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Gynecologic Cancer: From Molecular, Cellular Mechanisms to Novel Therapies
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Gynecologic Cancer: From Molecular, Cellular Mechanisms to Novel Therapies

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

Deadline for manuscript submissions: 31 July 2024 | Viewed by 2117

Special Issue Editor

Prof. Dr. Sun-Young Lee

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Guest Editor
Department of Radiation Oncology, Jeonbuk National University School of Medicine, Jeonju, Republic of Korea
Interests: radiation oncology; modulated electrohyperthermia; cancer therapy

Special Issue Information

Dear Colleagues,

Gynecological cancers caused by the female reproductive system, including cervical cancer, endometriosis, uterine fibroids, ovarian cancer, pelvic mass, uterine cancer, vaginal cancer and vulvar cancer, have long threatened the health of women around the world and are also widely studied. In recent years, great progress has been made in the diagnosis and treatment of gynecological diseases. With the advancement of genetic diagnosis and imaging equipment, diagnosis has become more accurate, and the advancement of chemotherapy has also effectively reduced the mortality of patients with gynecological tumors.

Despite impressive medical advances, many questions remain unresolved, and healthcare related to gynecological cancers remains a long-term scientific field of continuous development and exploration. This Special Issue will provide an overview of the latest advances in molecular and cellular mechanisms underlying gynecological cancers and their drug therapy and will provide a platform to demonstrate innovative approaches and results in the diagnosis and treatment of gynecological cancers.

We invite scholars to submit high-quality works related to molecular and cellular mechanisms, pathology, diagnosis and treatment of gynecological cancer. The formats for submission include original research articles, reviews, and communications.

Prof. Dr. Sun-Young Lee
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cervical cancer
  • endometriosis
  • uterine fibroids
  • ovarian cancer
  • pelvic mass
  • uterine cancer
  • vaginal cancer
  • vulvar cancer
  • molecular-targeted therapy
  • immunotherapy

Published Papers (4 papers)

