progesterone. 98

Atypical endometrial-like hyperplasia arising in an ovarian endometriotic cyst.

Early carcinoma in endometriosis

Early carcinoma developing in an endometriotic cyst has also been specifically described in detail in only a few studies. Seidman 113 reported 11 examples of ovarian endometriosis containing foci that fulfilled the Kurman and Norris 119 criteria for endometrioid carcinoma of the endometrium. Seven women were followed for a mean of 8.6 years; in ‘most’ of the cases the lesions had been completely excised. Nevertheless, three of them had an adverse outcome. One had a poorly differentiated adenocarcinoma of the anterior vaginal wall 8.1 years later, one had an endocervical-like mucinous borderline tumor in the contralateral ovary 7 years later and the third patient was found to have ‘early carcinoma’ in foci of endometriosis in the contralateral ovary and the omentum 3 months after the initial diagnosis. Thus, although the prognosis of an individual completely excised example of early carcinoma arising in endometriosis is excellent, carcinoma may arise in residual foci of endometriosis at the same or other sites. For this reason, close follow-up of women with early carcinoma arising in endometriosis is warranted.

Atypical cyst lining cells as a precursor lesion

Two additional atypical lesions encountered in endometriosis—but rarely, if ever, in the endometrium—are characterized by cells showing varying degrees of atypia lining endometriotic cysts without endometrial glandular hyperplasia. In the first type, which comprises most of these cases, the lining epithelium is composed of a single layer of large polygonal cells with abundant eosinophilic cytoplasm and large hyperchromatic, often smudged nuclei. Acute inflammation is frequently present ( Figure 7 ). 113 , 115 , 120 , 121 In the second less common type, large polygonal cells and hobnail cells are present with epithelial stratification and tufting. These cells may have eosinophilic, clear, or vacuolated cytoplasm and may contain intracytoplasmic mucin; their nuclei are usually markedly hyperchromatic and pleomorphic. This type of epithelium may also be associated with acute inflammation 111 , 113 , 114 , 120 , 122 , 123 and with mucinous endocervical-like (Mullerian) borderline tumors. 109 , 121 Seidman 113 obtained follow-up on 20 of 37 women with these two types of cyst lining atypias and found that the patients were all alive without the development of carcinoma after a mean of 8.6 years; ‘most’ of the lesions, however, were completely excised. Czernobilsky and Morris 111 reported that seven women with the second type of lining atypia were followed for 3–5 years without the development of carcinoma; again, most of the lesions were completely excised. Based on this data, Seidman 113 concluded that endometriotic cyst lining atypia was probably reactive or degenerative. In contrast, Moll et al 122 described a case in which a resected endometriotic cyst was lined by stratified, severely atypical hobnail cells; 3 years later, the patient had a clear cell carcinoma in the residual ovarian tissue; these authors suggested that such lining changes are preneoplastic. A single study of ploidy of atypical cyst lining cells has been performed. The investigators noted that all of the cases with ‘mild’ atypia and no stratification were diploid, but that three of six cases with ‘severe’ atypia, stratification and tufting, were aneuploid, suggesting a neoplastic potential. 120

Endometriotic cyst lined by atypical cells with eosinophilic cytoplasm.

• Endometriosis

A small number of studies have analyzed genetic alterations in endometriosis unassociated with carcinomas. 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 They have shown that most benign-appearing ovarian endometriotic cysts are monoclonal. 124 , 125 , 129 , 130 , 131 Jiang et al 124 , 132 have shown loss of heterozygosity at several loci on chromosomes 9q, 11q and 22q in less than 20% of ovarian endometriotic cysts and Sato et al 126 found a higher frequency of LOH of 56% at 10q23.3. PTEN mutations have been noted in 21% of endometriotic cysts. 126 Several studies have failed to demonstrate either mutations or overexpression of p53 127 , 128 , 133 or KRAS mutations 128 in benign endometriotic cysts.

Endometrioid carcinoma

Low-grade ovarian endometrioid adenocarcinomas have been shown to have different genetic alterations than other histologic subtypes. 126 , 127 , 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 Mutations of CTNNB1 , the gene that encodes β -catenin have been reported in 16–54% of cases. 134 , 135 , 136 , 137 , 138 , 139 , 140 Tumors associated with such mutations are more frequently low-grade and stage and have a favorable prognosis. 134 , 135 , 139 PTEN , which is frequently mutated in endometrioid carcinomas of the endometrium is mutated in approximately 20% of ovarian endometrioid carcinomas. 126 , 128 TP53 mutations or overexpression or both have been reported in 42–63% of ovarian endometrioid adenocarcinomas. 127 , 128 Microsatellite instability has been reported in 12–19% of ovarian endometrioid adenocarcinomas. 140 , 141

A small number of studies have examined ovarian endometrioid adenocarcinomas and adjacent synchronous endometriosis for common genetic events. Jiang et al 132 have demonstrated that endometriosis and adjacent endometrioid carcinoma share common genetic events such as loss of heterozygosity at the same loci involving the same allele, and have the same pattern of X chromosome inactivation (albeit in only two of two cases examined). Similarly, several groups of investigators have documented identical PTEN mutations and LOH patterns at 10q23 in endometriotic cysts or endometriosis coexisting with endometrioid carcinomas. 126 , 142 These findings are consistent with the morphologic observations of endometrioid carcinoma arising in endometriosis with mutations of PTEN and CTNNB1 .

In contrast, high-grade or poorly differentiated endometrioid carcinomas have demonstrated similar genetic alterations to high-grade serous carcinoma. 49

Clear cell carcinomas

Because of their rarity, much less data are available regarding the genetic alterations in clear cell adenocarcinomas. Recent molecular genetic studies have shown significantly lower TP53 mutation rates and LOH rates at 17p13 143 in clear cell carcinomas than in other types of ovarian carcinomas and several studies have demonstrated that gene expression profiles may distinguish clear cell carcinoma from other histologic subtypes. 144 , 145 One study has shown identical LOH patterns at 10q23 and PTEN mutations in endometriotic cysts adjacent to clear cell carcinomas. 126 These findings suggest that some clear cell tumors arise from ovarian and pelvic endometriosis.

At least a subset of low-grade endometrioid adenocarcinomas arise from ovarian endometriosis with mutations of CTNNB1 ( β -catenin) and PTEN , probably progressing through endometrial-like hyperplasia as an intermediate step. High-grade endometrioid carcinomas probably arise via a different pathway involving TP53 mutations.

The morphologic and molecular genetic data support different pathways of development for each of the major histologic types of ovarian carcinoma:

Low- and high-grade serous carcinoma most probably arise via different pathways, the former progressing along an adenoma–borderline tumor–carcinoma sequence involving mutations in KRAS and BRAF and the latter from alterations in surface epithelial inclusion glands involving mutations of TP53 and dysfunction of BRCA1 and/or BRCA2 .

Mucinous carcinomas most probably arise via an adenoma–borderline tumor–carcinoma sequence with mutations of KRAS .

Endometrioid carcinomas arise from endometriosis with mutations of CTNNB1 (the gene encoding β -catenin) and PTEN.

The genetic alterations in clear cell carcinoma are the least investigated but also support an origin from endometriosis.

The data also suggest that most lowgrade, relatively indolent ovarian carcinomas of serous, mucinous and endometrioid type arise from pre-existing cystadenomas or endometriosis, whereas most high-grade serous carcinomas arise without an easily identifiable precursor lesion.

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Debra A Bell

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Bell, D. Origins and molecular pathology of ovarian cancer. Mod Pathol 18 (Suppl 2), S19–S32 (2005). https://doi.org/10.1038/modpathol.3800306

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Received : 27 August 2004

Accepted : 27 August 2004

Published : 17 February 2005

Issue Date : February 2005

DOI : https://doi.org/10.1038/modpathol.3800306

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Ovarian cancer.

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• Continuing Education Activity

Ovarian cancer is one of the most common causes of cancer-related deaths in women of developed nations. They should be diagnosed early for better chances at curing it to avoid the high rates of morbidity and mortality. This article reviews the epidemiology, risk factors, pathophysiology, histopathology of ovarian cancer and also highlights the role of the interprofessional team in the management of this condition along with a discussion of few landmark trials and recent ongoing trials impacting the future treatment regimens and subsequent prognosis of patients with this disease.

• Describe the epidemiology of ovarian cancer.
• Review the evaluation of a patient with suspected ovarian cancer.
• Summarize the treatment options of ovarian cancer.
• Outline some interprofessional team strategies that can result in better care coordination for patients presenting with ovarian cancer.
• Introduction

Ovarian cancer is the leading cause of death in women diagnosed with gynecological cancers. It is also the fifth most frequent cause of death in women, in general. [1]  Most of the cases are diagnosed at an advanced stage, which leads to poor outcomes of this disease. The existing screening tests have a low predictive value contributing further to this misery. Detailed gynecological evaluation along with transvaginal ultrasound and laboratory marker like cancer antigen-125 (CA-125) assay are the key early detection strategies which have shown no significant beneficial effect in the morbidity or mortality of this cancer. [2]  

The standard line of care treatment includes surgery and platinum-based chemotherapy; however, anti-angiogenic bevacizumab and Poly(ADP-ribose) polymerase (PARP) inhibitors have gained momentum in the management of this gynecological malignancy in the past decade. [3]  

A high rate of recurrence following the initial treatment has been observed. Most of these relapsed cases are less curable and known to have an increased incidence of treatment failures. Hence, effective prevention and detection strategies and new treatment modalities based on a better understanding of molecular characterization of this cancer are the need of the hour. This article reviews the epidemiology, risk factors of ovarian cancer and also highlights the evaluation and multidisciplinary approach in the management of this condition, along with a discussion of a few of the recent ongoing trials.

There are various risk factors associated with ovarian cancer. It mostly affects postmenopausal women, where increasing age is associated with an increased incidence, advanced stage of this disease, and lower reported survival rates. Parity poses a protective role according to a few case-control studies with higher age at childbirth linked to a decreased risk of ovarian cancer. [4]  The strongest risk factor of ovarian cancer is a positive family history of breast or ovarian cancer, where a personal history of breast cancer also augments the risk. [5]  Several studies have shown an increased risk of smoking, especially the risk of mucinous epithelial tumors. [4]

• Epidemiology

In 2020, there are approximately 21,750 new ovarian cancer cases, which comprises 1.2% of all cancer cases. The estimated number of deaths related to it are 13,940. The 5-year relative survival rate is expected to be 48.6%. Around 15.7% of the ovarian cancer cases are diagnosed at the local stage, and about 58% at the metastasized stage, where the 5-year survival dips down to 30.2% instead of 92.6% if detected at an early stage of local spread. An average incidence rate per 100,000, age-adjusted to the 2000 US standard population is 11.1 in 2012-2016. The incidence is highest in non-Hispanic whites (11.6 per 100,000), followed by American Indians and Alaska Natives (10.3 per 100,000), Hispanics (10.1 per 00,000), non-Hispanic blacks, and Asian and Pacific Islanders. Ninety percent of ovarian cancers are epithelial, with the serous subtype being the most common. Age-adjusted rates of new ovarian cancer cases are on a reducing trend based on statistical models of analysis. [6]

• Histopathology

The four most common histological types of epithelial ovarian cancer are serous, endometrioid, clear cell, and mucinous tumor.  They have further subtypes based on their peculiar biology and treatment responses. The uncommon subtypes are Brenner and seromucinous.

