Molecular Pathogenesis of Ovarian Cancer and Therapeutic Strategies

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 20 May 2026 | Viewed by 4

Special Issue Editor


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Guest Editor
Women’s Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
Interests: gynecological cancers; ovarian cancers; drug resistance; DNA damage pathways; biomarkers of cancer

Special Issue Information

Dear Colleagues,

Epithelial ovarian cancer is the deadliest gynecological cancer in the U.S. and developed countries, often diagnosed late and developing drug resistance. It includes subtypes such as high-grade serous, low-grade serous, endometrioid, clear cell, and mucinous, with high-grade serous being the most lethal and the most difficult to treat. These cancers exhibit significant genetic diversity, particularly in high-grade serous (HGSC) tumors. Approximately 95% of HGSC cases harbor TP53 mutations, leading to S-phase checkpoint deficiency and a reliance on the G2/M checkpoint. In total, 40% also have mutations in tumor suppressor genes like BRCA1/2, affecting HR DNA repair, making them vulnerable to PARP inhibitors. However, resistance develops quickly, necessitating the identification of new molecular targets to extend survival.

Recent studies have identified molecular targets related to spindle assembly, PI3K pathways, cell cycle, DNA repair, and immune modulation. This review explores these findings, resultant therapeutic strategies, and/or their potential to develop new therapies, especially for hard-to-treat subtypes like high-grade serous ovarian cancer.

Dr. Jayakumar R. Nair
Guest Editor

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Keywords

  • ovarian cancer
  • pathogenic mutations
  • target therapy
  • genetic heterogeneity                                

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Published Papers

This special issue is now open for submission.
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