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Molecular Research on Genitourinary Cancers

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: 20 December 2024 | Viewed by 3319

Special Issue Editors


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Guest Editor
Department of Experimental and Clinical Medicine, University “Magna Graecia” Catanzaro, 88100 Catanzaro, Italy
Interests: molecular biology; cancer; cell line; cell culture; flow cytometry analysis; Western blotting; gene expression; sequencing; proteomics; seminoma cell line; prostate cancer cell lines
Special Issues, Collections and Topics in MDPI journals
Department of Experimental and Clinical Medicine, University “Magna Graecia” Catanzaro, 88100 Catanzaro, Italy
Interests: cancer endocrinology; molecular biology; signal transduction; p75NTR-signaling; apoptosis; autophagy; EMT; renal and peritoneal fibrosis; inflammation; biological activity of natural compounds in cancer and chronic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Genitourinary cancers encompass some of the most common solid tumors and have high rates of morbidity and mortality. Although much progress has been made in understanding the underlying tumorigenesis and progression of these malignancies, emerging evidence is focused on the characterization of further molecular mechanisms and novel molecular markers associated with early detection and predicting the response of therapeutic strategies. Finally, a great interest has been on the development of new drugs; some recent in vitro and in vivo studies reported that phytochemicals derived from plants have shown promise in discovering new anticancer treatments, which are both safe and effective. This Special Issue, “Molecular Research on Genitourinary Cancers”, welcomes original research and review articles with a focus on, but not limited to, the molecular and mechanistic basis for genitourinary cancers onset and progression, molecular markers, and the development of new drugs.

Dr. Sabrina Bossio
Dr. Anna Perri
Guest Editors

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Keywords

  • genitourinary cancer
  • molecular markers
  • oxi-inflammation
  • tumor microenvironmental
  • natural products

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Published Papers (2 papers)

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Research

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11 pages, 2315 KiB  
Article
Immunohistochemical Expression of p53 and FGFR3 Predicts Response to Enfortumab Vedotin in Metastatic Urothelial Carcinoma
by Yujiro Nagata, Akinori Minato, Hisami Aono, Rieko Kimuro, Katsuyoshi Higashijima, Ikko Tomisaki, Kenichi Harada, Hiroshi Miyamoto and Naohiro Fujimoto
Int. J. Mol. Sci. 2024, 25(19), 10348; https://doi.org/10.3390/ijms251910348 - 26 Sep 2024
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Abstract
Locally advanced or metastatic urothelial carcinoma is a genomically and molecularly heterogeneous disease associated with various clinical outcomes. We aimed to evaluate the association between the status of p53/FGFR3 expression and the efficacy of enfortumab vedotin (EV) in metastatic urothelial carcinoma. We evaluated [...] Read more.
Locally advanced or metastatic urothelial carcinoma is a genomically and molecularly heterogeneous disease associated with various clinical outcomes. We aimed to evaluate the association between the status of p53/FGFR3 expression and the efficacy of enfortumab vedotin (EV) in metastatic urothelial carcinoma. We evaluated the association between p53 (abnormal vs. wild-type) or FGFR3 (high vs. low) expression determined by immunohistochemistry and response to EV in 28 patients with metastatic urothelial carcinoma. Overall, 60.7% showed abnormal p53, and 17.9% had high FGFR3 expression. The rates of objective response to EV were statistically higher in patients with abnormal p53 than in those with wild-type p53 (p = 0.038). Patients with pure urothelial carcinoma (n = 18) and low FGFR3 showed significantly better response to EV than those with high FGFR3. When the statuses of p53 and FGFR3 were combined, abnormal p53/low FGFR3 (vs. wild-type p53/high FGFR3) was strongly associated with favorable outcomes in both the entire cohort (p = 0.002) and in cases of pure urothelial carcinoma only (p = 0.023). Immunohistochemically abnormal p53 tumors were found to respond well to EV, while high FGFR3 tumors had a poorer response. Thus, p53 and FGFR3 are potential biomarkers for predicting response to EV treatment in patients with urothelial carcinoma. Full article
(This article belongs to the Special Issue Molecular Research on Genitourinary Cancers)
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Review

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24 pages, 2606 KiB  
Review
GPCR-Gα13 Involvement in Mitochondrial Function, Oxidative Stress, and Prostate Cancer
by Di Wu and Patrick J. Casey
Int. J. Mol. Sci. 2024, 25(13), 7162; https://doi.org/10.3390/ijms25137162 - 28 Jun 2024
Cited by 1 | Viewed by 1728
Abstract
Gα13 and Gα12, encoded by the GNA13 and GNA12 genes, respectively, are members of the G12 family of Gα proteins that, along with their associated Gβγ subunits, mediate signaling from specific G protein-coupled receptors (GPCRs). Advanced prostate cancers have increased expression of GPCRs [...] Read more.
Gα13 and Gα12, encoded by the GNA13 and GNA12 genes, respectively, are members of the G12 family of Gα proteins that, along with their associated Gβγ subunits, mediate signaling from specific G protein-coupled receptors (GPCRs). Advanced prostate cancers have increased expression of GPCRs such as CXC Motif Chemokine Receptor 4 (CXCR4), lysophosphatidic acid receptor (LPAR), and protease activated receptor 1 (PAR-1). These GPCRs signal through either the G12 family, or through Gα13 exclusively, often in addition to other G proteins. The effect of Gα13 can be distinct from that of Gα12, and the role of Gα13 in prostate cancer initiation and progression is largely unexplored. The oncogenic effect of Gα13 on cell migration and invasion in prostate cancer has been characterized, but little is known about other biological processes such as mitochondrial function and oxidative stress. Current knowledge on the link between Gα13 and oxidative stress is based on animal studies in which GPCR-Gα13 signaling decreased superoxide levels, and the overexpression of constitutively active Gα13 promoted antioxidant gene activation. In human samples, mitochondrial superoxide dismutase 2 (SOD2) correlates with prostate cancer risk and prognostic Gleason grade. However, overexpression of SOD2 in prostate cancer cells yielded conflicting results on cell growth and survival under basal versus oxidative stress conditions. Hence, it is necessary to explore the effect of Gα13 on prostate cancer tumorigenesis, as well as the effect of Gα13 on SOD2 in prostate cancer cell growth under oxidative stress conditions. Full article
(This article belongs to the Special Issue Molecular Research on Genitourinary Cancers)
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