Ovarian Cancer is the Strongest Factor for Developing the Disease

Alice Sereka

Published Date: 2021-12-21

Alice Sereka*

Department of Reproductive Medicine, University of British Columbia, Vancouver, Canada

*Corresponding Author:
Alice Sereka
Department of Reproductive Medicine
University of British Columbia, Vancouver, Canada
E-mail: serekaalice@who.int

Received Date: December 11, 2021; Accepted Date: December 16, 2021; Published Date: December 21, 2021

Citation: Sereka A (2021) Ovarian Cancer is the Strongest Risk Factor for Developing the Disease. J Contracept Stud Vol 6 No.6:16.

Visit for more related articles at Journal of Reproductive Health and Contraception

Our understanding of the molecular epidemiology of breast and ovarian cancers has advanced dramatically during the last few decades. Various reproductive, demographic, and lifestyle factors elements that influence a woman's risk of breast or ovarian cancer ovarian cancer has been discovered. The classification of Hormonal and nutritional exposures, for example, are common risk factors. Demographic characteristics have thrown further light on the role of various environmental factors. The vulnerability to both diseases is determined by biological events. Because a family history of breast or ovarian cancer is the most common cause of cancer in women, The clarification of the strongest risk factor for getting the condition The study of hereditary genetics has been at the forefront of these endeavours. The discovery of the BRCA1 and BRCA2 genes, as well as their link with familial breast and ovarian cancers, ushered in a major shift in our knowledge of the significance of genetic factors in the aetiology of common malignancies two decades ago.

The clinical utility of BRCA1/2 in enhanced preventive strategies has sparked a lot of interest in the wake of these discoveries. Therapeutic testing for BRCA1/2 germline mutations, in combination with particular prophylactic clinical treatments (mastectomy, oophorectomy), has resulted in an unparalleled risk decrease in the population's high-risk individuals. In patients with BRCA1/2 mutations, preventive bilateral salpingo-oophorectomy virtually totally eliminates the risk of ovarian cancer. These major advancements show that the clinical care of patients with breast and ovarian cancer benefits greatly from important genetic markers are available, allowing for a more individualised assessment of Individual danger.

However, because BRCA1/2 mutations are linked to a small percentage of breast and ovarian malignancies, only a small percentage of people benefit from BRCA1/2-targeted preventative strategies. While hereditary breast and ovarian cancers account for 10%–20% of all cancer cases in the community, only 10% of hereditary instances are caused by mutations in BRCA1/2. This shows that there may be more genetic risk factors that have yet to be discovered. Moreover, whereas BRCA1/2 mutations pose the greatest risk, their age-specific penetrance is limited; carriers of BRCA1/2 mutations have an 80% lifetime risk of breast cancer, but only a 50% lifetime risk of ovarian cancer. This suggests that other genetic loci or environmental factors may influence the penetrance of BRCA1 and BRCA2 mutations

In the last few years, molecular epidemiology of breast and ovarian cancers has centred on answering these unanswered concerns. Genomewide association studies (GWASs) have revealed multiple common genetic variants conferring a risk of both breast and ovarian cancers in a sporadic population, some of which are related with risk effects in both illnesses, thanks to recent breakthroughs in genomic technologies. Many of the GWAS loci show distinct association patterns in BRCA1 (SNPs at 19p13) and BRCA2 (FGFR2, ZNF365) carriers, implying that common genetic variations affect BRCA1/2 penetrance as well. The GWAS loci, like BRCA1 and BRCA2 mutations, play a role in the clinical heterogeneity of breast and ovarian malignancies.

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