scholarly journals TERT Promoter Mutations and TERT mRNA but Not FGFR3 Mutations Are Urinary Biomarkers in Han Chinese Patients With Urothelial Bladder Cancer

2015 ◽  
Vol 20 (3) ◽  
pp. 263-269 ◽  
Author(s):  
Kun Wang ◽  
Tiantian Liu ◽  
Cheng Liu ◽  
Yan Meng ◽  
Xiaotian Yuan ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Han Chinese ◽  
Urinary Biomarkers ◽  
Chinese Patients ◽  
Urothelial Bladder Cancer ◽  
Tert Promoter ◽  
Tert Promoter Mutations ◽  
Urothelial Bladder ◽  
Promoter Mutations ◽  
Fgfr3 Mutations

scholarly journals The role of telomerase reverse transcriptase (TERT) promoter mutations in prognosis in bladder cancer

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 1495-1504
Author(s):  
Song Wan ◽  
Xuan Liu ◽  
Wei Hua ◽  
Ming Xi ◽  
Yulin Zhou ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Reverse Transcriptase ◽  
Telomerase Reverse Transcriptase ◽  
Tert Promoter ◽  
Tert Promoter Mutations ◽  
Promoter Mutations

Impact of body mass on recurrence and progression in Chinese patients with Ta, T1 urothelial bladder cancer

2015 ◽  
Vol 47 (7) ◽  
pp. 1135-1141 ◽  
Author(s):  
Tianyuan Xu ◽  
Zhaowei Zhu ◽  
Xianjin Wang ◽  
Leilei Xia ◽  
Xiaohua Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Body Mass ◽  
Chinese Patients ◽  
Urothelial Bladder Cancer ◽  
Urothelial Bladder

scholarly journals Urinary TERT promoter mutations are detectable up to 10 years prior to clinical diagnosis of bladder cancer: Evidence from the Golestan Cohort Study

EBioMedicine ◽  
2020 ◽  
Vol 53 ◽  
pp. 102643 ◽  
Author(s):  
Md Ismail Hosen ◽  
Mahdi Sheikh ◽  
Maria Zvereva ◽  
Ghislaine Scelo ◽  
Nathalie Forey ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cohort Study ◽  
Clinical Diagnosis ◽  
Tert Promoter ◽  
Tert Promoter Mutations ◽  
Promoter Mutations

scholarly journals Urine TERT promoter mutations‑based tumor DNA detection in patients with bladder cancer: A pilot study

2021 ◽  
Vol 15 (6) ◽  
Author(s):  
Mark Jain ◽  
David Kamalov ◽  
Alexander Tivtikyan ◽  
Alexander Balatsky ◽  
Larisa Samokhodskaya ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Pilot Study ◽  
Dna Detection ◽  
Tert Promoter ◽  
Tert Promoter Mutations ◽  
Promoter Mutations ◽  
Tumor Dna

scholarly journals BRAF V600E and TERT Promoter Mutations in Papillary Thyroid Carcinoma in Chinese Patients

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0153319 ◽  
Author(s):  
Jian Sun ◽  
Jing Zhang ◽  
Junliang Lu ◽  
Jie Gao ◽  
Xinyu Ren ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Braf V600e ◽  
Chinese Patients ◽  
Papillary Thyroid ◽  
Tert Promoter ◽  
Tert Promoter Mutations ◽  
Promoter Mutations

scholarly journals TERT Promoter Mutation Analysis of Whole-Organ Mapping Bladder Cancers

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 230
Author(s):  
Veronika Weyerer ◽  
Markus Eckstein ◽  
Pamela L. Strissel ◽  
Adrian Wullweber ◽  
Fabienne Lange ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Telomere Length ◽  
Hot Spot ◽  
Tumor Development ◽  
Non Invasive ◽  
Tert Promoter ◽  
Mutational Status ◽  
Tert Promoter Mutations ◽  
Promoter Mutations ◽  
Normal Urothelium