Ovarian cancer can be further classified into two subtypes- Type I or Type II tumors, the latter being a more fatal variant, thought to be caused by continuous ovarian cycles leading to inflammation and endometriosis. Type I tumor includes low-grade serous, endometrioid, clear-cell, and mucinous carcinomas, with the rare subtypes being seromucinous and Brenner tumors. Type I tumors mostly arise from atypical proliferative (borderline) tumors. Type II tumors include high-grade serous carcinoma, carcinosarcoma, and undifferentiated carcinoma, which mainly originate from serous tubal intraepithelial carcinoma. Type I tumors usually present at an early stage and are low grade except for clear cell, which is considered high grade. Their proliferative activity is usually low. They are diagnosed early and carry a good prognosis. In comparison, Type II tumors are high-grade tumors and almost always of advanced stage. They have high proliferative activity with rapid and aggressive progression and a high degree of chromosomal instability compared to type I with the presence of p53 mutations in most of the cases. [7]

Ovarian serous carcinoma is the most common subtype of ovarian carcinoma. It presents as low-grade (10% of all the serous subtype tumors) or high-grade carcinoma (90% of all the serous subtype tumors).  The low-grade subtype (LGSC) shows minimal nuclear atypia, rare mitosis, and lesser molecular abnormalities. In contrast, the high-grade subtype (HGSC) shows significant nuclear atypia and mitosis (>12 per 10 high-power fields) with more copies of molecular abnormalities as seen by cytogenetic analysis. [8] LGSCs are usually diagnosed at a young age and carry a better prognosis than HGSCs, which tend to present at an older age with a 10-year mortality rate of 70%. [9]  Further analysis revealed that a high frequency of KRAS and BRAF mutations are found in low-grade serous carcinoma, whereas high-grade serous carcinoma shows a high frequency of p53 and BRCA 1 and 2 genes mutations with an absence of KRAS/BRAF mutation. [8]  

Ovarian endometrioid carcinomas have been postulated to be derived from endometriosis. Morphologically, their cut sections reveal cystic areas showing soft masses and bloody fluid, with less common solid areas showing extensive hemorrhage and necrosis. No major molecular markers have been studied in this subtype; however, the beta-catenin gene mutation is noted to be one of the most common molecular abnormalities. One can differentiate between the endometrioid carcinoma arising from ovaries and uterus based on the molecular studies, even though they appear quite similar morphologically. Ovarian endometrioid cancers have microsatellite instability and PTEN alterations less frequently than the ones arising from the uterine cavity. [8]  Single ovarian carcinoma is found to have a less frequency of beta-catenin mutation as compared to synchronous tumors. [10] They are usually diagnosed at an earlier stage, offering a better prognosis to women with this histological subtype of ovarian cancer.

Ovarian mucinous carcinoma (MOC) is often heterogeneous, where a mixture of elements, including benign and malignant tumors, are found in a single specimen. KRAS mutations are common in these tumors. As commonly associated with metastases from the gastrointestinal tract (GI), the intestinal subtype will show the presence of glands with architectural and cytology clinical features of adenocarcinoma; however, it may lack stromal invasion. [8] It is hard to distinguish primary ovarian mucinous carcinomas from metastatic mucinous appendix tumors due to their close association, hence many gynecologic oncologists practice routine appendectomy in all these patients with MOC. [11] Evidence of micro invasions is less commonly found in intestinal subtype borderline tumors. Invasive mucinous carcinoma is uncommon, and the prognosis is found to be favorable compared to serous subtype, considering the mostly diagnosed at stage I itself, about 80%. [8] The molecular alterations responsible for malignant conversion of the benign mucinous tumor is still unknown.

Ovarian clear cell carcinomas are less prevalent and account for <5% of ovarian carcinoma. Histopathologically they show cellular clearing, cystic growth pattern, and a characteristic hobnail growth pattern. Immunohistochemically, overexpression of BAX in stage I and stage II tumors is predominant, whereas anti-apoptotic protein BCL-2 is expressed more in metastatic lesions than in primary lesions.  A lower relative BCL-2/BAX ratio is found in early-stage ovarian clear cell carcinoma tumors as compared to the higher relative ratio found in metastatic lesions. [8] They are also commonly diagnosed in earlier stages and hence carry a good prognosis, similar to endometrioid cancers.

Cytokeratin-7 (CK7) shows diffuse and strong staining in all serous ovarian tumors. It is positive in 80% to 100% of mucinous ovarian tumors, and other ovarian epithelial tumors also show positivity for CK7. About 96% of ovarian adenocarcinomas were positive for CK7 compared to metastatic colorectal, which shows about a 25% positivity.

• History and Physical

Symptoms of ovarian cancer are non-specific, and hence they can be easily missed at an early stage as the symptoms can be attributed to other possible disease processes. The symptoms often become apparent in the late stage (stage III or stage IV). The presenting symptoms include a combination of abdominal fullness, bloating, nausea, abdominal distention, early satiety, fatigue, change in bowel movements, urinary symptoms, back pain, dyspareunia, and loss of weight. The symptoms occur vaguely months before the diagnosis of ovarian cancer. [12]

A thorough physical examination should be done, including rectovaginal examination on an empty bladder to look for pelvic and abdominal masses in clinical cases of high suspicion. In advanced cases, a palpable pelvic mass or ascites or diminished breath sounds due to the presence of pleural effusions can also be found. As a result of metastases to the umbilicus, a sister Mary Joseph nodule will rarely be seen. Sign of Lesar-Trélat, which refers to a sudden increase in the finding of seborrheic keratosis, also gives a clinical clue indicating the presence of occult cancer. [13]

Paraneoplastic syndromes can be infrequently associated with ovarian cancer. Subacute cerebellar degeneration due to tumor-induced autoimmune reactivity against cerebellar antigens can lead to symptoms like ataxia, dysarthria, nystagmus vertigo, and diplopia. This condition commonly precedes the occurrence of the primary ovarian tumor by months or years. Trousseau's syndrome has also been associated with ovarian cancer. Increased levels of circulating parathyroid hormone-releasing protein can lead to hypercalcemia, which can manifest as altered mental status, fatigue, constipation, abdominal pain, and increased thirst and urinary frequency. Such early warning signs of various paraneoplastic syndromes should be considered well in advance to avoid the diagnosis of ovarian cancer directly at an advanced stage where the patient may not be amenable to curative therapy. [14] [13]

In patients with a high degree of clinical suspicion, radiological imaging including transvaginal ultrasonography (TVUS, highly sensitive and preferred) and/or abdominal and pelvic ultrasonography is done. It gives a fair idea about the size, location, and complexity of the ovarian mass. For defining tumor extension, further imaging with chest and abdomen pelvis CT scan, pelvic MRI, and/or PET scan can be done. 

Measurement of CA-125 levels is usually done in adjunction with the imaging. CA-125 is elevated in most of the epithelial ovarian cancers overall, but only half of the early stage epithelial ovarian cancers. [15] The specificity and positive predictive value is found to be higher in postmenopausal women than in premenopausal women. Increased CA-125 levels are also observed in other physiological or benign pathological conditions such as endometriosis, pregnancy, ovarian cysts, inflammatory peritoneal diseases. Hence, other biomarkers are currently being studied to improve specificity for ovarian cancer biomarkers. Human epididymis protein 4 (HE4) is a new biomarker that is currently being evaluated. It is found to be more sensitive for ovarian cancer and found in approximately 100% of serous and endometrioid subtypes. Based on recent studies, a combination of higher CA-125 and HE4 levels are thought to be predictive of malignant ovarian tumors and may serve as a useful diagnostic tool in the future. [16] CA-125 levels can also be used to calculate the risk of malignancy index (RMI), which also utilizes TVUS findings and menopausal status. RMI above 200 is associated with a high risk of malignancy, with a greater than 96 % specificity. [13]

The malignancy algorithm (ROMA) risk utilizes a mathematical formula that incorporates HE-4 and CA 125 levels adjusted for pre and post-menopausal status to determine the risk of malignancy. [17]  The ROMA is a valuable screening test that takes advantage of the high specificity of HE4 and high-sensitivity of CA-125 to detect more patients of ovarian cancer overall, especially in the early stages. The risk of malignancy index (RMI) index is usual for the patient, where the score incorporates TVUS findings, menopausal status, and CA-125 levels. [13] Currently, multimarker longitudinal models are being worked on for the early detection of ovarian cancer. [18]

Optimal staging with exploratory laparotomy and close evaluation of abdominal and pelvic region for disease, including inspection of peritoneal surfaces with biopsy and/or pelvic washings, is done. It establishes the stage using the International Federation of Gynecology and Obstetrics (FIGO) staging of ovarian cancer. It is followed by total abdominal hysterectomy and bilateral salpingo-oophorectomy (BSO) with para-aortic and pelvic lymph node dissection and omentum. The tissue biopsies evaluated by a pathologist help provide the final diagnosis concerning the histological type, grade, and staging. [9]

• Treatment / Management

Debulking Surgery

Treatment of ovarian cancer conventionally includes a combination of chemotherapy and surgery. In the early stage of invasive epithelial ovarian carcinoma, unilateral salpingo-oophorectomy while preserving the uterus and contralateral ovary is done, with comprehensive surgical staging where lesions show a low likelihood of progressing to malignancy. However, for advanced-stage ovarian cancer, a debulking surgery comprising hysterectomy/bilateral salpingo-oophorectomy (BSO) has shown better outcomes. It is imperative to determine whether debulking surgery would be beneficial for a patient by initially performing exploratory laparoscopic surgery. The presence of a large or residual tumor burden can block perfusion to the affected region leading to damaged tissue and increase chances of further cellular damage with multidrug chemotherapy resistance. [9]   Laparoscopic surgeries are noted to be less invasive with decreased recovery time as opposed to debulking surgeries. Patients with ovarian cancer should have genetic risk evaluation and germline, somatic (BRCA 1/2) testing done if previously not tested, as the latter guides the maintenance therapy.

