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      Ovarian Cancer Statistics, 2018

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          Abstract

          In 2018, there will be approximately 22,240 new cases of ovarian cancer diagnosed and 14,070 ovarian cancer deaths in the US. Herein, the American Cancer Society provides an overview of ovarian cancer occurrence based on incidence data from nationwide population-based cancer registries and mortality data from the National Center for Health Statistics. The status of early detection strategies is also reviewed. In the US, overall ovarian cancer incidence declined by 29% from 1985 (16.6 per 100,000) to 2014 (11.8 per 100,000), while mortality declined 33% from 1976 (10.0 per 100,000) to 2015 (6.7 per 100,000). Ovarian cancer encompasses a heterogenous group of malignancies that vary in etiology, molecular biology, and numerous other characteristics. Ninety percent of ovarian cancers are epithelial, the most common being serous carcinoma, for which incidence is highest in non-Hispanic whites (NHWs; 5.2 per 100,000) and lowest in non-Hispanic blacks (NHBs; 3.4 per 100,000) and Asian/Pacific Islanders (APIs; 3.4 per 100,000). Notably, however, APIs have the highest incidence of endometrioid and clear cell carcinoma, which occur at younger ages and help explain comparable epithelial cancer incidence for APIs and NHWs younger than 55 years. Most serous carcinomas are diagnosed at stage III (51%) or IV (29%), for which the 5-year cause-specific survival is 42% and 26%, respectively. For all stages of epithelial cancers combined, five-year survival is highest in APIs (57%) and lowest in NHBs (35%), who have the lowest survival for almost every stage of diagnosis across cancer subtype. Epithelial ovarian cancer survival has plateaued in NHBs for decades, whereas it continues to increase in NHWs, from 40% for cases diagnosed during 1992–1994 to 47% during 2007–2013. Although there has been progress in reducing ovarian cancer incidence and mortality overall, further research is needed to determine the source of racial disparities and identify effective mechanisms for early ovarian cancer detection and prevention.

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          Most cited references45

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          Cancer risks associated with germline mutations in MLH1, MSH2, and MSH6 genes in Lynch syndrome.

          Providing accurate estimates of cancer risks is a major challenge in the clinical management of Lynch syndrome. To estimate the age-specific cumulative risks of developing various tumors using a large series of families with mutations of the MLH1, MSH2, and MSH6 genes. Families with Lynch syndrome enrolled between January 1, 2006, and December 31, 2009, from 40 French cancer genetics clinics participating in the ERISCAM (Estimation des Risques de Cancer chez les porteurs de mutation des gènes MMR) study; 537 families with segregating mutated genes (248 with MLH1; 256 with MSH2; and 33 with MSH6) were analyzed. Age-specific cumulative cancer risks estimated using the genotype restricted likelihood (GRL) method accounting for ascertainment bias. Significant differences in estimated cumulative cancer risk were found between the 3 mutated genes (P = .01). The estimated cumulative risks of colorectal cancer by age 70 years were 41% (95% confidence intervals [CI], 25%-70%) for MLH1 mutation carriers, 48% (95% CI, 30%-77%) for MSH2, and 12% (95% CI, 8%-22%) for MSH6. For endometrial cancer, corresponding risks were 54% (95% CI, 20%-80%), 21% (95% CI, 8%-77%), and 16% (95% CI, 8%-32%). For ovarian cancer, they were 20% (95% CI, 1%-65%), 24% (95% CI, 3%-52%), and 1% (95% CI, 0%-3%). The estimated cumulative risks by age 40 years did not exceed 2% (95% CI, 0%-7%) for endometrial cancer nor 1% (95% CI, 0%-3%) for ovarian cancer, irrespective of the gene. The estimated lifetime risks for other tumor types did not exceed 3% with any of the gene mutations. MSH6 mutations are associated with markedly lower cancer risks than MLH1 or MSH2 mutations. Lifetime ovarian and endometrial cancer risks associated with MLH1 or MSH2 mutations were high but do not increase appreciably until after the age of 40 years.
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            Inherited Mutations in Women With Ovarian Carcinoma.

