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Genetic Mechanisms and Therapeutic Strategies in Ovarian Cancer
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Genetic Mechanisms and Therapeutic Strategies in Ovarian Cancer

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: 25 January 2027 | Viewed by 997

Editor

Dr. Aimee Stablewski

E-Mail Website
Guest Editor
Department of Molecular and Cellular Biology, Roswell Park Cancer, Buffalo, NY, USA
Interests: CRISPR technology; ovarian cancer research; creation of genetically modified cells and preclinical models; genetics

Special Issue Information

Dear Colleagues,

Epithelial ovarian cancer (EOC), which accounts for approximately 95% of all ovarian cancers, is the most lethal subtype with a poor prognosis of recurrence. Ovarian cancer is responsible for nearly 65% of all gynecologic cancer-related deaths. The 5-year survival rate is less than 30% and the tumor usually spreads to distant sites. Platinum-based chemotherapeutics remain the first-line treatment for ovarian cancer; however, a significant proportion of patients develop resistance to the treatment. Additionally, immunotherapeutic approaches have also failed in ovarian cancer due to metabolic, genomic, and immune perturbations in the tumor microenvironment.

Ovarian cancer is characterized by genetic and epigenetic alterations as well as changes in amplification of genes, copy number variations and single nucleotide variants. Epigenetic modifications including DNA methylation, histone modifications, non-coding RNAs, chromatin remodeling, and RNA methylation have been shown in ovarian cancer development, progression, and treatment resistance and offer a promising strategy for use in treatment.

In this Special Issue, we will report on the latest advances in the research and therapeutic intervention strategies to define the Genetic Mechanisms and Therapeutic Strategies in Ovarian Cancer.

Dr. Aimee Stablewski
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • epithelial ovarian cancer (EOC)
  • genetic alterations
  • epigenetic regulation
  • tumor microenvironment
  • therapeutic strategies

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Published Papers (1 paper)

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Research

26 pages, 12331 KB  
Article
Integrated Single-Cell and Bulk Transcriptomic Analyses Identify a B Cell- and Plasma Cell-Associated Prognostic Signature and a Candidate Tumor-Suppressive Role for FUT8 in Ovarian Cancer
by Yiya Wang, Yuan Shi, Ruibin Zhu, Cong Yu, Guoying Wu, Zihan Li, Ju Zhu, Yuxin Lei and Qingqing Wang
Genes 2026, 17(7), 784; https://doi.org/10.3390/genes17070784 - 8 Jul 2026
Viewed by 510
Abstract
Background: Ovarian cancer (OC) exhibits substantial tumor heterogeneity and an immunosuppressive tumor microenvironment (TME), both contributing to its unfavorable clinical outcomes. Recent studies have increasingly demonstrated that dysregulated glycosylation significantly impacts tumor progression and immune modulation. However, the specific functions and implications of [...] Read more.
Background: Ovarian cancer (OC) exhibits substantial tumor heterogeneity and an immunosuppressive tumor microenvironment (TME), both contributing to its unfavorable clinical outcomes. Recent studies have increasingly demonstrated that dysregulated glycosylation significantly impacts tumor progression and immune modulation. However, the specific functions and implications of glycosylation-associated regulators in OC remain poorly understood. This study integrates single-cell and bulk transcriptomic data to uncover crucial genes within the TME and investigates the potential role of Fucosyltransferase 8 (FUT8) in OC development. Methods: Single-cell RNA sequencing (scRNA-seq) data from OC and normal ovarian tissues (GSE184880, n = 12) were analyzed using Seurat and Harmony for clustering and annotation. Ro/e analysis identified B cells and plasma cells as enriched immune populations. Their marker genes were integrated with The Cancer Genome Atlas (TCGA) cohort as the training set, while internal testing and an independent external validation cohort (GSE63885) were used to construct and validate the prognostic model. FUT8 function was evaluated in OC cell lines using quantitative real-time PCR (qRT-PCR), cell counting kit-8 (CCK-8) assays, flow cytometry, and transcriptomic sequencing. Gene Set Variation Analysis (GSVA), Gene Set Enrichment Analysis (GSEA), and virtual knockout analyses were performed to explore FUT8-associated pathways. Results: We constructed a single-cell atlas consisting of 46,235 cells classified into seven principal cell populations, highlighting significant enrichment of B and plasma cells in OC tissues. The prognostic signature could stratify patients into high- and low-risk groups across training, internal validation, and external validation cohorts, showing consistent prognostic stratification capacity. FUT8 expression was elevated in OC samples and was associated with favorable overall survival (OS). Experimental overexpression of FUT8 in OC cell lines resulted in reduced cell proliferation and increased apoptosis. Both transcriptomic analyses and virtual knockout studies consistently associated FUT8 with pathways related to N-glycosylation. High-risk patients exhibited predicted activation of Wnt/β-catenin, Hedgehog, and Kras pathways, coupled with diminished immune cell infiltration. Conclusions: We developed a prognostic signature informed by single-cell data for OC and identified FUT8 as a potential regulator associated with N-glycosylation processes in OC. These results offer insights into OC molecular characteristics and highlight FUT8 as a candidate biomarker with potential prognostic relevance. Further experimental studies are necessary to validate and elucidate the precise molecular mechanisms involved. Full article
(This article belongs to the Special Issue Genetic Mechanisms and Therapeutic Strategies in Ovarian Cancer)
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