Primary Debulking Surgery versus Neoadjuvant Chemotherapy

A gynecologic oncologist initially evaluates patients with suspected advanced stage IIIC or IV ovarian cancer to determine if they are appropriate surgical candidates or not. Neoadjuvant chemotherapy is recommended to decompress the tumor burden for the ones deemed poor surgical candidates with a low likelihood of optimal cytoreduction.  According to the Society of Gynecologic Oncology (SGO) and American Society of clinical oncology (ASCO), clinical practice guidelines state that women with a favorable surgical profile can receive either neoadjuvant chemotherapy or undergo cytoreduction surgery. But if they have a high likelihood of attaining cytoreduction to less than 1 cm with acceptable morbidity, primary cytoreductive surgery should be preferred. Before administering neoadjuvant chemotherapy, patients should carry a histological diagnosis of invasive ovarian cancer confirmed by biopsy preferred over specimens obtained from fine-needle aspiration of paracentesis. [19]

Various clinical trials have compared neoadjuvant chemotherapy with interval cytoreduction surgery versus primary cytoreductive surgery upfront, showing equal overall median survival. Two of the phase III trials have shown non-inferiority of neoadjuvant chemotherapy compared to cytoreductive surgery followed by chemotherapy in women with stage IV disease. This proves that neoadjuvant chemotherapy can be significantly utilized in patients with advanced-stage invasive ovarian cancer patients who are poor surgical candidates with high tumor burden. The European organization for research and treatment of cancer (EORTC), phase III trial EORTC 55971 recruited women with stage IIIC-IV epithelial ovarian cancer (n=670) and CHORUS trial had a similar recruitment profile with women of stage III A-B besides (n= 550). They showed non-inferiority of median overall survival with neoadjuvant chemotherapy when compared to primary cytoreductive surgery upfront. In a pooled analysis of individual patient data from these two trials, EORTC 55971 and CHORUS trials, women with stage IV disease had better survival outcomes with neoadjuvant chemotherapy followed by cytoreductive surgery. [20]   An exploratory analysis of the EORTC 55971 randomized trial found that patients with stage IIIC (<4.5 cm) and less invasive metastatic tumors had better survival outcomes with primary cytoreductive surgery. In contrast, patients with stage IV disease (>4.5cm) and more invasive metastatic tumors had better survival outcomes with neoadjuvant chemotherapy. [21]

Maximal Cytoreductive Surgery

One of the most powerful independent determinants of improved median survival among patients with stage III or IV ovarian carcinoma is to achieve maximal cytoreduction. Hence, irrespective of the surgery sequence, before or after neoadjuvant chemotherapy, optimal cytoreduction is strongly recommended to achieve ideally no residual disease. A meta-analysis of 6885 patients with stage III and IV ovarian cancer showed a 5.5% increase in overall median survival with a 10% increase in maximal cytoreduction in one of the studies. When the actuarial survival was being estimated comparing cohorts with less than or equal to 25% maximal cytoreduction and more than 75% maximal cytoreduction, there was an increase of 50% of mean weighted median survival time.  However, platinum dose intensity did not have a statistically significant relation to the log median survival time. [22]  If interval cytoreduction surgery is being performed after neoadjuvant chemotherapy, it is usually done after four or fewer cycles ensuring early surgical intervention in the disease course. However, if the patient has received bevacizumab as a part of their initial neoadjuvant chemotherapy regimen, there should be a gap of at least 20 days before surgical intervention due to the risk of highly compromised postoperative healing. [23]  

Primary Chemotherapy and Neoadjuvant Therapy

• Early-stage ovarian cancer:Adjuvant chemotherapy in women with early-stage ovarian cancer has been studied extensively and based on the evidence. The final clinical decision has to be individualized for every patient. Based on four randomized control trials (ACTION 2003; Bolis 1995; ICON1 2003; trope 2000) which studied platinum-based chemotherapy, women with early-stage epithelial ovarian cancer showed better overall survival (OS) (HR 0.71; 95% CI 0.53 to 0.93) and progression-free survival (PFS) (HR 0.67; 95% CI 0.53 to 0.84) with adjuvant chemotherapy than the ones who did not receive it.  However, one of those trials, ICON1 2003, showed similar evidence in high-risk patients with adjuvant chemotherapy but not among others. Based on the pooled data in a meta-analysis, which included all the patients (total of 772) in ICON1 2003 and two-thirds of patients in ACTION 2003, evidence of overall benefit in early-stage ovarian cancer women was observed after sub-optimal staging. [24]  In stage IA or 1B epithelial ovarian cancer or grade 1 endometrioid carcinomas, considering the good survival rates, surgical treatment alone is recommended over adjuvant chemotherapy with close observation. [23]  Another prospective randomized phase III trial was done. Patients were randomly assigned to either adjuvant platinum-based chemotherapy or observation followed by surgery, with endpoints being overall survival and recurrence-free survival (RFS). It provided evidence that chemotherapy improves both overall and recurrence-free survival in the non-optimally staged patients (patients with residual disease); however, these findings were not observed in optimally staged patients (patients with a slight chance of residual disease). This suggests that adjuvant chemotherapy in early-stage ovarian cancer affects the micro-metastasis that goes unnoticed at the time of surgical staging. [25]  A meta-analysis of all the randomized clinical trials that studied women of stages I-II epithelial ovarian cancer compared to adjuvant chemotherapy with observation showed no overall survival benefit of adjuvant chemotherapy (hazard ratio 0.91, 0.51 to 1.61). [23] Overall, the available evidence supports the use of adjuvant chemotherapy in patients with early-stage ovarian cancer with high-risk features like the stage IC and stage II disease and clear cell or high-grade histology. While the optimal regimen is unclear, most clinicians use carboplatin with paclitaxel extrapolating their evidence in the advanced stage of ovarian cancer.
• Advanced stage ovarian cancer:The standard approach in treating patients with advanced ovarian cancer uses platinum and a taxane. The option of intravenous (IV) and intraperitoneal (IP) chemotherapy depends on the optimal debulking of the tumor. A phase III trial, GOG111, showed improved overall survival in patients with a combination of cisplatin and paclitaxel when compared to the cohort receiving cisplatin and cyclophosphamide combination. The first line chemotherapeutic agent for epithelial ovarian cancer is platinum-based cisplatin or carboplatin along with a taxane family agent, paclitaxel or docetaxel. There have been many studies concluding that carboplatin is as effective as cisplatin and better tolerated. Also, weekly dose-dense chemotherapy with carboplatin and paclitaxel combination has not shown any additional benefit in PFS than standard three-weekly chemotherapy or an additional third agent or a longer period of the chemotherapy cycle. [23]  Chemotherapeutic agents are administered IV or IP or a combination of both. In advanced age ovarian cancer patients, IP carboplatin chemotherapy is well-tolerated. There have been four landmark trials, namely GOG 104, GOG 114, GOG 172, and GOG 252, which have shown improved survival benefit of intraperitoneal or intravenous chemotherapy, with strong evidence supporting the same, however clinically, its use has been inconsistent. [26] [27] This is mostly due to increased frequency of toxicity, especially neutropenia, thrombocytopenia, neurotoxicity, and adverse gastrointestinal symptoms affecting the quality of life of patients treated with intraperitoneal chemotherapy as well as due to the addition of bevacizumab studied in GOG 252 didn't show any advantage of IV/IP compared to IV with bevacizumab. [28]  

Chemotherapy in Elderly

Elderly patients aged over 70 years or older with comorbidities who have stage III-IV ovarian cancer were studied in a randomized control trial, which showed worse survival outcomes with carboplatin monotherapy versus carboplatin-paclitaxel three weekly/weekly. [23]  But when combination therapy is being used, a modified dose-dense regimen of weekly carboplatin plus paclitaxel has shown to be better tolerated with a lower toxicity profile than the conventional dosing (three weeks schedule). Still, it did not prolong progression-free survival, as shown in a MIT07 phase III trial, which can also be used for elderly patients with comorbidities. [29] [30] The frail elderly patients were found to have decreased high-grade neutropenia, febrile neutropenia, thrombocytopenia, and neuropathy. [23]   An ongoing prospective trial of older women of age equal to or greater than 70 on different chemotherapy regimen combinations will help us predict chemotherapy tolerance. However, preliminary results have commented on patients with higher baseline instrumental activities of the daily living score are more likely to complete four chemotherapy cycles and less likely to experience high-grade toxicity. [31]

Maintenance Therapy

Maintenance therapy is conceptualized to ensure the effective killing of residual slowly dividing cells by decelerating the cell turnover so that the dormant population of cancer cells does not progress to grow enough to be detected by either elevation of biomarkers or clinical evidence of recurrent disease. Several randomized trials have been done to compare maintenance therapy versus observation. 

