Molecular Mechanisms, Novel Diagnostics and Treatments of Gynecologic Cancer

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 757

Special Issue Editor


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Guest Editor
Department of Cell Systems and Anatomy, Greehey Children's Cancer Research Institute (GCCRI), The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
Interests: biomarker; cancer biology; novel drug targets and therapeutics; cancer stem cells; tumorigenesis

Special Issue Information

Dear Colleagues,

A Special Issue on “Molecular Mechanisms, Novel Diagnostics and Treatments of Gynecologic Cancer” is in preparation for the esteemed journal Biomolecules (Impact Factor 4.8 and CiteScore 9.4).

This Special Issue aims to highlight recent advancements in gynecologic cancer research, focusing on cervical, ovarian, uterine, vaginal, and vulvar cancers. We invite submissions of original research articles, reviews, clinical trials, and case reports, particularly those that explore the molecular mechanisms of gynecologic cancer biology, novel therapeutic drug targets, biomarkers, and the development of targeted therapies. Contributions that utilize innovative technologies such as single-cell RNA sequencing, CRISPR knockout screening, and proteomics to investigate tumorigenesis, therapy resistance, and cancer stem cells are encouraged. By examining these aspects, this issue seeks to provide insights into innovative approaches for precision oncology, ultimately improving early detection and treatment outcomes for gynecologic cancers.

Dr. Panneerdoss Subbarayalu
Guest Editor

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Keywords

  • biomarker
  • cancer biology
  • novel drug targets and therapeutics
  • cancer stem cells
  • tumorigenesis

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Published Papers (1 paper)

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Research

15 pages, 4739 KB  
Article
EC359 Enhances Trametinib Efficacy in Ras/Raf-Driven Ovarian Cancer by Suppressing LIFR Signaling
by William C. Arnold, Durga Meenakshi Panneerdoss, Baskaran Subramani, Megharani Mahajan, Behnam Ebrahimi, Paulina Ramirez, Bindu Santhamma, Suryavathi Viswanadhapalli, Edward R. Kost, Yidong Chen, Zhao Lai, Hareesh B. Nair, Ratna K. Vadlamudi and Yasmin A. Lyons
Biomolecules 2025, 15(10), 1396; https://doi.org/10.3390/biom15101396 - 30 Sep 2025
Viewed by 490
Abstract
Ovarian cancer (OCa) remains the most lethal gynecologic malignancy in the United States, with low-grade serous and mucinous subtypes frequently driven by KRAS mutations. These mutations activate downstream MAPK and PI3K/AKT signaling pathways, contributing to tumor progression and resistance to therapy. Although the [...] Read more.
Ovarian cancer (OCa) remains the most lethal gynecologic malignancy in the United States, with low-grade serous and mucinous subtypes frequently driven by KRAS mutations. These mutations activate downstream MAPK and PI3K/AKT signaling pathways, contributing to tumor progression and resistance to therapy. Although the MEK inhibitor trametinib is used to target these pathways, its efficacy is limited in KRAS-mutant OCa due to compensatory activation of the leukemia inhibitory factor (LIF)/LIF receptor (LIFR) axis. In this study, we evaluated the therapeutic potential of combining trametinib with EC359, a selective LIFR inhibitor, in Ras/Raf-driven OCa models. EC359 significantly reduced cell viability, clonogenic survival, and induced cell death via ferroptosis in vitro. Mechanistic studies revealed that EC359 suppressed trametinib-induced activation of LIFR downstream signaling. RNA-seq analysis showed that combination therapy downregulated mitochondrial translation and MYC target genes while upregulating apoptosis-related genes. In vivo, EC359 and trametinib co-treatment significantly reduced tumor growth in xenograft and PDX models without inducing toxicity. Our studies identify LIFR signaling as a critical vulnerability in Ras/Raf-mutant and low grade serous OCa. Further, it provides strong preclinical rationale for EC359 and trametinib combination therapy as a new therapeutic strategy for treating Ras/Raf-driven OCa and low-grade serous OCa. Full article
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