International Journal of Molecular Sciences

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Molecular Studies in Gynecological Oncology: Advancing Diagnosis and Treatment

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Dear Colleagues,

The molecular characterization of gynecological cancers, including ovarian, uterine, cervical, vaginal, and vulvar cancer, has advanced rapidly and has remarkably influenced clinical and translational research. The analysis of molecular parameters and genomic alterations has improved therapeutic approaches to surgical and medical treatment for gynecological malignant diseases. Our aim in launching this Special Issue is to expand our current understanding of cancer initiation and progression and to collect the latest discoveries toward molecular guided diagnosis, treatment, and monitoring, including potential prognostic or predictive biomarkers for therapy response or resistance, emerging targeted therapeutics, and novel technical developments in molecular gyneco-oncology. Authors are invited to submit original research and review articles revealing new knowledge concerning molecular features of gynecologic oncology, which may contribute to improving diagnostic options and treatment choices.

Topics of interest include, but are not limited to, the following:

Clinical and translational research;
Cellular mechanisms and biological processes;
The molecular pathology of tumors and tumor microenvironment;
Intratumor heterogeneity;
Single-cell analysis;
Omics technologies and database applications;
Biomarkers for early diagnosis, targeted and systemic therapy response, and resistance.

Dr. Ivonne Nel
Guest Editor

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Keywords

biomarker
cancer screening
clinical trial
DNA repair
invasion
metastasis
methylation
molecular diagnostics
molecular tumor pathology
next-generation sequencing
omics
personalized medicine
prognosis
single-cell analysis
targeted therapy
translational cancer research
treatment response
tumor microenvironment

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Research

22 pages, 3252 KB

Open AccessArticle

Disseminated Tumor Cells (DTCs) in Patients with Cervical Cancer Reveal Mesenchymal Properties and Potential Therapeutic Targets—A New Perspective?

by Elisa Brochwitz, Ivonne Nel, Anne Eckardt, Laura Weydandt, Anne Kathrin Höhn, Karsten Winter and Bahriye Aktas

Int. J. Mol. Sci. 2026, 27(11), 4875; https://doi.org/10.3390/ijms27114875 - 28 May 2026

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Abstract

Despite effective primary treatment, approximately 20% of cervical cancer patients experience recurrence, which may be driven by early hematogenous dissemination. While circulating (CTCs) and disseminated tumor cells (DTCs) are established prognostic markers in breast cancer, their role in cervical cancer remains poorly defined. Current detection methods rely predominantly on cytokeratin (CK) expression, but epithelial–mesenchymal transition (EMT) may lead to CK downregulation, potentially compromising detection sensitivity. We analyzed bone marrow (n = 43) and blood samples (collected pre-surgically and at follow-up) from cervical cancer patients. DTCs and CTCs were detected using a standardized CK based immunocytochemical assay. A multi-parameter immunofluorescence (IF) approach was employed to simultaneously assess CK, vimentin (Vim), p16, PD-L1 and VEGF on DTCs. Marker expression profiles were compared with matched tumor tissue and correlated with clinical and pathological parameters. CTCs were detected in 16% (7/43) of pre-surgical blood samples. DTC positivity increased from 56% (24/43) using CK based detection to 74% (32/43) when assessed via multi-parameter IF. A total of 248 DTCs were identified (median: 7 per patient). The most prevalent DTC phenotype was Vim+ (54%), followed by CK+ (12%), Vim+/VEGF+/p16+ (7%), and CK+/Vim+ (4%). Significant correlations were observed between p16 and VEGF (r = 0.631, p < 0.001) and between PD-L1 (r = 0.323, p < 0.001). Discordance between DTCs and tumor tissue reached 43–64%, primarily attributable to PD-L1 gain in DTCs. Over 70% of DTCs lacked CK, with majority exhibiting vimentin positivity, indicative of a mesenchymal phenotype. Vim+ and VEGF+ DTCs were associated with disease recurrence, suggesting their prognostic value. These findings underscore the limitations of relying solely on CK for DTC detection and highlight the potential of EMT and immune-related markers as novel biomarkers in cervical cancer. Further validation in larger, prospective cohorts is warranted. Full article

(This article belongs to the Special Issue Molecular Studies in Gynecological Oncology: Advancing Diagnosis and Treatment)

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14 pages, 2437 KB

Open AccessArticle

NRF2 Drives Aggressiveness and Chemoresistance in Ovarian Cancer Stem-like Cells

by Yu-Hsun Chang, Kai-Hung Wang and Dah-Ching Ding

Int. J. Mol. Sci. 2026, 27(6), 2820; https://doi.org/10.3390/ijms27062820 - 20 Mar 2026

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Abstract

Advanced-stage ovarian cancer remains a major clinical challenge because of its aggressive behavior and the frequent development of chemoresistance. The nuclear factor erythroid-derived 2–like 2 (NRF2) signaling pathway regulates cellular redox homeostasis. However, its role in ovarian cancer stem-like cells remains unclear. Therefore, we aimed to investigate the effects of NRF2 overexpression on acetaldehyde dehydrogenase (ALDH)⁺ KURAMOCHI ovarian cancer cells in vitro and in vivo. In particular, we investigated the effects of NRF2 on tumor-associated behaviors, chemoresistance, and signaling pathways. Lentivirus-mediated NRF2 overexpression activated extracellular signal-regulated kinase and AKT signaling. Moreover, it modulated tumor-associated phenotypes, including proliferation, migration, and invasion. NRF2-overexpressing cells exhibited significantly enhanced migratory and invasive capacities, increased resistance to paclitaxel and carboplatin, and reduced apoptosis. Furthermore, the expression of anti-apoptotic proteins was upregulated, and caspase-3 activation was attenuated. In xenograft models, NRF2 overexpression promoted tumor growth and increased the expression of antioxidant and angiogenic factors, including heme oxygenase-1 and vascular endothelial growth factor A. Collectively, these findings demonstrate that NRF2 regulates ovarian cancer aggressiveness and chemoresistance by coordinating stress response signaling, survival pathways, and tumor progression. Therefore, targeting NRF2-mediated signaling represents a promising therapeutic strategy for overcoming drug resistance and improving outcomes in patients with ovarian cancer. Full article

(This article belongs to the Special Issue Molecular Studies in Gynecological Oncology: Advancing Diagnosis and Treatment)

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