• Platinum-based agent:A phase III trial, GOG 178, randomized patients to 12 months versus 3 months of maintenance therapy with paclitaxel after complete clinical response with platinum/paclitaxel therapy in patients with stage III-IV ovarian cancer. After 50% accrual interval analysis, improved PFS was seen favoring the extended therapy cohort. However, the study closed early. A follow-up study later showed no overall survival benefit compared to the same maintenance monotherapy for 22 months versus 14 months. [32]  Another trial, GOG 175, showed no significant difference in 5-year survival or recurrence-free interval (RFI) where high-risk early-stage ovarian cancer patients were randomized to observational versus weekly paclitaxel 40 mg/m²x 24 weeks after completion of 6 cycles of carboplatin and paclitaxel for 3 cycles. [33]  A three-arm phase III trial following standard chemotherapy, GOG 0212, compared observation without immediate therapy to 12 months of paclitaxel or polyglutamated paclitaxel but showed disappointing results. [34]  To conclude, the results of maintenance, chemotherapy trials have been discouraging.
• Anti-angiogenic inhibitor:Pazopanib, an oral multikinase inhibitor of vascular endothelial growth factor receptor (VEGFR) -1/2/3, platelet-derived growth factor (PDGFR) alpha/beta and c-kit, has also been studied as maintenance therapy in a study of 940 patients with patients of ovarian cancer stage II-IV. These patients had a complete clinical response to five cycles of platinum-taxane chemotherapy and were randomized to pazopanib versus placebo for 24 months showing a median improvement in PFS in the pazopanib arm; no benefit was seen in overall survival data. BRCA1/2 carriers were noted to have an additional significant benefit. [35]  Bevacizumab is a humanized monoclonal antibody against vascular endothelial growth factor (VEGF) that has been studied in combination with chemotherapy followed by bevacizumab, single agent, maintenance therapy in two major landmark trials (ICON7 and GOG0218) of patients with advanced-stage ovarian cancer. The studies showed an improved PFS in the maintenance bevacizumab cohort when compared with surveillance only. [36]  The FDA eventually approved it. Bevacizumab has also been associated with serious side effects like hemorrhage, thrombosis, hypertension, proteinuria, bowel perforation. [23] In a subset analysis of the ICON 7 trial, patients with large volume residual disease after their primary cytoreductive surgery or stage IV disease who fall into the high-risk category showed a greater median overall survival benefit. Secondary analysis of GOG0128 revealed improved overall survival in a particular subgroup of patients with ascites, who are at high risk of recurrence and mortality from stage IV disease. [36]  This targeted therapy should be individualized in patients. However, it does show significant benefit in PFS when used as concurrent therapy followed by single-agent maintenance therapy but without any clear clinical benefit in overall survival.
• Poly(ADP)-ribose polymerase (PARP) inhibitors:PARP inhibitors have recently gained momentum for the maintenance treatment of ovarian cancer. Olaparib was the first FDA-approved drug in this subgroup indicated to treat advanced BRCA mutated ovarian cancer after platinum-based chemotherapy, based on SOLO-1, phase III randomized double-blind, placebo-controlled trial. It showed a reduction in disease progression or death by 70% (hazard ratio 0.30, 0.23 to 0.41; P<0.001). [37] PAOLA-1 trial, a phase III randomized controlled trial of 806 women with stage III-IV high-grade serous or endometrioid ovarian cancer, showed a PFS benefit of 4.5 months in the group that received olaparib and bevacizumab maintenance versus placebo and bevacizumab. [38] This combination of olaparib and bevacizumab achieved FDA approval as a first-line maintenance treatment for these patients with ovarian cancer after initial platinum-based chemotherapy with partial or complete response or tumors associated with homologous recombination deficiency (HRD) defined by the presence of deleterious BRCA mutation. Further noted clinical trials include the VELIA trial and PRIMA trial using Veliparib and Niraparib maintenance therapy, respectively, showing markedly improved PFS compared to the placebo group in patients with newly diagnosed advanced-stage ovarian cancer who initially responded to first-line platinum-based chemotherapy. [39] [40]
• Immunotherapy:It has recently shown significant benefits in solid malignant tumors. However, published data do not show any benefit in patients with ovarian cancers so far. The resulting controversial data diverted the focus on combination strategies involving immune- checkpoint inhibitors with PARPs, chemotherapy, anti-angiogenic agents, and more. A combination of such therapies shows more significant anti-tumor activity than concentrating on a single pathway. This promising data is from initial phase trials, and further results from ongoing phase II and III trials are awaited. [41]
• Vaccines:Vaccines are currently being studied for ovarian cancer, where the basis lies in activating the immune cells to destroy the cancer cells. The potential tumor-associated antigen molecules targeted in ovarian cancer in ongoing ovarian cancer vaccine researches are CA-125, p53 protein, HER-2, and more. [41] There are currently ongoing pilot and phase I or II trials for the use of therapeutic vaccines in ovarian cancer patients by employing novel techniques. Other emerging therapies being studied in clinical trials are using adoptive T-cell transfer and chimeric antigen receptor therapy (CAR-T) as a part of future strategies to ensure reduced cancer burden and improved life expectancy in this patient population.

Recurrent Ovarian Cancer

About 80% of women with advanced-stage ovarian cancer more commonly have tumor progression or recurrence. Platinum free interval (PFI) is one of the most reliable predictors indicating the response of recurrent ovarian cancer to subsequent chemotherapy. PFI refers to the interval between the completion of the last platinum-based chemotherapy and the occurrence of relapse. [42]  However, platinum sensitivity is generally used to refer to an interval of greater than 6 months between the last platinum-based chemotherapy (PBC) cycle and commencement of subsequent PBC.

The role of surgery in cases of recurrent ovarian cancer is yet quite undefined. GOG 213, a phase III multicenter randomized clinical trial enrolled patients with platinum-sensitive recurrent ovarian cancer, randomized patients to surgical cytoreductive surgery followed by adjuvant PBC or only PBC with a primary endpoint of overall survival showed no improved benefit in patients receiving secondary surgical cytoreduction followed by chemotherapy and chemotherapy alone (HR for death 1.29, 0.97 to 1.72; P=0.08). [23]   Desktop III trial, which compares surgery followed by chemotherapy versus chemotherapy only in recurrent platinum-sensitive ovarian cancer, is currently ongoing whose results are eagerly awaited.  They had announced their preliminary results in ASCO 2017 showing improvement in PFS and longer interval of the period to the start of subsequent chemotherapy in favor of surgery followed by chemotherapy. There are two other trials- Surgery for Ovarian Cancer Recurrence (SOCceR) and Surgery or Chemotherapy in Recurrent Ovarian Cancer (SOC 1) comparing surgery and chemotherapy with surgery alone in such groups of patients, with awaited results. To conclude, none of the studies have resulted in longer overall survival with second-degree surgical cytoreduction in patients with platinum-sensitive recurrent epithelial ovarian cancer diagnosed surgery. [43]

Large phase III trials have also resulted in the approval of bevacizumab, as discussed above, which was studied in combination with chemotherapy for the treatment of recurrent ovarian cancer as well as for maintenance therapy (GOG 218, or OCEANS and AURELIA trials). [42]  The studies have shown an objective improvement of PFS. However, they failed to prove a benefit in overall survival. Nevertheless, antiangiogenic agents have shown activity in these platinum-sensitive recurrent ovarian cancer however further studies are needed to define their benefit clearly. Evidence shows the use of aromatase inhibitors like letrozole for the treatment of recurrent low-grade serous and endometrioid epithelial ovarian cancer based on large retrospective cohort studies.

PARP inhibitors have been under clinical development at various stages and have shown their efficacy in patients with germline BRCA mutations. They were first approved as monotherapy in ovarian cancer patients with deleterious germline or somatic BRCA mutations who have not responded to chemotherapy. Further studies showed significant PFS benefit in patients with an initial response to be BC with maintenance PARP inhibitor therapy. An overall survival benefit is yet to be proven, which requires a longer follow-up. SOLO-2 study assessed maintenance monotherapy with olaparib in patients with platinum-sensitive recurrent ovarian cancer and BRCA mutation showing significantly improved PFS for the patients receiving olaparib with no significant detrimental effect on patient's quality of life. [44]  

PAOLA-1, a phase III trial, studied olaparib with bevacizumab in platinum-sensitive recurrent ovarian cancer showing PFS benefit in the patients receiving the combination. The results were quite consistent with those observed in the SOLO 1 trial. The safety profile of olaparib was quite consistent in the trials, with a higher incidence of serious adverse events noted in the group receiving a combination of olaparib and bevacizumab than with placebo plus bevacizumab, the most common one being anemia. [38]  Many phase III trials have shown PARP inhibitor maintenance therapy in patients with platinum-sensitive recurrent ovarian cancer with clinical benefits.  Recently in the 2019 SGO annual meeting, an abstract was presented which described a retrospective study of a few patients who have been previously treated with PARP inhibitor for epithelial ovarian cancer, where a second PARP inhibitor treatment was used; however, the most common reason for discontinuation of treatment was toxicity. [23]  Further studies using PARP inhibitors as maintenance therapy and predicting their resistance would be areas of further research.

Platinum resistance poses a very poor prognosis, where these patients have a recurrence of the disease within 6 months of completion of cytoreductive surgery and adjuvant chemotherapy.  It is imperative to have goals of care discussion with these patients as their overall survival rates are quite grim. Focusing on newer targets like tumor vasculature, DNA repair, intracellular signaling inhibition, and other molecular targets will provide more avenues to be explored for optimizing the treatment of recurrent ovarian cancer.

To conclude, advanced-stage ovarian cancer patients are treated with primary reductive surgery, followed by platinum-based chemotherapy. But poor surgical candidates or patients who might not achieve effective cytoreductive surgery are recommended to undergo neoadjuvant chemotherapy. Optimal cytoreductive surgery is very important to achieve as it is one of the most powerful predictors of survival of these patients. There is a high rate of relapse in patients with advanced-stage whose response to subsequent platinum-based chemotherapy depends on various factors. Targeted therapies are the new emerging treatment strategies where bevacizumab and PARP inhibitors have become first-line therapies for maintenance and PARP inhibitors as the first line for recurrent cases. Genetic screening for all newly diagnosed ovarian cancer is recommended.

• Differential Diagnosis

The differential diagnosis for ovarian cancer includes:

• Colon cancer
• Embryologic remnants
• Gastric adenocarcinoma
• Metastatic gastrointestinal carcinoma
• Ovarian torsion
• Peritoneal cyst
• Retroperitoneal mass
• Uterine fibroids
• Papillary adenocarcinoma
• Serous adenocarcinomas
• Undifferentiated adenocarcinomas
• Small-cell adenocarcinomas
• Brenner tumors
• Radiation Oncology

Historically, whole abdomen radiation was practiced during early times; however, due to the increased frequency of toxicity and complications, its use became nonexistent. Currently, the role of radiation in ovarian cancer is limited to palliation, either for symptom control or to treat a localized spread of disease. Adjuvant radiotherapy has not even shown any survival benefit in the early stages of clear cell carcinoma, including a high-risk subset of patients. [45]

Due to the advent of advanced systemic therapies, radiation has taken a backseat in the management of ovarian cancer, offering limited use. Stereotactic body radiotherapy (SBRT) is one of the newer techniques for palliative radiation. There is still evidence of high rates of distant progression of lesions with its use, even when local control is achieved. [46]

Currently, with the emergence of new techniques like SBRT, intensity-modulated radiotherapy, and low dose hypofractionation, the role of radiation is strongly considered for local-regionally recurrent ovarian cancer, especially for chemotherapy-resistant lesions. [47] [48]

Ovarian cancer is staged according to the 8th edition American Joint Committee of Cancer (AJCC), International Federation of Gynecology and Obstetrics (FIGO) staging system and corresponding Tumor, Node, Metastasis (TNM) classification.

