ArticleBritish journal of cancer2002
Genetic aberrations of c-myc and CCND1 in the development of invasive bladder cancer.
Article in British journal of cancer, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 48 citations in OpenAlex.
- The role of circular RNA targeting IGF2BPs in cancer-a potential target for cancer therapy.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Integrating Genetic Alterations and Histopathological Features for Enhanced Risk Stratification in Non-Muscle-Invasive Bladder Cancer.Diagnostics (Basel, Switzerland) · 2024Article
- Review
- USP43 stabilizes c-Myc to promote glycolysis and metastasis in bladder cancer.Cell death & disease · 2024Article
- The urothelial gene regulatory network: understanding biology to improve bladder cancer management.Oncogene · 2024Review
- Targeting microRNA-145-mediated progressive phenotypes of early bladder cancer in a molecularly definedMolecular therapy. Nucleic acids · 2023Article
- Expression of proto-oncogene c-Myc in patients with urinary bladder transitional cell carcinoma.Current urology · 2021Article
- Biological significance of MYC and CEBPD coamplification in urothelial carcinoma: Multilayered genomic, transcriptional and posttranscriptional positive feedback loops enhance oncogenic glycolysis.Clinical and translational medicine · 2021Article
- CircPTPRA blocks the recognition of RNA NMolecular cancer · 2021Article
- Copy number variations in primary tumor, serum and lymph node metastasis of bladder cancer patients treated with radical cystectomy.Scientific reports · 2020Article
- Article
- DANCR Promotes Metastasis and Proliferation in Bladder Cancer Cells by Enhancing IL-11-STAT3 Signaling and CCND1 Expression.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Suppression of FGFR3- and MYC-dependent oncogenesis by tubacin: association with HDAC6-dependent and independent activities.Oncotarget · 2018Article
- Synthetic regulatory RNAs selectively suppress the progression of bladder cancer.Journal of experimental & clinical cancer research : CR · 2017Article
- Heterogeneous nuclear ribonucleoprotein K is associated with poor prognosis and regulates proliferation and apoptosis in bladder cancer.Journal of cellular and molecular medicine · 2017Article
- Prognostic Value of Beta-Tubulin-3 and c-Myc in Muscle Invasive Urothelial Carcinoma of the Bladder.PloS one · 2015Article
- Copy number analysis of 24 oncogenes: MDM4 identified as a putative marker for low recurrence risk in non muscle invasive bladder cancer.International journal of molecular sciences · 2014Article
- Targeted therapies in the management of metastatic bladder cancer.Biologics : targets & therapy · 2007Article
- HER2/neu overexpression in the development of muscle-invasive transitional cell carcinoma of the bladder.British journal of cancer · 2003Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Detrusor muscle invasive transitional cell carcinoma is associated with poor prognosis and is responsible for the majority of bladder cancer related deaths. Amplifications of c-myc and CCND1 are associated with detrusor-muscle-invasive transitional cell carcinoma, however, their precise role in driving disease progression is unclear. Fluorescence in situ hybridisation on archival tissue from 16 patients with primary diagnosis of > or = pT2 transitional cell carcinoma and 15 cases with primary pTa/pT1 disease subsequently progressing to detrusor-muscle-invasion was performed, in the latter group both pre and post muscle invasive events were studied. No patients presenting with >/=pT2 had amplification of c-myc, two out of 16 (12.5%) had CCND1 amplification. Of patients who developed > or = pT2, two out of 15 (13.3%) had amplification of c-myc, both in > or = pT2, five out of 15 (33.3%) had CCND1 amplification, two in pTa/pT1 tumours, three in > or = pT2 transitional cell carcinomas. In total, two out of 31 (6.5%) of patients' > or = pT2 TCCs were amplified for c-myc and six out of 31 (19%) were amplified for CCND1. Eighty-seven per cent (40 out of 46) of tumours were polysomic for chromosome 8 and 80% (37 out of 46) were polysomic for chromosome 11 and this reflected the high copy numbers of c-myc and CCND1 observed. In almost all cases an increase in c-myc/CCND1 copy number occurred prior to invasion and persisted in advanced disease. Amplification of CCND1 or alterations in c-myc/CCND1 early in bladder cancer may have clinical relevance in promoting and predicting progression to detrusor-muscle-invasive transitional cell carcinoma.
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