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Research

12 pages, 857 KiB  
Article
The Role of Glutathione Transferase Omega-Class Variant Alleles in Individual Susceptibility to Ovarian Cancer
by Petar Simic, Vesna Coric, Igor Pljesa, Ana Savic-Radojevic, Nebojsa Zecevic, Jovana Kocic, Tatjana Simic, Vladimir Pazin and Marija Pljesa-Ercegovac
Int. J. Mol. Sci. 2024, 25(9), 4986; https://doi.org/10.3390/ijms25094986 - 03 May 2024
Viewed by 143
Abstract
The tumor microenvironment is affected by reactive oxygen species and has been suggested to have an important role in ovarian cancer (OC) tumorigenesis. The role of glutathione transferases (GSTs) in the maintenance of redox balance is considered as an important contributing factor in [...] Read more.
The tumor microenvironment is affected by reactive oxygen species and has been suggested to have an important role in ovarian cancer (OC) tumorigenesis. The role of glutathione transferases (GSTs) in the maintenance of redox balance is considered as an important contributing factor in cancer, including OC. Furthermore, GSTs are mostly encoded by highly polymorphic genes, which further highlights their potential role in OC, known to originate from accumulated genetic changes. Since the potential relevance of genetic variations in omega-class GSTs (GSTO1 and GSTO2), with somewhat different activities such as thioltransferase and dehydroascorbate reductase activity, has not been clarified as yet in terms of susceptibility to OC, we aimed to investigate whether the presence of different GSTO1 and GSTO2 genetic variants, individually or combined, might represent determinants of risk for OC development. Genotyping was performed in 110 OC patients and 129 matched controls using a PCR-based assay for genotyping single nucleotide polymorphisms. The results of our study show that homozygous carriers of the GSTO2 variant G allele are at an increased risk of OC development in comparison to the carriers of the referent genotype (OR1 = 2.16, 95% CI: 0.88–5.26, p = 0.08; OR2 = 2.49, 95% CI: 0.93–6.61, p = 0.06). Furthermore, individuals with GST omega haplotype H2, meaning the concomitant presence of the GSTO1*A and GSTO2*G alleles, are more susceptible to OC development, while carriers of the H4 (*A*A) haplotype exhibited lower risk of OC when crude and adjusted haplotype analysis was performed (OR1 = 0.29; 95% CI: 0.12–0.70; p = 0.007 and OR2 = 0.27; 95% CI: 0.11–0.67; p = 0.0054). Overall, our results suggest that GSTO locus variants may confer OC risk. Full article
(This article belongs to the Special Issue Gynecologic Cancer: From Molecular, Cellular Mechanisms to Novel Therapies)
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16 pages, 13046 KiB  
Article
Tobacco Smoke Condensate Induces Morphologic Changes in Human Papillomavirus-Positive Cervical Epithelial Cells Consistent with Epithelial to Mesenchymal Transition (EMT) with Activation of Receptor Tyrosine Kinases and Regulation of TGFB
by Zaniya A. Mark, Linda Yu, Lysandra Castro, Xiaohua Gao, Noelle R. Rodriguez, Deloris Sutton, Erica Scappini, Charles J. Tucker, Rob Wine, Yitang Yan, Evangeline Motley and Darlene Dixon
Int. J. Mol. Sci. 2024, 25(9), 4902; https://doi.org/10.3390/ijms25094902 - 30 Apr 2024
Viewed by 214
Abstract
High-risk human papillomavirus (HR-HPV; HPV-16) and cigarette smoking are associated with cervical cancer (CC); however, the underlying mechanism(s) remain unclear. Additionally, the carcinogenic components of tobacco have been found in the cervical mucus of women smokers. Here, we determined the effects of cigarette [...] Read more.
High-risk human papillomavirus (HR-HPV; HPV-16) and cigarette smoking are associated with cervical cancer (CC); however, the underlying mechanism(s) remain unclear. Additionally, the carcinogenic components of tobacco have been found in the cervical mucus of women smokers. Here, we determined the effects of cigarette smoke condensate (CSC; 3R4F) on human ectocervical cells (HPV-16 Ect/E6E7) exposed to CSC at various concentrations (10−6–100 μg/mL). We found CSC (10−3 or 10 μg/mL)-induced proliferation, enhanced migration, and histologic and electron microscopic changes consistent with EMT in ectocervical cells with a significant reduction in E-cadherin and an increase in the vimentin expression compared to controls at 72 h. There was increased phosphorylation of receptor tyrosine kinases (RTKs), including Eph receptors, FGFR, PDGFRA/B, and DDR2, with downstream Ras/MAPK/ERK1/2 activation and upregulation of common EMT-related genes, TGFB SNAI2, PDGFRB, and SMAD2. Our study demonstrated that CSC induces EMT in ectocervical cells with the upregulation of EMT-related genes, expression of protein biomarkers, and activation of RTKs that regulate TGFB expression, and other EMT-related genes. Understanding the molecular pathways and environmental factors that initiate EMT in ectocervical cells will help delineate molecular targets for intervention and define the role of EMT in the initiation and progression of cervical intraepithelial neoplasia and CC. Full article