Stage I - Tumor limited to ovaries (one or both) or fallopian tube(s)

• IA - Tumor limited to one ovary (capsule intact) or fallopian tube, no tumor on ovarian or fallopian tube surface; no malignant cells in ascites or peritoneal washings
• IB - Tumor limited to both ovaries (capsules intact) or fallopian tubes; no tumor on ovarian or fallopian tube surface; no malignant cells in ascites or peritoneal washings
• IC - Tumor limited to one or both ovaries or fallopian tubes, with any of the following:
• IC1    Surgical spill
• IC2    Capsule rupture before surgery or tumor on the ovarian or fallopian tube surface
• IC3    Malignant cells in ascites or peritoneal washings

Stage II - Tumor involves one or both ovaries or fallopian tubes with a pelvic extension below pelvic brim or primary peritoneal cancer

• IIA - Extension and/or implants on the uterus and/or fallopian tube(s) and/or ovaries
• IIB - Extension to and/or implants on other pelvic tissues

Stage III - Tumor involves one or both ovaries or fallopian tubes, or primary peritoneal cancer, with microscopically confirmed peritoneal metastasis outside the pelvis and/or metastasis to the retroperitoneal (pelvic and/or para-aortic) lymph nodes

• IIIA1 - Positive retroperitoneal lymph nodes only (histologically confirmed)
• IIIA1i  Metastasis up to and including 10 mm in greatest dimension
• IIIA1ii  Metastasis more than 10 mm in greatest dimension
• IIIA2   Microscopic extrapelvic (above the pelvic brim) peritoneal involvement with or without positive retroperitoneal lymph nodes
• IIIB - Macroscopic peritoneal metastasis beyond pelvis 2 cm or less in greatest dimension with or without metastasis to the retroperitoneal lymph nodes
• IIIC - Macroscopic peritoneal metastasis beyond the pelvis more than 2 cm in greatest dimension with or without metastasis to the retroperitoneal lymph nodes (includes an extension of tumor to the capsule  of liver and spleen without parenchymal involvement of either organ)

Stage IV - Distant metastasis, including pleural effusion with positive cytology; liver or splenic parenchymal metastasis; metastasis to extra-abdominal organs (including inguinal lymph nodes and lymph nodes outside the abdominal cavity), and transmural involvement of intestine

• IVA - Pleural effusion with positive cytology
• IVB - Liver or splenic parenchymal metastases; metastases to extra-abdominal organs (including inguinal lymph nodes and lymph nodes outside the abdominal cavity); transmural involvement of intestine

The prognosis of ovarian cancer is directly dependent on the disease stage at the time of diagnosis. It is also significantly associated with baseline performance status, FIGO stage, and volume of residual disease post-primary cytoreductive surgery. The median survival of ovarian cancer is approximately around 40% to 50% at 10 years, with stage-related survival for stage I between 70% to 92% compared to stage IV being less than 6%. [49]  

In women with a disease that spread to adjacent tissues, 5-year survival rates drop down to 80% and 25% for the ones with metastatic disease. [9]  Patients with recurrent disease can be treated. However, they are usually incurable. Recurrent platinum-sensitive ovarian cancer median survival is approximately 3 years; however, it is about just 1 year for platinum-resistant patients. [49] [50]  

Most of these patients with ovarian cancer develop malignant bowel obstruction in the late-stage, which is quite difficult to manage. Palliative symptom management is the mainstay in such patients. Debulking surgery is the strongest predictor of prognosis, where the volume of residual disease post-surgery is directly correlated to overall survival and PFS. [51]

• Complications

Women who succumbed to ovarian cancer are found to have various complications in the last 6 months of life, the most common ones being:

• Fatigue or weakness (75%)
• Nausea or vomiting (71%)
• Constipation (49%)
• Pedal edema (44%)
• Anemia (34%) 

Women who could not be offered treatment are frequently found to have serious complications like ascites, bowel obstruction, pleural effusion, and bladder obstruction, apart from disorders of nutrition. [52]

• Deterrence and Patient Education

The patient should be explained and counseled about all the treatment options available along with prognosis at the time of diagnosis, depending on the stage of presentation. Counseling for genetic testing should also be done, which does have an impact on treatment at times. The palliative care team and other related consultants' involvement should be sought timely regardless of cancer stage to enable comprehensive care, anticipate the disease course, and make a great impact on the quality of life of the patients. Patients should also be explained about the recent ongoing clinical trials if pertinent to their particular case.

• Enhancing Healthcare Team Outcomes

Ovarian cancer remains one of the lethal malignancies in women despite the leading ongoing clinical trials and the introduction of new treatment lines in the past few decades. The poor clinical outcome is majorly due to the failure of effective strategies for the early detection of ovarian cancer. [53] There is also evidence regarding the deviation of care from the recommended guidelines, possibly due to clinical variation seen in ovarian cancer care. [54]

With the goal of ovarian cancer to be diagnosed at an earlier and more curable stage, we are still in need of the development of effective strategies. The volume of residual disease post cytoreduction surgery is one of the powerful determinants of patients' survival. Hence it should be done only by an experienced gynecologic oncologist who sees a high number of cases at a large busy hospital (>20 cases/year). [55]

Shared decision-making in terms of management of patients regarding newly available treatment strategies or clinical trials by going through benefits, safety profile, symptom control, and a discussion about the prognosis is one of the key elements. A close interprofessional team play with major roles played by medical oncologists and surgical oncologists helps in the smooth and effective management of the patients. Involvement of palliative care early helps fully optimize the treatment course and improve the quality of life. [56] [57]

Patients in clinical remission should be offered affordable yet effective strategies for close surveillance follow-ups where patients should also be educated about the symptoms indicating recurrence of the disease and should be encouraged for genetic risk counseling if not done previously in the early disease course.

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Disclosure: Taruna Arora declares no relevant financial relationships with ineligible companies.

Disclosure: Sanjana Mullangi declares no relevant financial relationships with ineligible companies.

Disclosure: Manidhar Reddy Lekkala declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Arora T, Mullangi S, Lekkala MR. Ovarian Cancer. [Updated 2023 Jun 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Introduction. Cancer is the most common cause of mortality in most parts of the world, 1 and currently is the most common impediment to achieving desirable life expectancy in most countries. 2 Ovarian cancer is one of the most common gynecologic cancers that rank third after cervical and uterine cancer. 2 It also has the worst prognosis and the highest mortality rate. 3 Although ovarian cancer ...

ovarian cancer in hospitals that have high volume of both surgery and chemotherapy for ovarian cancer [2]. A population based study from Australia found variation ... thesis [16]. Results A total of 2012 papers were identified during the search, after removing duplicates 1683 studies were left. Screening

Patients with Ovarian Cancer Min Liu A Thesis Submitted to the Faculty of The Harvard Medical School in Partial Fulfillment of the Requirements for the Degree of Master of Medical Sciences in Immunology Harvard University Boston, Massachusetts. May, 2021

Objective: To provide an overview of the risk factors, modifiable and non-modifiable, for ovarian cancer as well as prevention, diagnostic, treatment, and long-term survivorship concerns. This article will also examine current and future clinical trials surrounding ovarian cancer. Data sources: A review of articles dated 2006-2018 from CINAHL, UpToDate, and National Comprehensive Cancer ...

In fact, over 70% of ovarian cancers are not diagnosed until the disease has progressed to stage III or IV. The latest research has survival rates for ovarian cancer after 5years to be 47.4%. 2., 5. Interestingly, data suggest that ovarian cancer does not usually start in the ovaries.

ADH1B mutations have been extensively studied and have been linked to various types of cancer. The functional polymorphism ADH1B rs1229984 (Arg47His) has been associated with esophageal, head and neck, and colorectal cancers [8-10]. However, the biological roles of ADH1B in metastasis and residual disease are unknown.

Abstract. Ovarian carcinoma is characterized by heterogeneity at the molecular, cellular and anatomical levels, both spatially and temporally. This heterogeneity affects response to surgery and/or ...

Ovarian cancer (OC) is a highly malignant disease that seriously threatens women's health and poses challenges for clini-cians. MicroRNAs (miRNAs) have recently been intensively studied in the field of oncology due to their regulatory roles in gene expressions through RNA degradation and/or translation inhibition.

PDF | On Sep 5, 2013, Feras Abu Saadeh published Hypercoagulability in Ovarian cancer. MD thesis | Find, read and cite all the research you need on ResearchGate

This qualitative study focused on the patient path to ovarian cancer diagnosis as described by patients and providers in a US-based multi-payer healthcare system. In contrast to prior record-based studies, we were able to characterize time intervals that occur prior to the patient entering the healthcare system.

The worldwide distribution of and international variation in histological groups of ovarian cancer was examined, as an approach to understanding international differences in overall ovarian cancer survival. International comparisons of ovarian cancer survival have traditionally analysed ovarian cancer as a single homogenous group.

Although ovarian cancer may occur at any age, it is more common in patients older than 50 years. Ovarian cancer has an age-adjusted incidence of 12.5 per 100,000 women [32]. The median age of ...

Abstract. Epithelial ovarian cancer comprises the majority of malignant ovarian tumors in adult women. These neoplasms are classified into distinct morphologic categories based on the appearance ...

metastatic progression of ovarian cancer and suggest that inhibiting pathways that drive mesenchymal pro-grams may suppress tumor cell invasion of peritoneal tissues. Introduction Ovarian cancer has the highest mortality rate of all gynecological cancers and the fifth highest mortality rate of all cancers in the United States (1).

The World Ovarian Cancer Atlas 2020 is a comprehensive report that provides the latest data and insights on the global burden, diagnosis, treatment and outcomes of ovarian cancer. It reveals the significant disparities and challenges that women with ovarian cancer face across regions and countries, and highlights the urgent need for action to improve survival and quality of life. The report ...

Approximately 13.7% of cases of ovarian cancer are detected at a local stage, and about 52% of cases are detected at the metastasized stage, in which the survival rate of five years gets as low as 29.7% instead of 91.8% if diagnosed earlier before spreading locally. 90% of ovarian carcinomas are of the

Trends. The incidence of ovarian cancer has declined slightly since the mid-1970s, when the incidence was approximately 16 new cases per 100,000 women ( Howlader et al., 2015 ). Mortality from ovarian cancer has also declined—from 9.8 deaths per 100,000 women in 1975 to 7.4 deaths per 100,000 women in 2012. However, the decline in mortality ...

Polycystic ovary syndrome (PCOS), which affects 5-20% of women in their reproductive age, is the most common endocrinopa-thy affecting women worldwide. It is a condition characterized by ...

Ovarian cancer is the leading cause of death in women diagnosed with gynecological cancers. It is also the fifth most frequent cause of death in women, in general.[1] Most of the cases are diagnosed at an advanced stage, which leads to poor outcomes of this disease. The existing screening tests have a low predictive value contributing further to this misery. Detailed gynecological evaluation ...

catamarans over 50 feet for sale

Better sailing.

Best Catamarans Over 50 Feet

All kinds of high-end luxury sailing you could ever imagine can be experienced on Catamarans Over 50 Feet. It just depends on the boat at hand. Why spend your holiday cruising or liveaboard on a monohull when comfortable catamarans exist?

A catamaran is quite different from a regular monohull. Catamarans are typically designed with two equal-sized hulls and derive their stability from their wide beam; unlike a one-hulled boat deriving stability from a loaded undersurface.

The average catamaran is 38-47 feet in size. Usually, they are equipped with four large cabins with double or queen-sized beds, each cabin having an in-suite head. These vessels, originally designed for fishing, have, over the years, evolved and have become very popular in recent years. Lately, many boatbuilders are focusing more and more on building large catamarans over 50 feet as more and more people are starting to liveaboard and put more emphasis on comfort and luxury than their sailing performance.

In 2011, the biggest catamaran ever was built by Pendennis Shipyard in the UK, at 145 feet in length! It is equipped with a trampoline, a jacuzzi and can accommodate 12 guests in 5 cabins. This boat is designed to accommodate all the luxuries and adornments that can be found on a watercraft.