Background: Multifocal occurrence is a main characteristic of urothelial bladder cancer (UBC). Whether urothelial transformation is caused by monoclonal events within the urothelium, or by polyclonal unrelated events resulting in several tumor clones is still under debate. TERT promoter mutations are the most common somatic alteration identified in UBC. In this study, we analyzed different histological tissues from whole-organ mapping bladder cancer specimens to reveal TERT mutational status, as well as to discern how tumors develop. Methods: Up to 23 tissues from nine whole-organ mapping bladder tumor specimens, were tested for TERT promoter mutations including tumor associated normal urothelium, non-invasive urothelial lesions (hyperplasia, dysplasia, metaplasia), carcinoma in situ (CIS) and different areas of muscle invasive bladder cancers (MIBC). The mutational DNA hotspot region within the TERT promoter was analyzed by SNaPshot analysis including three hot spot regions (−57, −124 or −146). Telomere length was measured by the Relative Human Telomere Length Quantification qPCR Assay Kit. Results: TERT promoter mutations were identified in tumor associated normal urothelium as well as non-invasive urothelial lesions, CIS and MIBC. Analysis of separate regions of the MIBC showed 100% concordance of TERT promoter mutations within a respective whole-organ bladder specimen. Polyclonal events were observed in five out of nine whole-organ mapping bladder cancers housing tumor associated normal urothelium, non-invasive urothelial lesions and CIS where different TERT promoter mutations were found compared to MIBC. The remaining four whole-organ mapping bladders were monoclonal for TERT mutations. No significant differences of telomere length were observed. Conclusions: Examining multiple whole-organ mapping bladders we conclude that TERT promoter mutations may be an early step in bladder cancer carcinogenesis as supported by TERT mutations detected in tumor associated normal urothelium as well as non-invasive urothelial lesions. Since mutated TERT promoter regions within non-invasive urothelial lesions are not sufficient alone for the establishment of cancerous growth, this points to the contribution of other gene mutations as a requirement for tumor development.

scholarly journals GABPA is a master regulator of luminal identity and restrains aggressive diseases in bladder cancer

2019 ◽  
Vol 27 (6) ◽  
pp. 1862-1877 ◽  
Author(s):  
Yanxia Guo ◽  
Xiaotian Yuan ◽  
Kailin Li ◽  
Mingkai Dai ◽  
Lu Zhang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Transcription Factors ◽  
Gene Methylation ◽  
Tert Promoter ◽  
Tumorigenic Potential ◽  
Tert Promoter Mutations ◽  
Geo Dataset ◽  
Ets Family ◽  
Promoter Mutations

AbstractTERT promoter mutations occur in the majority of glioblastoma, bladder cancer (BC), and other malignancies while the ETS family transcription factors GABPA and its partner GABPB1 activate the mutant TERT promoter and telomerase in these tumors. GABPA depletion or the disruption of the GABPA/GABPB1 complex by knocking down GABPB1 was shown to inhibit telomerase, thereby eliminating the tumorigenic potential of glioblastoma cells. GABPA/B1 is thus suggested as a cancer therapeutic target. However, it is unclear about its role in BC. Here we unexpectedly observed that GABPA ablation inhibited TERT expression, but robustly increased proliferation, stem, and invasive phenotypes and cisplatin resistance in BC cells, while its overexpression exhibited opposite effects, and inhibited in vivo metastasizing in a xenograft transplant model. Mechanistically, GABPA directly activates the transcription of FoxA1 and GATA3, key transcription factors driving luminal differentiation of urothelial cells. Consistently, TCGA/GEO dataset analyses show that GABPA expression is correlated positively with luminal while negatively with basal signatures. Luminal tumors express higher GABPA than do basal ones. Lower GABPA expression is associated with the GABPA gene methylation or deletion (especially in basal subtype of BC tumors), and predicted significantly shorter patient survival based on TCGA and our cohort of BC patient analyses. Taken together, GABPA dictates luminal identity of BC cells and inhibits aggressive diseases in BC by promoting cellular differentiation despite its stimulatory effect on telomerase/TERT activation. Given these biological functions and its frequent methylation and/or deletion, GABPA serves as a tumor suppressor rather than oncogenic factor in BC. The GABPA effect on oncogenesis is context-dependent and its targeting for telomerase inhibition in BC may promote disease metastasizing.

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