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Special Issue "Molecular Pathogenesis and Therapeutics in Urothelial Carcinoma"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 4132

Special Issue Editors

Institute of Medical Science and Technology, National Sun Yat-sen University, Kaohsiung, Taiwan
Interests: Urothelial cancer; Epigenetics; Genomics; Signal transduction

Special Issue Information

Dear Colleagues,

Urothelial carcinoma (UC) is one of the most common malignancies worldwide. UC might arise from the upper urinary tract (UTUC) or lower urinary tract (UBUC). Of these, UTUC is relatively rare and only accounts for 5–10% of UC in Western countries while demonstrating an unusually high prevalence in certain regions. Histologically, UC can be driven by two different genetic pathways and are defined as noninvasive low-grade papillary carcinoma and high-grade non-invasive/invasive carcinomas. Somatic genetic effects play a critical role in the pathogenesis of UC. The deletion of the short arm or long arm of chromosome 9 leads to the depleted expression of CDKN2A and TSC1, respectively, and is the most frequent genetic abnormality in the urothelial tumorigenesis. The mutation of FGFR3, HRAS and PIK3CA, which are involved in the MAPK and PI3K pathways, is associated with the growth of non-invasive low-grade papillary urothelial carcinomas, while the deficiency of TP53 and retinoblastoma 1 (RB) related to cell-cycle regulation at the G1/S checkpoint are usually occurreds in high-grade in situ and invasive carcinomas. Moreover, epigenetic gene regulation has also been shown to be involved in the progression of UC. In general, hypomethylation is commonly observed in non-invasive UCs, while the highly methylated DNA was widespread in invasive UC. Although some genetic hallmarks have been disclosed for urothelial carcinogenesis, the underlying mechanism responsible for urothelial carcinoma initiation and progression remains largely unknown. Moreover, the treatment of UC is also limited by only a few targeted therapeutic agents avaible in the current stage. Accordingly, we organize this Special Issue to focus on the most updated concepts regarding molecular profiling and biological effects on novel biomarkers to understand their clinical unility and therapeutic relavance.

Prof. Dr. Chien-Feng Li
Prof. Dr. Yow Ling Shiue
Guest Editors

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  • Urothelial carcinoma
  • Molecular
  • Pathogenesis
  • Prognosis
  • Predictive
  • Therapy
  • Theranostic

Published Papers (1 paper)

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15 pages, 5424 KiB  
Establishment of Canine Transitional Cell Carcinoma Cell Lines Harboring BRAF V595E Mutation as a Therapeutic Target
Int. J. Mol. Sci. 2021, 22(17), 9151; https://doi.org/10.3390/ijms22179151 - 25 Aug 2021
Cited by 6 | Viewed by 3509
Transitional cell carcinoma (TCC) is the most common malignant tumor of the canine urinary tract and tends to have a poor prognosis due to its invasive potential. Recent studies have reported that up to 80% of canine urothelial carcinoma has the BRAF V595E [...] Read more.
Transitional cell carcinoma (TCC) is the most common malignant tumor of the canine urinary tract and tends to have a poor prognosis due to its invasive potential. Recent studies have reported that up to 80% of canine urothelial carcinoma has the BRAF V595E mutation, which is homologous to the human V600E mutation. Activating the BRAF mutation is an actionable target for developing effective therapeutic agents inhibiting the BRAF/mitogen-activated protein kinase (MAPK) pathway in canine cancer as well as human cancer. We established novel canine TCC cell lines from two tumor tissues and one metastatic lymph node of canine TCC patients harboring the BRAF V595E mutation. Tumor tissues highly expressed the BRAF mutant and phosphorylated extracellular signal-related kinases (ERK)1/2 proteins. The derived cell lines demonstrated activated MAPK pathways. We also evaluated the cell lines for sensitivity to BRAF inhibitors. Sorafenib, a multiple kinase inhibitor targeting RAF/vascular endothelial growth factor receptor (VEGFR), successfully inhibited the BRAF/MAPK pathway and induced apoptosis. The established canine TCC cell lines responded with greater sensitivity to sorafenib than to vemurafenib, which is known as a specific BRAF inhibitor in human cancer. Our results demonstrated that canine TCC cells showed different responses compared to human cancer with the BRAF V600E mutation. These cell lines would be valuable research materials to develop therapeutic strategies for canine TCC patients. Full article
(This article belongs to the Special Issue Molecular Pathogenesis and Therapeutics in Urothelial Carcinoma)
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