Here are the best sailing catamarans over 50 feet, in no particular order.

Length: 50 Feet

Price: From $500k to $1.5 Million USD On the Used Market

Back in 2019, the Lagoon 50 was awarded the best multihull of Sail Magazine. A product of the world’s largest boat manufacturer Lagoon, established in 1984, is majorly famous for the design and construction of cruising catamarans, which infuse top-notch designs, upscale comfort, and great sailing performances to one’s boating experience. Every detail is carefully thought out to establish novel and spacious architecture with a homely ambiance.

It’s a perfect balance between the model Lagoon 450 and the lofty 52. The Lagoon 50 has an encompassing view, generous volumes with a self-tacking jib, and a shorter mast for easily simplified maneuvers. It has two cockpits, one large one facing the sea and the other for seating at foredeck or on a deck chair. The hulls being large enough to contain more than 2 cabins, you can have up to six cabins. Italian agency Nauto Design Studio set a standard for their innovative interior designs every time. This vessel boasts of a unique brand signature, providing increased performance and a detailed wood finish to be fitted for the owner. Unconventional lines are linked with luxury, versatility, and a layout of technical options to cater to everyone’s needs.

>>Also Read: Jeanneau 64 Review

Length: 52 Feet

Looking for something contemporary and luxurious? Lagoon 52 takes the cake in that way. This boat signified a new stage in the design of cruising catamarans. The Lagoon 52 is a product of the prolonged conversations between Lagoon’s customary VPLP, Nauto design agency, and the Lagoon design department. It comes in two versions: The Lagoon 52 FlyBridge, known as Lagoon 52F, and Lagoon 52 SporTop.

The combination of onboard comfort with its sailing performance is perfect and in sync. The wide side decks allow easy movement onboard. The cockpit and saloon also offer spacious living areas. The vertical bows of the boat have a diamond-shaped appearance with diagonal shaped hull and a lifting deck house.

The boat is easily accessible and safe thanks to the open rear skirts. Most of the features in this luxurious watercraft can be found in the aforementioned Lagoon 50. It has a perfect blend for its easy use, a comfy, elegant interior, amazing space, and lighting. You’re sure to get your money’s worth with the LAGOON 52.

Privilege Series 5

Price: Around $1-1.5 Million USD

At 50 feet, this boat is quite marvelous and a privilege to spend your time in as a cruiser or owner. The Privilège Series 5 is the world’s first 50 feet sailing catamaran. This vessel was built by Privilège Marine, a French company based in Les Sables-d’Olonne, France. They are famous for building premium luxury catamarans and designed by French Naval Architect Marc Lombard. The Privilège Series 5 is equipped with three or four double and a full-sized owner’s cabin located in the yacht’s center. It’s a lightweight boat at 48500 pounds and could go up to 52900 depending on the size.

It has great customization options, and it can be designed to suit the boat owner’s taste. The attention to detail on the boat is nothing short of perfection as the interior design, woodwork, safety measurements laid out by the boat’s design, aesthetics, ventilation, etc., was thought out good. The vessel’s finishing is really phenomenal as everything has a high level of craftsmanship.

Leopard 50L

Length: 50 Ft 6 In

Price: Around $1 Million USD

The Leopard 48, which was launched in 2012, was one of the most popular cruising cats ever designed. But the design was beginning to become dated, even as new orders kept coming in. So, Robertson & Caine, who build the Leopard cats, set out to improve on what was already great. The new 50 was their answer and comes with many innovations that will make owners happy. We test sailed the 50L last winter in Florida. The L version has the optional lounge on top of the hardtop over the cockpit. Unlike some cats with flying bridges and lounges up high, the 50L doesn’t feel like a layer wedding cake.

The steering station is a traditional raised helm to starboard, and the lounge is just up a few stairs from there. The helmsman is in contact with those in the main cockpit and those in the lounge. Out sailing, we got the 50L up to 10 knots in a good breeze, so the boat is fast. It is also commodious and will make a very comfortable home for a family or a charter party.

>>Also Read: 10 Best Catamaran Brands

Length: 58 Feet

Price: From $450k To $1.5 Million on the Used Market

Leopard 58 is a superb layout from Leopard, skilfully modeled by award-winning designers Robertson & Caine. This extravagant catamaran is suited to the prolific and innovative catamarans that have made Leopard famous while still giving out fresh features and various design options.

This expansive FlyBridge takes space to a whole new dimension as it is larger than its siblings with their award-winning aspects. A Flybridge is basically a version of catamarans that affords you the luxury of outdoor space, come rain or shine. Leopard 58 is more about space, bragging about 750 square feet in just the saloon alone. It gives you amazing comfort and is naturally luminous. With an open plan layout, the galley available means the meal making and interaction will be easy. Highly recommended for a family outdoor gathering.

Price: Around $1 Million USD New ; Not many options on the used market since its a newer model

Popularly called the Seawind 52 because of its 52 feet size. The Seawind 52′ 1600 is designed by world-renowned architects Reichel Pugh. Like the Lagoon 52, it’s a perfect balance for onboard comfort and performance sailing and sea safety. Perfect for sailors or boat lovers who are looking for a little extra.

This catamaran sets a standard for offshore sailing because of its simple sailing methods, large open cockpit space, and twin protected helms. Equipped with a three or four-cabin design that affords the owner’s cabin expansive living space, great storage, high aspect riders, daggerboards, an elegant fit/finish, and infused carbon-reinforced construction.

Seawind 1600

Price: Around $1 Million USD New

The new Seawind 1600 has been in the works for a while and has finally arrived on the market. The Reichel Pugh design is a departure from the more conservative looks of the other Seawinds and embraces a very Euro-style with plumb bows, hard chines, a swept-back cabin, and a large open cockpit with helm stations on both sides. The boat is a pure performance cruiser that was conceived as a blue water voyaging boat for a family. At 52 feet, it falls within the size range that an experienced couple can handle, so it would make a great platform for a couple to explore the world. The 1600 like all of the Seawinds and Corsairs, are built in Vietnam.

Nautitech 542

Length: 54 Feet

Price: Around $1.2 Million USD New

Nautitech 542 is the typical example of offshore meeting first class. This boat has ideally tweaked fittings for smooth sailing under any circumstances. Furnished with a single wheel on its roof for perfect views of the boat and a comfy 2-person seat. The idea of this boat is mostly based on performance and quality. Asides from the positions of the helm, Nautitech 541 and 542 are very similar. Nautitech 542 is large and luxurious. The sail controls at the helm stations for easy sailing maneuvers and perfect for all weather conditions. The interior was designed by French designer Franck Darnet. Equipped with state of the art furniture and cabin experience, a sleek experience is assured.

>>Also Read: Best Sailboats Under 100k

Xquisite X5

Length: 51 Feet

Price: Around $1.5 Million USD

Once you have met your first Xquisite X5, you will never forget its absolute distinctive looks and almost space-traveling styling. The whole look of the boat, with its large reverse curving arches and cat’s eye windows, says right out loud that you need to pay attention. The boat itself is a very modern design with a classic and comfortable interior. It sails better than most of its peers in the 50-foot range and is set up cleverly so one watchstander can hand, reef, and steer all from the protected comfort of the raised steering station. Tomas and Sara, who build the boats in South Africa, are veteran cruisers and owned hull number one of the X5 line before taking over the company. Their attention to detail and the innovations they have incorporated into the boats all stem from their time living aboard and blue water sailing.

Privilege 615

Length: 61 Feet

Price: From $800k to $1.3 Million USD on the Used Market

When it comes to onboard luxury, Marc Lombard, who designed this catamaran, is an expert in that field. This lovely boat is in touch with the latest style, sporting a flybridge complete with two wheels and a broad sunbed suitable for the crew to relax the day away. The 615 is a combination of simplistic and superior design with an outstanding crew, results in the ultimate luxury Caribbean cruising experience. The impeccable elegance of the interior with a lavish owner’s suite and the boat’s perfect wood quality are two great reasons to make you get the boat. The freedom to choose a four or five-double cabin is another, depending on the size of the family.

Followed closely by its outstanding exterior, you’re sure to fall in love with it on sight, from the cockpit to the foredeck. With an impressive platform and lustrous profile, the Privilède 615 contradicts the volume and versatility of its interior. One wonders how they fit into the other, gives it a great ambiance.

>>Also Read: Best Catamarans Under 200k

Balance 526

Length: 52ft 6in

Price: From $1.3 to $1.6 Million USD New

Multihull impresario, dealer, and broker Phil Berman (The Multihull Company) has sold more multihulls over the last 30 years than just about anyone. His latest project has been the development of the Balance line of performance cruising cats. The queen of the line is the Balance 526 that was introduced a few years ago and has proven to be a very successful player in the 50-foot plus segment of the cat market. Built in South Africa by noted composite experts, the 526 offers a well-conceived combination of great sailing performance and luxury living in a boat that can be handled by an experienced couple.

The boat has plenty of innovations, among them a helm that can be tilted up so you can steer from the raised helm station or tilted down so you can steer from the protection of the cockpit. Very cool. The design does not take any particular element to the “extreme.” Instead, Berman and his crew have sought to provide a boat that is truly well balanced in all aspects. And, they’ve done it.

>>Also Read: How Long Do Sailboats Last?

Length: 62 Feet

Price: From $700k to $1.7 Million USD on the Used Market

Manufactured in 2014, this luxury catamaran is ideal for those who enjoy watersports and healthy activities. It was designed by world-renowned designer Van Peteghem-Lauriot Prvost (VPLP) and built to top-notch quality with a focus on stability, performance, luxury, and spaciousness. The maximum capacity of this boat is 12 guests in 4-double and 2-twin cabins. The Sunreef 620 is the very first to feature a newly developed rig. From the large cabins, saloon, galley, and sail performance, the 620 is one boat you’d get a memorable experience on. As you can understand, this is a great catamaran over 50 feet to use as a liveaboard.

Outremer 5X

Length: 69 Feet

Price: From $1.3 to $1.8 Million USD on the Used Market

The Outremer 5X is unlike any other in the yacht market as it is fast, sturdy, but luxurious all at the same time. Also, it possesses finely finished cabinetwork, spacious accommodations, and an excellent payload carrying ability. Modeled great agility to make even a single person handle any maneuver, its retractable high aspect ratio daggerboards assure a shallower drift giving access to the most remote of harbors.

When it comes to the interior, every Outremer model is trying to outdo the last in elegance, neatness, and modernity. She offers an unrestricted view and functional comfort. The port hull suite includes a king-sized bed, superb sea view portlight, an office, and a separate private entrance from the rear. It’s a semi-custom interior designed by VPLP in conjunction with Patrick le Quement. It won the ‘European Yacht of the Year’ and Cruising World’s ‘Boat of the Year’ in 2013 and 2014. This catamaran is as affordable as a luxury catamaran over 50 feet can get. Beautiful isn’t she?

