Bladder cancer subtypes defined by genomic alterations

Knowles, Margaret A.

doi:10.1080/03008880802284605

Cited by 40 publications

(15 citation statements)

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“…Other authors have reviewed the field of UBC molecular pathogenesis in detail [25][26][27][28][29][30], and there has been general consensus on a divergent pathway for the development of Ta/T1 disease and Tis/T2þ disease [28,[40][41][42][43][44][45]. However, Dancik et al [46] recently identified a cell of origin gene signature for basal cells and umbrella cells of the urothelium.…”

Section: Molecular Pathways To Non-muscle-invasive and Muscle-invasivmentioning

confidence: 99%

Cell adhesion and urothelial bladder cancer: the role of cadherin switching and related phenomena

Bryan

2015

Phil. Trans. R. Soc. B

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Cadherins are mediators of cell-cell adhesion in epithelial tissues. E-cadherin is a known tumour suppressor and plays a central role in suppressing the invasive phenotype of cancer cells. However, the abnormal expression of N-and P-cadherin ('cadherin switching', CS) has been shown to promote a more invasive and m alignant phenotype of cancer, with P-cadherin possibly acting as a key mediator of invasion and metastasis in bladder cancer. Cadherins are also implicated in numerous signalling events related to embryonic development, tissue morphogenesis and homeostasis. It is these wide ranging effects and the serious implications of CS that make the cadherin cell adhesion molecules and their related pathways strong candidate targets for the inhibition of cancer progression, including bladder cancer. This review focuses on CS in the context of bladder cancer and in particular the switch to P-cadherin expression, and discusses other related molecules and phenomena, including EpCAM and the development of the cancer stem cell phenotype.

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Section: Molecular Pathways To Non-muscle-invasive and Muscle-invasivmentioning

confidence: 99%

Cell adhesion and urothelial bladder cancer: the role of cadherin switching and related phenomena

Bryan

2015

Phil. Trans. R. Soc. B

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“…The 4 probes were selected since increased copy numbers (polysomies) of the chromosomes 3, 7 and 17 had been found to be particularly frequent in bladder cancer. Deletion of 9p21, the site of the tumor-suppressor gene P16, is also common and occurs early in the development of both papillary and flat urothelial neoplasia [17]. Subsequent progression is associated with chromosomal instability leading to aneuploidy with multiple chromosomal aberrations.…”

Section: Introductionmentioning

confidence: 99%

Multiprobe Fluorescence in situ Hybridization (UroVysion) for the Detection of Urothelial Carcinoma – FISHing for the Right Catch

Bubendorf¹

2011

Acta Cytologica

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Urinary cytology has a well-established role in the detection and monitoring of urothelial carcinoma. The main strength of cytology is the high specificity for high-grade urothelial carcinoma and carcinoma in situ, but it has a low sensitivity for low-grade, non-invasive tumors. There are several other limitations of cytology. Cytology of the upper urinary tract and after intravesical therapy with bacillus Calmette-Guerin is notoriously difficult to interpret. In addition, there is a poorly defined but commonly used category of atypical cytology of uncertain significance. The UroVysion multiprobe fluorescence in situ hybridization has emerged as a helpful tool to address these limitations. It consists of fluorescently labeled DNA probes to detect increased copy numbers (polysomy) of the chromosomes 3, 7 and 17 and deletion of 9p21, the site of the P16 tumor suppressor gene. Multiple studies have shown that fluorescence in situ hybridization in voided urine and washing specimens can help in patient management due to its superior sensitivity over cytology in different situations. It can be particularly useful to clarify equivocal cytological findings. However, some aspects remain to be further addressed including cost efficiency, optimal cut-off values and the true performance under real-life conditions.

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“…Superficial tumors, which account for the large majority (~75%-85%), typically have a favorable prognosis, while the 5-yr survival for patients with invasive bladder cancer (~25% of all bladder tumors) can be less than 10% (Jemal et al 2005). Notably, superficial and invasive bladder cancers are associated with distinct genotypic and phenotypic patterns (Wu 2005;CordonCardo 2008;Knowles 2008). In particular, chromosome 9 deletions and mutations of RAS and FGFR3 occur in most, if not all, superficial papillary noninvasive tumors, but only in a small subset of invasive bladder tumors.…”

mentioning

confidence: 99%

Inactivation of p53 and Pten promotes invasive bladder cancer

Puzio-Kuter

Castillo-Martín²,

Kinkade³

et al. 2009

Genes Dev.

271

277

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Although bladder cancer represents a serious health problem worldwide, relevant mouse models for investigating disease progression or therapeutic targets have been lacking. We show that combined deletion of p53 and Pten in bladder epithelium leads to invasive cancer in a novel mouse model. Inactivation of p53 and PTEN promotes tumorigenesis in human bladder cells and is correlated with poor survival in human tumors. Furthermore, the synergistic effects of p53 and Pten deletion are mediated by deregulation of mammalian target of rapamycin (mTOR) signaling, consistent with the ability of rapamycin to block bladder tumorigenesis in preclinical studies. Our integrated analyses of mouse and human bladder cancer provide a rationale for investigating mTOR inhibition for treatment of patients with invasive disease.Supplemental material is available at http://www.genesdev.org.

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Bladder cancer subtypes defined by genomic alterations

Cited by 40 publications

References 100 publications

Cell adhesion and urothelial bladder cancer: the role of cadherin switching and related phenomena

Cell adhesion and urothelial bladder cancer: the role of cadherin switching and related phenomena

Multiprobe Fluorescence in situ Hybridization (UroVysion) for the Detection of Urothelial Carcinoma – FISHing for the Right Catch

Inactivation of p53 and Pten promotes invasive bladder cancer

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