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Biomedicines
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Current Perspectives on Gynecologic Cancers
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Current Perspectives on Gynecologic Cancers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 2748

Special Issue Editor

Dr. Kecheng Huang

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Guest Editor
Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Interests: epidemiology; genetics; meta-analysis; gynecologic cancer

Special Issue Information

Dear Colleagues,

Gynecologic cancers—encompassing malignancies of the cervix, ovaries, uterus, vulva, and vagina—remain a critical global health challenge, accounting for significant morbidity and mortality among women worldwide. Despite advancements in screening and treatment, these cancers persistently highlight disparities in access to care, variable therapeutic responses, and unmet needs in survivorship. This Special Issue, Current Perspectives on Gynecologic Cancers, seeks to illuminate the rapidly evolving landscape of research and clinical practice, offering a synthesis of cutting-edge discoveries, translational innovations, and multidisciplinary approaches that are reshaping the field.

Recent years have witnessed transformative progress in understanding the molecular underpinnings of gynecologic malignancies. Breakthroughs in genomic and epigenomic profiling have unraveled tumor heterogeneity, identified driver mutations (e.g., TP53, BRCA1/2, PIK3CA), and uncovered biomarkers predictive of treatment response or resistance. The rise of immunotherapy, particularly immune checkpoint inhibitors targeting PD-1/PD-L1 in cervical and endometrial cancers, has reinvigorated hope for patients with advanced or recurrent disease. Similarly, PARP inhibitors have become a cornerstone in managing BRCA-mutated ovarian cancer, while antibody-drug conjugates like mirvetuximab soravtansine offer precision targeting of folate receptor-alpha-positive tumors.

Equally groundbreaking are advances in early detection and prevention. Liquid biopsy technologies, including circulating tumor DNA (ctDNA) and exosome-based assays, now enable non-invasive monitoring of minimal residual disease and recurrence. Meanwhile, HPV vaccination campaigns and AI-enhanced cervical screening programs are driving progress in primary prevention. Beyond biology, the integration of artificial intelligence (AI) into diagnostic imaging, risk prediction models, and treatment planning exemplifies the fusion of technology and oncology. Furthermore, it highlights the role of the tumor microenvironment, microbiome interactions, and metabolic reprogramming in tumor progression, offering novel therapeutic targets.

By compiling reviews and original research, this collection underscores the importance of interdisciplinary collaboration—bridging oncology, genetics, bioengineering, and public health—to translate scientific discovery into equitable clinical practice. We invite readers to explore these contributions, which collectively aim to redefine standards of care and inspire future innovation in the fight against gynecologic cancers.

Dr. Kecheng Huang
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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines 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

  • gynecology
  • genetics
  • biology
  • bioinformatics
  • review
  • predictive model
  • artificial intelligence

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Published Papers (3 papers)

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Research

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15 pages, 1844 KB  
Article
Lactate Enhances Non-Homologous End Joining Repair and Chemoresistance Through Facilitating XRCC4–LIG4 Complex Assembly in Ovarian Cancer
by Jingyi Lu, Jiayu Zhu, Huanxiao Zhang, Zhou Zhou, Haoyuan Li, Cuimiao Zheng, Xi Huang, Siqi Chen, Chaoyun Pan, Jie Li and Hao Tan
Biomedicines 2025, 13(12), 2949; https://doi.org/10.3390/biomedicines13122949 - 30 Nov 2025
Viewed by 316
Abstract
Background: Non-homologous end joining (NHEJ) is a crucial pathway for repairing DNA double-strand breaks and a key contributor to chemoresistance in cancer. The assembly of the DNA Ligase IV (LIG4)–XRCC4 complex is essential for NHEJ fidelity, however, the regulatory mechanisms governing this [...] Read more.
Background: Non-homologous end joining (NHEJ) is a crucial pathway for repairing DNA double-strand breaks and a key contributor to chemoresistance in cancer. The assembly of the DNA Ligase IV (LIG4)–XRCC4 complex is essential for NHEJ fidelity, however, the regulatory mechanisms governing this complex in cancer remain poorly understood. This study aims to investigate whether and how lactate, a key metabolic byproduct of the Warburg effect, regulates the XRCC4–LIG4 complex and influences chemoresistance. Methods: The functional role of lactate in NHEJ was assessed using DNA repair reporter assays in ovarian cancer cells. Protein–protein interactions were examined through co-immunoprecipitation and pull-down assays. The molecular mechanism of lactate’s action was delineated using a combination of site-directed mutagenesis, in vitro binding assays, and molecular docking. Finally, the physiological relevance of lactate-mediated NHEJ was validated in a preclinical ovarian cancer mouse model treated with cisplatin. Results: We demonstrated that lactate enhances NHEJ repair efficiency and confers resistance to DNA-damaging chemotherapeutics. Mechanistically, lactate directly binds to XRCC4 at key residues, including Y66, E55, and S110, thereby strengthening the XRCC4–LIG4 association. This interaction is independent of protein lactylation. In vivo studies confirmed that lactate-driven NHEJ promotes chemoresistance in ovarian cancer. Conclusions: Our findings reveal lactate as a novel metabolic regulator of the NHEJ pathway by directly allosterically modulating the XRCC4–LIG4 complex. This work establishes a direct molecular link between the Warburg effect and DNA repair-driven chemoresistance, offering new insights into potential therapeutic strategies for ovarian cancer. Full article
(This article belongs to the Special Issue Current Perspectives on Gynecologic Cancers)
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Review