Length: 51 Feet

Price: From $450k to $550k On the Used Market

Aimed at Blue-water sailors looking to sail fast and far, Switch 51 has proved itself and regarded in this day as a remarkable ocean cruising catamaran. This classic high-performance voyage was designed by VPLP and is said to combine a level of comfort, performance, and safety. It was built by Sud Composites in France with high tech materials. Sud initially built about 18 of these classic catamarans from 2001 to 2007.

Switch 51 hulls are built with vinyl ester sandwiched with a Klegecelle PVC foam core, thereby creating a hull light enough to be real quick and heavy enough to handle the ocean waves and swells. The saloon and galley are huge, with the cockpit spacious. The layout and accommodation are perfect for a small family with classic amenities aimed at making your stay on board a memorable one. This also a pretty affordable option in this category with prices on the used market as low as 450k.

>>Also Read: Best Sailboats to Live On

Final Thoughts

If you are looking for a large catamaran to either spend your summer vacation with your family or to liveaboard, this list of the best catamarans over 50 feet will point you in the right direction. Obviously, there are many options on the used market, but you should pick the one that you like best and fits your budget.

While the prices vary with their manufactured year, options, location, etc., buying any of the above-mentioned catamarans will certainly offer you state of the art onboard luxury and comfort. Why not try one of them out on your next boat cruise to see for yourself before you buy?

Peter is the editor of Better Sailing. He has sailed for countless hours and has maintained his own boats and sailboats for years. After years of trial and error, he decided to start this website to share the knowledge.

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Recent news, the multihull company announces the sale of the first pre-owned balance 482.

The Multihull Company is pleased to announce the closing on the Balance 482 "SeaLife" We wanted to take a moment and thank her new owners on their amazing new catamaran, and to also congratulate our team handling the sale. TMC agent Andrew Hodgdon successfully represented the buyers on the sale of the vessel, while TMC CEO Will Miller represented the...

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Visit Us at the 2023 Miami Boat Show

The Multihull Company is thrilled to announce our participation in the Miami Boat Show, taking place on February 15-19, 2023. As one of the premier boat shows in the world, this event is the perfect platform for us to showcase our wide range of high-quality multihulls for sale.  We are committed to providing our customers with the best experience possible,...

Introducing the Tao 452: On Display At The Annapolis Boat Show October 12 – 15, 2023

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The Multihull Company is thrilled to announce the appointment of Ian Edmonson as a yacht broker at its newly opened Fort Pierce location. Ian brings a unique blend of boating passion, brokerage experience, real estate expertise, and customer-focused mentality to the team. Ian's love for boating began at an early age and has only continued to grow, leading him to...

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We are thrilled to announce that Alan Prater has joined The Multihull Company team as a Yacht Broker in Virginia covering the Hampton Roads area of Virginia. With a lifelong passion for the water and a career spent in the US Navy and as a maritime training professional, Alan brings a wealth of experience and expertise to our team. Alan...

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I bought a yacht that I had never seen. I did this because I trusted my broker Andrew Holland. It was not an easy job for Andrew, as I am an experienced boat builder and owner of previous yachts, but work in West Africa. Imagine how hard it was to communicate what I was looking for. Andrew came up with exactly what I wanted. He dealt with time delays, all my questions at odd hours, and was there for the survey. He reported honestly and professionally. After buying the yacht, I arrived at the boat on a Sunday night, after dark, after travelling from West Africa to the Caribbean, and found it was better than expected. He never pulled punches and made me aware of shortfalls. I expected to spend my one month leave working on the boat, but actually spent less than one week, and was able to spend 3 weeks sailing – wonderful bonus.

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2006 LIDGARD 73 ft Type: Sail | Condition: Used Model: Executive 73 Catamaran for Sale Gloucestar Virginia

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2022 SUNREEF 70 ft Type: Power | Condition: Used Model: Sunreef 70 PC Catamaran for Sale Palma Spain

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2020 SUNREEF 70 ft Type: Sail | Condition: Used Model: Sunreef 70 Catamaran for Sale St Thomas U.S. Virgin Islands

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Used Motor Yachts for Sale from 50 to 60 Feet

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Power Boats over 50ft | Used Boats For Sale

Strange Glow Over Moscow Skies Triggers Panic as Explosions Reported

B right flashes lit up the night sky in southern Moscow in the early hours of Thursday morning, new footage appears to show, following reports of an explosion at an electrical substation on the outskirts of the city.

Video snippets circulating on Russian-language Telegram channels show a series of flashes on the horizon of a cloudy night sky, momentarily turning the sky a number of different colors. In a clip shared by Russian outlet MSK1.ru, smoke can be seen rising from a building during the flashes lighting up the scene.

Newsweek was unable to independently verify the details of the video clips, including when and where it was filmed. The Russian Ministry of Emergency situations has been contacted via email.

Several Russian Telegram accounts said early on Thursday that residents of southern Moscow reported an explosion and a fire breaking out at an electrical substation in the Leninsky district, southeast of central Moscow.

Local authorities in the Leninsky district told Russian outlet RBC that the explosion had happened in the village of Molokovo. "All vital facilities are operating as normal," Leninsky district officials told the outlet.

The incident at the substation in Molokovo took place just before 2 a.m. local time, MSK1.ru reported.

Messages published by the ASTRA Telegram account, run by independent Russian journalists, appear to show residents close to the substation panicking as they question the bright flashes in the sky. One local resident describes seeing the bright light before losing access to electricity, with another calling the incident a "nightmare."

More than 10 villages and towns in the southeast of Moscow lost access to electricity, the ASTRA Telegram account also reported. The town of Lytkarino to the southeast of Moscow, lost electricity, wrote the eastern European-based independent outlet, Meduza.

Outages were reported in the southern Domodedovo area of the city, according to another Russian outlet, as well as power failures in western Moscow. Electricity was then restored to the areas, the Strana.ua outlet reported.

The cause of the reported explosion is not known. A Telegram account aggregating news for the Lytkarino area described the incident as "an ordinary accident at a substation."

The MSK1.ru outlet quoted a local resident who speculated that a drone may have been responsible for the explosion, but no other Russian source reported this as a possible cause.

Ukraine has repeatedly targeted Moscow with long-range aerial drones in recent months, including a dramatic wave of strikes in late May.

On Sunday, Moscow Mayor Sergei Sobyanin said the region's air defense systems had intercepted an aerial drone over the city of Elektrostal, to the east of Moscow. No damage or casualties were reported, he said.

The previous day, Russian air defenses detected and shot down another drone flying over the Bogorodsky district, northeast of central Moscow, Sobyanin said.

There is currently no evidence that an aerial drone was responsible for the reported overnight explosion at the electrical substation in southern Moscow.

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Elektrostal

Elektrostal Localisation : Country Russia , Oblast Moscow Oblast . Available Information : Geographical coordinates , Population, Area, Altitude, Weather and Hotel . Nearby cities and villages : Noginsk , Pavlovsky Posad and Staraya Kupavna .

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2005 Catamaran TS 50. US$626,812. US $4,905/mo. Raiatea Yacht | Tahiti, French Polynesia. <. 1. >. * Price displayed is based on today's currency conversion rate of the listed sales price. Boats Group does not guarantee the accuracy of conversion rates and rates may differ than those provided by financial institutions at the time of transaction.

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Used sail Catamaran for sale - EXTRA NAUTI 2019 Lagoon 50 (50ft)-Vessel Summary. Inquire About this Boat Full Specifications Image Gallery BASIC SUMMARY. Boat Length: 50 ft: Asking Price: $995,000: Boat Name: "EXTRA NAUTI" Manufacturer: LAGOON: Model: Lagoon 50: Type of Yacht: Sail: Boat Condition: Used : Boat Status: Catamaran for Sale: Model ...

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Used 50 Foot Boats & Yachts For Sale. Explore used yachts and boats for sale worldwide between 50-59 feet. Often, people who are considering a 50 foot yacht are looking to extend their time on the water. A 50 foot boat frequently offers two or three staterooms, making cruising or fishing with family and friends much more comfortable.

2020 SUNREEF 70 ft Type: Sail | Condition: Used Model: Sunreef 70 Catamaran for Sale St Thomas U.S. Virgin Islands Price: $5,800,000 Inquire Now Images Gallery Save

Listed below are used motor yachts for sale between 50 - 60 feet. Motor yachts vary greatly in their hull design, interior accommodations, engine packages, and performance capabilities. They often feature multiple staterooms for owners and guests as well as bathrooms, showers, full galleys and a wide range of other amenities to make life on ...

Tutte 25 km 50 km 100 km 200 km 300 km 500 km 1000 km 2000 km 5000 km. from your location. Condition. All. New. Used. ... These vessels range in size from 19 feet to over 100 feet. ... Power Catamaran boats pricing. Power Catamaran boats for sale on YachtWorld are available in a range of prices from $37,160 on the more modest side up to ...

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B right flashes lit up the night sky in southern Moscow in the early hours of Thursday morning, new footage appears to show, following reports of an explosion at an electrical substation on the ...

Elektrostal Geographical coordinates: Latitude: 55.8, Longitude: 38.45 55° 48′ 0″ North, 38° 27′ 0″ East Elektrostal Area: 4,951 hectares 49.51 km² (19.12 sq mi): Elektrostal Altitude: 164 m (538 ft) Elektrostal Climate: Humid continental climate (Köppen climate classification: Dfb)

Elektrostal, city, Moscow oblast (province), western Russia.It lies 36 miles (58 km) east of Moscow city. The name, meaning "electric steel," derives from the high-quality-steel industry established there soon after the October Revolution in 1917. During World War II, parts of the heavy-machine-building industry were relocated there from Ukraine, and Elektrostal is now a centre for the ...

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Find company research, competitor information, contact details & financial data for BETA GIDA, OOO of Elektrostal, Moscow region. Get the latest business insights from Dun & Bradstreet.

eastward ho sailboat for sale

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24' eastward ho cruisers.

ARCHIVED: This is a previously listed vessel and is no longer offered for sale If you would like assistance locating a similar vessel, Click Here to locate a similar boat

Designed by Eldredge-McInnis and built by Portsmouth Yacht Co., the Eastward Ho is a compact yet roomy sloop designed for family cruising in comfort. She is a proven design which combines traditional elegance with practical accommodations. Nothing has been overlooked to satisfy both the sailor and the cruising enthusiast. Her generous headroom, two berths, full galley, and enclosed head are unique on a boat of this size. Her spacious cockpit affords seats long enough for an afternoon nap or additional overnight guests. Sailing or under power she is lively and responsive with a motion reminiscent of a much larger boat. Her ample beam and sufficient ballast make her very stiff without sacrificing valuable draft.

