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This review summarizes genetic drivers across high-grade serous, endometrioid, and clear-cell ovarian carcinomas, linking subtype-specific mutations to personalized therapeutic strategies. It highlights TP53 centrality, mutation prevalence differences, and the clinical relevance of BRCA1/2 for genetic risk and PARP inhibitor therapy. The article also discusses platinum-resistance alterations, including ARID1A, PIK3CA, and PTEN, and explores pathway-targeted approaches such as PI3K/AKT/mTOR inhibition and concepts for restoring WT p53 function.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/complexity-of-the-genetic-background-of-oncogenesis-in-ovarian-cancer-genetic-instability-and-clinical-implications/331867/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/complexity-of-the-genetic-background-of-oncogenesis-in-ovarian-cancer-genetic-instability-and-clinical-implications/331867.png","ImageObject",300,407,{"name":92,"@type":93},"Patrick","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-29","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":52},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"Which ovarian cancer subtypes are covered, and what is the focus of the review?","Question",{"text":112,"@type":113},"The review addresses high-grade serous, endometrioid, and clear-cell ovarian carcinomas, focusing on genetic aspects of oncogenesis, genetic instability, and clinical implications for personalized care.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"Why are TP53 and BRCA1/2 mutations emphasized?",{"text":117,"@type":113},"TP53 is highlighted as pivotal for mutational analysis, including discussion of p53 immunohistochemical staining. 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Complexity of the Genetic Background of Oncogenesis in Ovarian Cancer—Genetic Instability and Clinical Implications. Cells 2024, 13, 345. [https://doi.org/10.3390/](https://doi.org/10.3390/)[ ](https://doi.org/10.3390/)cells13040345  \nAcademic Editors: Marek Nowak and Miłosz Wilczy ´nski  \nReceived: 9 January 2024  \nRevised: 29 January 2024  \nAccepted: 13 February 2024  \nPublished: 15 February 2024  \nCopyright: © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \n1 1st Clinical Department of Gynecology and Obstetrics, Wroclaw Medical University, 50-367 Wroclaw, Poland; [marek.murawski@umw.edu.pl](marek.murawski@umw.edu.pl)  \n2 Laboratory of Biology of Stem and Neoplastic Cells, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, 53-114 Wroclaw, Poland;  \n[aleksandra.bielawska-pohl@hirszfeld.pl](aleksandra.bielawska-pohl@hirszfeld.pl) (A.B.-P.); [aleksandra.klimczak@hirszfeld.pl](aleksandra.klimczak@hirszfeld.pl) (A.K.)  \n* Correspondence: [a.jagodzinski@umw.edu.pl](a.jagodzinski@umw.edu.pl)  \nAbstract: Ovarian cancer is a leading cause of death among women with gynecological cancers, and is often diagnosed at advanced stages, leading to poor outcomes. This review explores genetic aspects of high-grade serous, endometrioid, and clear-cell ovarian carcinomas, emphasizing personalized treatment approaches. Specific mutations such as TP53 in high-grade serous and BRAF/KRAS in low-grade serous carcinomas highlight the need for tailored therapies. Varying mutation prevalence across subtypes, including BRCA1/2, PTEN, PIK3CA, CTNNB1, and c-myc amplification, offers potential therapeutic targets. This review underscores TP53’s pivotal role and advocates p53 immunohistochemical staining for mutational analysis. BRCA1/2 mutations’ significance as genetic risk factors and their relevance in PARP inhibitor therapy are discussed, emphasizing the importance of genetic testing. This review also addresses the paradoxical better prognosis linked to KRAS and BRAF mutations in ovarian cancer. ARID1A, PIK3CA, and PTEN alterations in platinum resistance contribute to the genetic landscape. Therapeutic strategies, like restoring WT p53 function and exploring PI3K/AKT/mTOR inhibitors, are considered. The evolving understanding of genetic factors in ovarian carcinomas supports tailored therapeutic approaches based on individual tumor genetic profiles. Ongoing research shows promise for advancing personalized treatments and refining genetic testing in neoplastic diseases, including ovarian cancer. Clinical genetic screening tests can identify women at increased risk, guiding predictive cancer risk-reducing surgery.  \nKeywords: genetic instability; oncogenesis; ovarian cancer; RRSO; TP53 mutations; BRCA1 mutations; BRCA2 mutations; BRAF mutations; RAS mutations; ARID1A mutations; PIK3CA mutations; PTEN mutations; CTNNB1 mutations; c-myc amplification  \n1. Introduction  \nOvarian cancer (OC) is the malignant neoplasm of the female reproductive organs associated with the highest mortality rate [1,2] and ranks eighth in terms of the incidence of malignant tumors worldwide according to 2020 data [2] . The population risk of developing OC is 1.3% . Ovarian cancer includes a heterogeneous group of malignant tumors, within which there are differences regarding, among other things, etiology and molecular biology. Most ovarian maligna","cbCain6kPA2IoGhx","https://ap.wps.com/l/cbCain6kPA2IoGhx","pdf",313255,16,"English","# Abstract\n# Keywords\n# 1. Introduction","[{\"question\":\"Which ovarian cancer subtypes are covered, and what is the focus of the review?\",\"answer\":\"The review addresses high-grade serous, endometrioid, and clear-cell ovarian carcinomas, focusing on genetic aspects of oncogenesis, genetic instability, and clinical implications for personalized care.\"},{\"question\":\"Why are TP53 and BRCA1/2 mutations emphasized?\",\"answer\":\"TP53 is highlighted as pivotal for mutational analysis, including discussion of p53 immunohistochemical staining. BRCA1/2 mutations are emphasized as genetic risk factors with relevance to PARP inhibitor therapy.\"},{\"question\":\"How do KRAS/BRAF and other alterations relate to prognosis and treatment resistance?\",\"answer\":\"The review notes a paradoxical better prognosis associated with KRAS and BRAF mutations. It also describes platinum resistance contributions from ARID1A, PIK3CA, and PTEN alterations and considers pathway-targeted therapeutic strategies.\"}]","Complexity of the Genetic Background of Oncogenesis in Ovarian Cancer - Genetic Instability and Clinical Implications | PDF",1789995551]