(This article belongs to the Special Issue Gynecologic Cancer: From Molecular, Cellular Mechanisms to Novel Therapies)
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17 pages, 6279 KiB  
Article
The Clinicopathological Significance of the Cyclin D1/E1–Cyclin-Dependent Kinase (CDK2/4/6)–Retinoblastoma (RB1/pRB1) Pathway in Epithelial Ovarian Cancers
by Ayat Lashen, Mashael Algethami, Shatha Alqahtani, Ahmed Shoqafi, Amera Sheha, Jennie N. Jeyapalan, Nigel P. Mongan, Emad A. Rakha and Srinivasan Madhusudan
Int. J. Mol. Sci. 2024, 25(7), 4060; https://doi.org/10.3390/ijms25074060 - 05 Apr 2024
Viewed by 631
Abstract
Cyclin-dependent kinases (CDK2, CDK4, CDK6), cyclin D1, cyclin E1 and phosphorylated retinoblastoma (pRB1) are key regulators of the G1/S cell cycle checkpoint and may influence platinum response in ovarian cancers. CDK2/4/6 inhibitors are emerging targets in ovarian cancer therapeutics. In the current study, [...] Read more.
Cyclin-dependent kinases (CDK2, CDK4, CDK6), cyclin D1, cyclin E1 and phosphorylated retinoblastoma (pRB1) are key regulators of the G1/S cell cycle checkpoint and may influence platinum response in ovarian cancers. CDK2/4/6 inhibitors are emerging targets in ovarian cancer therapeutics. In the current study, we evaluated the prognostic and predictive significance of the CDK2/4/6–cyclin D1/E1–pRB1 axis in clinical ovarian cancers (OC). The CDK2/4/6, cyclin D1/E1 and RB1/pRB1 protein expression were investigated in 300 ovarian cancers and correlated with clinicopathological parameters and patient outcomes. CDK2/4/6, cyclin D1/E1 and RB1 mRNA expression were evaluated in the publicly available ovarian TCGA dataset. We observed nuclear and cytoplasmic staining for CDK2/4/6, cyclins D1/E1 and RB1/pRB1 in OCs with varying percentages. Increased nuclear CDK2 and nuclear cyclin E1 expression was linked with poor progression-free survival (PFS) and a shorter overall survival (OS). Nuclear CDK6 was associated with poor OS. The cytoplasmic expression of CDK4, cyclin D1 and cyclin E1 also has predictive and/or prognostic significance in OCs. In the multivariate analysis, nuclear cyclin E1 was an independent predictor of poor PFS. Tumours with high nuclear cyclin E1/high nuclear CDK2 have a worse PFS and OS. Detailed bioinformatics in the TCGA cohort showed a positive correlation between cyclin E1 and CDK2. We also showed that cyclin-E1-overexpressing tumours are enriched for genes involved in insulin signalling and release. Our data not only identified the prognostic/predictive significance of these key cell cycle regulators but also demonstrate the importance of sub-cellular localisation. CDK2 targeting in cyclin-E1-amplified OCs could be a rational approach. Full article
(This article belongs to the Special Issue Gynecologic Cancer: From Molecular, Cellular Mechanisms to Novel Therapies)
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17 pages, 2712 KiB  
Article
Different Patterns of Platinum Resistance in Ovarian Cancer Cells with Homologous Recombination Proficient and Deficient Background
by Michela Chiappa, Federica Guffanti, Chiara Grasselli, Nicolò Panini, Alessandro Corbelli, Fabio Fiordaliso and Giovanna Damia
Int. J. Mol. Sci. 2024, 25(5), 3049; https://doi.org/10.3390/ijms25053049 - 06 Mar 2024
Viewed by 629
Abstract
Platinum compounds are very active in first-line treatments of ovarian carcinoma. In fact, high rates of complete remission are achieved, but most patients eventually relapse with resistant disease. Many mechanisms underlying the platinum-resistant phenotype have been reported. However, there are no data in [...] Read more.
Platinum compounds are very active in first-line treatments of ovarian carcinoma. In fact, high rates of complete remission are achieved, but most patients eventually relapse with resistant disease. Many mechanisms underlying the platinum-resistant phenotype have been reported. However, there are no data in the same isogenic cell system proficient and deficient in homologous recombination (HR) on platinum-acquired resistance that might unequivocally clarify the most important mechanism associated with resistance. We generated and characterized cisplatin (DDP)-resistant murine ovarian ID8 cell lines in a HR-deficient and -proficient background. Specific upregulation of the NER pathway in the HR-proficient and -resistant cells and partial restoration of HR in Brca1−/−-resistant cells were found. Combinations of different inhibitors of the DNA damage response pathways with cisplatin were strongly active in both resistant and parental cells. The data from the ID8 isogenic system are in line with current experimental and clinical evidence and strongly suggest that platinum resistance develops in different ways depending on the cell DNA repair status (i.e., HR-proficient or HR-deficient), and the upregulation and/or restoration of repair pathways are major determinants of DDP resistance. Full article
(This article belongs to the Special Issue Gynecologic Cancer: From Molecular, Cellular Mechanisms to Novel Therapies)
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