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35 pages, 1089 KB  
Review
Estrogen Receptors as Key Factors in Carcinogenesis
by Oliwia Gruszka, Magdalena Jurzak and Ilona Anna Bednarek
Biomedicines 2025, 13(11), 2620; https://doi.org/10.3390/biomedicines13112620 - 26 Oct 2025
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Abstract
Despite continuous advances in the development of methodologies for the diagnosis and therapeutic treatment of cancer, the disease remains a primary cause of mortality worldwide. A comprehensive understanding of the molecular mechanisms underlying cancer could ultimately lead to increasingly effective therapeutic interventions. One [...] Read more.
Despite continuous advances in the development of methodologies for the diagnosis and therapeutic treatment of cancer, the disease remains a primary cause of mortality worldwide. A comprehensive understanding of the molecular mechanisms underlying cancer could ultimately lead to increasingly effective therapeutic interventions. One approach that could be adopted is to formulate methodologies that impede cell signalling and/or the expression of genes pivotal to carcinogenesis. A notable example of this strategy is the focus on the estrogen receptor, a key player in the development of various types of cancer. The deregulation of this receptor, and the subsequent impact on cell function, is a critical factor in the progression of these diseases. This renders it a significant therapeutic target. Furthermore, the microenvironment has been demonstrated to exert a significant influence on the development of cancers. A mounting body of evidence indicates that the abnormal physical properties of the tumour microenvironment can induce widespread changes, leading to the selection of characteristic tumour cell abilities and subsequent clonal proliferation. This process is accompanied by an increased capacity for invasive growth and, notably, the induction of multidrug resistance. The present article focuses on presenting the structure and role of the estrogen receptor in selected hormone-dependent cancers, its involvement in the formation of the tumor microenvironment, currently used therapeutic methods in the treatment of these cancers, and the challenges associated with them. Each new discovery in the field of cancer biology offers the prospect of developing new potential treatments, including targeted therapies aimed at improving the survival of patients suffering from hormone-dependent malignant tumours. Although the role of the estrogen receptor in their development is well established, further research is required to develop a detailed understanding of how its specific isoforms act in different types of cancer. Full article
(This article belongs to the Special Issue Current Perspectives on Gynecologic Cancers)
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17 pages, 2396 KB  
Review
Early Non-Response to Neoadjuvant Chemotherapy Will Increase the Recurrence of Cervical Cancer: A Systematic Review
by Shiqing Huang, Runfeng Yang, Li Yang, Shiyi Kong and Kecheng Huang
Biomedicines 2025, 13(8), 2016; https://doi.org/10.3390/biomedicines13082016 - 19 Aug 2025
Viewed by 811
Abstract
Objectives: Cervical cancer remains a significant global health burden for women. While neoadjuvant chemotherapy (NACT) has emerged as a potential treatment option, the prognostic implications of early non-response to NACT remain inadequately characterized. This systematic review aims to elucidate the association between [...] Read more.
Objectives: Cervical cancer remains a significant global health burden for women. While neoadjuvant chemotherapy (NACT) has emerged as a potential treatment option, the prognostic implications of early non-response to NACT remain inadequately characterized. This systematic review aims to elucidate the association between early non-response to NACT and long-term disease-free survival (DFS) in cervical cancer patients. Methods: A comprehensive systematic review was conducted following PRISMA guidelines. PubMed, Embase, Elsevier, Springer, EBSCO, and Cochrane Library were systematically searched to identify eligible studies. Pooled hazard ratios (HRs) for DFS with 95% confidence intervals (CIs) were calculated using R software (version 4.5.1). Heterogeneity was assessed via Cochran’s Q test and I2 statistics. Publication bias was evaluated using funnel plots, Begg’s test, Egger’s test, and trim-and-fill methods. Sensitivity analyses further validated result robustness. Results: Eleven studies (n = 2064 patients; 1546 responders, 518 non-responders) met inclusion criteria. The pooled early non-response rate ranged from 13% to 39%. Early non-response significantly correlated with poorer DFS (HR = 3.29, 95% CI 2.35–4.62). Subgroup analyses by response criteria showed HRs of 2.94 (95% CI 1.72–5.03) for WHO criteria and 4.00 (95% CI 2.52–6.34) for RECIST criteria. No significant publication bias was detected (Begg’s p = 0.35; Egger’s p = 0.28). Sensitivity analyses and trim-and-fill adjustments confirmed result stability. Conclusions: Early non-response to NACT predicts worse DFS in women with cervical cancer. These findings proposed the need for large-scale or prospective studies to validate the prognostic value of early non-response and optimize treatment strategies for non-responders. Future prospective trials with standardized protocols are essential to validate these findings and establish criteria for optimizing patient selection for NACT-based therapeutic strategies. Full article
(This article belongs to the Special Issue Current Perspectives on Gynecologic Cancers)
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