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Molecular Genetics in Ovarian Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 379

Special Issue Editor


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Guest Editor
Department of Life Sciences, University of Trieste, Valerio 28, 34127 Trieste, Italy
Interests: biological fluids; cancer; cancer biomarkers; cfDI; cfDNA; cfNA; copy number variation; ctDNA; ddPCR; disease-free survival; epigenetic; epigenetic sequencing; exosome; extracellular vesicle; genotyping; liquid biopsy; miRNA; mRNA; mutation; ncRNA; next- generation sequencing; overall survival; progression-free survival; recurrence-free survival; whole-exome sequencing
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Special Issue Information

Dear Colleagues,

Ovarian cancer (OC) is one of the deadliest malignancies in women worldwide due to its heterogeneity and high probability of recurrence, mainly due to chemotherapy resistance in its advanced stages (stages III and IV).

Common germline and somatic gene mutations in OCs such as BRCA and other driver mutations and their association with survival outcomes have recently been of great interest. In addition, OCs are characterised by genomic structural variations with frequent DNA gains and losses, making them a chromosomally unstable malignancy, especially the high-grade serous subtype. These structural changes are important mechanisms for the inactivation of tumour suppressors and cell cycle control genes in OCs.

In addition, there are an increasing number of studies demonstrating models based on differential gene expression that can help classify favourable and poor patient outcomes in patients with advanced-stage OC.

A better understanding of the mechanisms involved in these OC renegade cells’ metastasis and treatment response within the tumour microenvironment is therefore crucial for the implementation of rational oncotherapeutic strategies to prevent recurrence, ultimately improving patients' chances of survival.

Overall, this Special Issue highlights the recent advances in studies unravelling molecular trajectories toward a deeper understanding of molecular genetics and mechanistic pathways in OCs in terms of diagnosis, prognosis, therapeutic response, and chemotherapy resistance.

Dr. Bruna Scaggiante
Guest Editor

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Keywords

  • chemotherapy resistance
  • differential gene expression
  • genomic structural variation
  • ovarian cancer mutations
  • ovarian cancer metastasis
  • ovarian cancer treatment
  • novel molecular targets

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Published Papers (1 paper)

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Research

15 pages, 35957 KiB  
Article
Establishment of a Novel In Vitro and In Vivo Model to Understand Molecular Carcinogenesis of Endometriosis-Related Ovarian Neoplasms
by Hasibul Islam Sohel, Tohru Kiyono, Umme Farzana Zahan, Sultana Razia, Masako Ishikawa, Hitomi Yamashita, Kosuke Kanno, Shahataj Begum Sonia, Kentaro Nakayama and Satoru Kyo
Int. J. Mol. Sci. 2025, 26(5), 1995; https://doi.org/10.3390/ijms26051995 - 25 Feb 2025
Viewed by 106
Abstract
The molecular mechanisms through which endometriosis-related ovarian neoplasms (ERONs) develop from benign endometrioma remain unclear. It is especially a long-standing mystery why ovarian endometrioma has the potential to develop into two representative histological subtypes: endometrioid ovarian carcinoma or clear cell ovarian carcinoma. This [...] Read more.
The molecular mechanisms through which endometriosis-related ovarian neoplasms (ERONs) develop from benign endometrioma remain unclear. It is especially a long-standing mystery why ovarian endometrioma has the potential to develop into two representative histological subtypes: endometrioid ovarian carcinoma or clear cell ovarian carcinoma. This study aimed to investigate the molecular carcinogenesis of ERONs using newly developed in vitro and in vivo carcinogenesis models. Epithelial cells were isolated and purified from surgically removed benign endometrioma samples, followed by immortalization by overexpressing cyclinD1/CDK4 in combination with the human TERT gene. Immortalized cells were subjected to various molecular manipulations by combining knockout or overexpression of several candidate drivers, including ARID1A, KRAS, PIK3CA, AKT, and MYC, based on previous comprehensive genome-wide studies of ERONs. These cells were then inoculated into immunocompromised mice and evaluated for malignant transformation. Inoculated cells harboring a combination of three genetic alterations successfully developed tumors with malignant features in mice, whereas those with two genetic manipulations failed to do so. Especially, ARID1A gene knockout, combined with overexpressing the KRAS oncogenic mutant allele (or overexpressing AKT) and c-Myc overexpression led to efficient tumor formation. Of note, these three combinations of genetic alterations produced tumors that histologically represented typical clear cell carcinoma in SCID mice, while the same combination led to tumors with endometrioid histology in nude mice. A combination of ARID1A mutation, KRAS mutation or AKT activation, and c-Myc overexpression were confirmed to be the main candidate drivers for the development of ERONs, as suggested by comprehensive genetic analyses of ERONs. A tumor immune microenvironment involving B-cell signaling may contribute to the diverse histological phenotypes. The present model may help to clarify the molecular mechanisms of ERON carcinogenesis and understand their histological diversity and novel molecular targets. Full article
(This article belongs to the Special Issue Molecular Genetics in Ovarian Cancer)
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