Attabuoy  is in need of general cleaning inside and out and some cosmetic work. The keel will need some minor fiberglass work. The sails are like new. The engine turns over, but has not been operated for a number of years. Take a look and you will fall in love!

• Specifications
• Description

Hull color - white

Deck color - cream

Keel - internal lead

Cockpit Cushions

Stern Ladder

Opening Ports - 2

Pressure Water

Refrigerator

Battery - 1 (most likely is dead)

Shorepower 110V

Roller Furling

Depthsounder

Cradle - steel

Anchors - 3

Anchor Rode - 2

Fire Extinguisher

Life Jackets

Main - white, Dacron, The Yacht Sailmakers

Main Cover - blue, Sunbrella

Genoa - white, Dacron, The Yacht Sailmakers

Summer & Winter - Torresen Marine, Inc., Muskegon, Michigan

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eastward ho 24 for sale

• eastward ho 24

1976 CE Ryder Eastward Ho 24 sailboat for sale in Connecticut

Ce ryder eastward ho 24.

Built by CE Ryder (USA) and finished by Portsmouth Yacht Co., Rhode Island, USA, this stout pocket cruiser is a solid full-keel sailing vessel. Omoo has had a lot...

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Sales Department phone 2012 Yamaha SX240 HO 1 of 111 View Large Images Description Stock #075952 - If you are in the market for a jet, look no further...

Marine Connection Boat Sales 1.phone West Palm Beach, FL 2011 Yamaha SX240 HO 2011 Yamaha SX240 HO Jet Boat Combines Performance & Family Friendly Fun!! $34,900...

Marine Connection Boat Sales 1.phone West Palm Beach, FL 2011 Yamaha SX240 HO NICE! 2011 Yamaha SX240 HO Jet Boat, Twin 180HP Engines, Financing! $34,900 ConditionUsed...

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This boat has approximately 53 hours and in like new condition and only used in fresh water. Boat has been in dry storage when not in use. It's powered by twin 180...

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Portsmouth Eastward Ho Boats for sale

1976 PORTSMOUTH Eastward Ho

Neptune, New Jersey

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Model Eastward Ho

Category Sailboats

Posted Over 1 Month

1976 PORTSMOUTH Eastward Ho All of the prep work has been done and she's just about ready for paint. This is a great opportunity for someone looking to customize an Eastward Ho their way and do it cheap!   Seller has all parts to complete this project. Also available separately is the completely rebuilt 14HP Volvo MD7A Diesel engine, ready to be placed in the boat.  Top to Bottom rebuild was performed by world renowned Monmouth Marine Engines of Brielle NJ. $3000 Invested.

Belmar, New Jersey

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• Sailboat Guide

Eastward HO 24

Eastward HO 24 is a 23 ′ 7 ″ / 7.2 m monohull sailboat designed by Walter McInnis and built by C. E. Ryder starting in 1975.

Rig and Sails

Auxilary power, accomodations, calculations.

The theoretical maximum speed that a displacement hull can move efficiently through the water is determined by it's waterline length and displacement. It may be unable to reach this speed if the boat is underpowered or heavily loaded, though it may exceed this speed given enough power. Read more.

Classic hull speed formula:

Hull Speed = 1.34 x √LWL

Max Speed/Length ratio = 8.26 ÷ Displacement/Length ratio .311 Hull Speed = Max Speed/Length ratio x √LWL

Sail Area / Displacement Ratio

A measure of the power of the sails relative to the weight of the boat. The higher the number, the higher the performance, but the harder the boat will be to handle. This ratio is a "non-dimensional" value that facilitates comparisons between boats of different types and sizes. Read more.

SA/D = SA ÷ (D ÷ 64) 2/3

• SA : Sail area in square feet, derived by adding the mainsail area to 100% of the foretriangle area (the lateral area above the deck between the mast and the forestay).
• D : Displacement in pounds.

Ballast / Displacement Ratio

A measure of the stability of a boat's hull that suggests how well a monohull will stand up to its sails. The ballast displacement ratio indicates how much of the weight of a boat is placed for maximum stability against capsizing and is an indicator of stiffness and resistance to capsize.

Ballast / Displacement * 100

Displacement / Length Ratio

A measure of the weight of the boat relative to it's length at the waterline. The higher a boat’s D/L ratio, the more easily it will carry a load and the more comfortable its motion will be. The lower a boat's ratio is, the less power it takes to drive the boat to its nominal hull speed or beyond. Read more.

D/L = (D ÷ 2240) ÷ (0.01 x LWL)³

• D: Displacement of the boat in pounds.
• LWL: Waterline length in feet

Comfort Ratio

This ratio assess how quickly and abruptly a boat’s hull reacts to waves in a significant seaway, these being the elements of a boat’s motion most likely to cause seasickness. Read more.

Comfort ratio = D ÷ (.65 x (.7 LWL + .3 LOA) x Beam 1.33 )

• D: Displacement of the boat in pounds
• LOA: Length overall in feet
• Beam: Width of boat at the widest point in feet

Capsize Screening Formula

This formula attempts to indicate whether a given boat might be too wide and light to readily right itself after being overturned in extreme conditions. Read more.

CSV = Beam ÷ ³√(D / 64)

Originally designed for wood contruction. The hulls of the later, FG version were built by CE Ryder (USA) and finished by Portsmouth Yacht Co. Diesel power was available as an option.

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Eastward ho 24 preowned sailboats for sale by owner. Eastward ho 24 used sailboats for sale by owner.

Both salon settees turn into two twin beds so can sleep 4 adults. YEAR: 1977 MAKE: Portsmouth Yacht Co MODEL: Eastward Ho CLASS: Sloop, Pocket Cruiser LENGTH: 26' (24' with 2' boomkin) HULL MATERIAL: FIberglass reinforced plastic FUEL TYPE: Diesel. AIR CONDITIONING: Drop in Cruise Air. ALL PHOTOS ARE RECENT.

1978. 31'. 10'. 4.2'. Florida. $12,900. Description: Airyella is a classic New England style sloop - has incredible character, is very distinctive, and is a pleasure to sail. She is perfect for anyone looking for a boat that will sail, and anchor overnight with 1-5 people, comfortably in the bay and the Keys and beyond, at a fantastic price.

1976. 24'. 9'. 4'. Connecticut. $12,000. Description: Built by CE Ryder (USA) and finished by Portsmouth Yacht Co., Rhode Island, USA, this stout pocket cruiser is a solid full-keel sailing vessel. Omoo has had a lot of updates including new diesel engine (Kubota Beta marine), rebuilt gearbox (2021), new standing and running rigging (2020), new ...

Broker: Designed by Eldredge-McInnis and built by Portsmouth Yacht Co., the Eastward Ho is a compact yet roomy sloop designed for family cruising in comfort. She is a proven design which combines traditional elegance with practical accommodations. Nothing has been overlooked to satisfy both the sailor and the cruising enthusiast.

A boat with a BN of 1.6 or greater is a boat that will be reefed often in offshore cruising. Derek Harvey, "Multihulls for Cruising and Racing", International Marine, Camden, Maine, 1991, states that a BN of 1 is generally accepted as the dividing line between so-called slow and fast multihulls.

Model McInnis. Category Sailboats. Length 31'. Posted Over 1 Month. 1985 #1 Hull McInnis,31 ft., 4.5ft. draft, McInnis Cutter rig Eastward Ho series. 28hp Yanmar diesel, All hardwood Interior, Complete custom finished, In bristol condition. Completely blue water equipt.Leave Message at 772/283-0853. $40000.

Go to Sailing Texas classifieds for current sailboats for sale . Eastward HO 24, 1977 LOA 25'5" LWL 20' Beam 8'8" Draft 3'10" SA 283 sq ft Ballast 3,600 Displacement 7,000 Keel Full Designed by Thomas F. Eldredge/Walter J. Mcinnis and built by the Portsmouth Boat Company (UK).

Used 1978 Eastward Ho 31 for sale is located in Bienville National Forest (Mississippi, United States of America). This vessel was designed and built by the Eastward shipyard in 1978. Key features 1978 Eastward Ho 31: length 9.45 meters. engine: fuel type - diesel. 1978 Eastward Ho 31 refers to classes: sailing yachts , sailboats and sailing ...

Seller's Description. Portsmouth Eastward Ho 24, 1978 sailboat for sale I am selling my 1978 Portsmouth Eastward Ho 24 for $12,500. The boat is in Alamitos Bay (Seal Beach, CA / Long Beach, CA) where the buyer may assume the slip at $320 a month. Very nice location, across the street from the new 2nd and PCH outdoor mall.

Go to Sailing Texas classifieds for current sailboats for sale Eastward Ho, 24 ft., 1975 No. 55, 1975. Highly regarded Eldridge/McGinnis cruising design- Full keel, 4 ft. draft. ... The lower a boat's ratio is, the less power it takes to drive the boat to its nominal hull speed or beyond. Read more. Formula. D/L = (D ÷ 2240) ÷ (0.01 x LWL)³ ...

Seller's Description. 1980 Portsmouth Yacht Co Eastward Ho 31. She is a classic designed in 1959, built in 1980. Similar to the Sea Sprite 33 that Robin Graham sailed around the world. Custom interior Volvo Penta MD2B 25hp Nice thick teak toe rail Electric Windlass Auto Helm Updated hardware above deck Updated rigging Bimini, dodger frames ...

Search eastward ho 24 prices - more than 1 listings - Built by CE Ryder (USA) and finished by Portsmouth Yacht Co., Rhode Island, USA, this stout pocket cruiser is a solid full-keel sailing vessel. ... 1976 CE Ryder Eastward Ho 24 sailboat for sale in Connecticut. Ce Ryder eastward ho 24 . Built by CE Ryder (USA) and finished by Portsmouth ...

Boat Trader currently has 3 Eastward boats for sale, including 1 new vessels and 2 used boats listed by both private sellers and professional yacht brokers and boat dealerships mainly in United States. The oldest model listed is a contemporary boat built in 2018 and the newest model year of 2021.

Join Date: Aug 2018. Posts: 3. Eastward Ho 31 Sailboat. Cutter Rig. Eldredge McInnis design, built in RI by C. Ryder Yachts. Roller furling jib. Jib boom & roller for twin furlers. Re-built Volvo Penta 30hp with spare engine & transmission. Bimini & dodger.

35.5' Endeavour E35 Presently on the hard for winter storage at Morgans Marina, New Jersey Asking $35,000

2015 Malibu Wakesetter 22 VLX. Battle Creek, MI. $40,000. 2008 Hydra-Sports 2200 CC. Sarasota, FL. $26,500. 2 new and used Portsmouth Eastward Ho boats for sale at smartmarineguide.com.

First S-400 bltn, Elektrostal, Moscow.

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Advertisement. Eastward HO 24 is a 23′ 7″ / 7.2 m monohull sailboat designed by Walter McInnis and built by C. E. Ryder starting in 1975.