            Germline mutations in BRCA1 and BRCA2 are relatively common in women with ovarian, fallopian tube, and peritoneal carcinoma (OC) causing a greatly increased lifetime risk of these cancers, but the frequency and relevance of inherited mutations in other genes is less well characterized.
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              Mutation of FOXL2 in granulosa-cell tumors of the ovary.

              Granulosa-cell tumors (GCTs) are the most common type of malignant ovarian sex cord-stromal tumor (SCST). The pathogenesis of these tumors is unknown. Moreover, their histopathological diagnosis can be challenging, and there is no curative treatment beyond surgery. We analyzed four adult-type GCTs using whole-transcriptome paired-end RNA sequencing. We identified putative GCT-specific mutations that were present in at least three of these samples but were absent from the transcriptomes of 11 epithelial ovarian tumors, published human genomes, and databases of single-nucleotide polymorphisms. We confirmed these variants by direct sequencing of complementary DNA and genomic DNA. We then analyzed additional tumors and matched normal genomic DNA, using a combination of direct sequencing, analyses of restriction-fragment-length polymorphisms, and TaqMan assays. All four index GCTs had a missense point mutation, 402C-->G (C134W), in FOXL2, a gene encoding a transcription factor known to be critical for granulosa-cell development. The FOXL2 mutation was present in 86 of 89 additional adult-type GCTs (97%), in 3 of 14 thecomas (21%), and in 1 of 10 juvenile-type GCTs (10%). The mutation was absent in 49 SCSTs of other types and in 329 unrelated ovarian or breast tumors. Whole-transcriptome sequencing of four GCTs identified a single, recurrent somatic mutation (402C-->G) in FOXL2 that was present in almost all morphologically identified adult-type GCTs. Mutant FOXL2 is a potential driver in the pathogenesis of adult-type GCTs. 2009 Massachusetts Medical Society
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                Author and article information

                Journal
                0370647
                2683
                CA Cancer J Clin
                CA Cancer J Clin
                CA: a cancer journal for clinicians
                0007-9235
                1542-4863
                4 July 2019
                29 May 2018
                July 2018
                11 July 2019
                : 68
                : 4
                : 284-296
                Affiliations
                [1 ]Senior Epidemiologist, Surveillance and Health Services Research, American Cancer Society, Atlanta, GA
                [2 ]Earl Stadtman Investigator, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD
                [3 ]Director, Breast and Gynecologic Cancer Surveillance, Surveillance and Health Services Research, American Cancer Society, Atlanta, GA
                [4 ]Epidemiologist, Surveillance and Health Services Research, American Cancer Society, Atlanta, GA
                [5 ]Program Director, Breast and Gynecologic Cancer Research Group, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD
                [6 ]Executive Associate Dean for Academic Affairs and Professor, Florida International University Herbert Wertheim College of Medicine, Miami, FL
                [7 ]Strategic Director, Breast and Gynecologic Cancer Research, Behavioral and Epidemiologic Research Group, American Cancer Society, Atlanta, GA
                [8 ]Vice President, Surveillance and Health Services Research, American Cancer Society, Atlanta, GA
                [9 ]Strategic Director, Surveillance Information Services, Surveillance and Health Services Research, American Cancer Society, Atlanta, GA
                Author notes
                Corresponding author: Lindsey A. Torre, MSPH, Surveillance and Health Services Research, American Cancer Society, 250 Williams Street NW, Atlanta, Georgia 30303; lindsey.torre@ 123456cancer.org
                Article
                PMC6621554 PMC6621554 6621554 nihpa1039849
                10.3322/caac.21456
                6621554
                29809280
                915639f2-c7e9-46b4-bcb8-8cfb42af0de4
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