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Genetic alterations in bladder cancer
Abstract
To see whether genetic alterations follow a sequence of events leading to bladder cancer progression, 60 paired bladder tumours and normal tissues were analysed with polymorphic DNA markers, correlating loss of heterozygosity (LOH) at candidate tumour suppressor gene sites with pathological indices of poor clinical outcome. Distinct genotypic patterns were associated with early and late stages of bladder cancer. 9q deletions were observed in all superficial papillary tumours (Ta) and almost all tumours invading the lamina propria (T1), suggesting that this event associates with the development of superficial bladder tumours. However, 3p, 5q, and 17p deletions were absent in the Ta tumours but were identified in invasive bladder cancers. Two genetic pathways characterise the evolution of superficial bladder tumours. 9qLOH was detected in most Ta tumours, but in only 43% of muscle invasive neoplasms. Our hypothesis is that certain chromosomal abnormalities have a defined role in bladder tumour development, whereas others correlate with pathological indices of poor clinical outcome.
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“Similarly, Mad2 was significantly increased in many bladder carcinomas when compared to normal urothelium (data not shown), particularly in the more advanced tumours, where Rb inactivation is common 19 (Fig. 3a, middle panels).”
From Rb inactivation promotes genomic instability by uncoupling cell cycle progression from mitotic control (2004) · cites this paper as [19]
In the citing paper
“particularly in the more advanced tumours, where Rb inactivation is common 19”
From Rb inactivation promotes genomic instability by uncoupling cell cycle progression from mitotic control (2004) · cites this paper as [19]
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Hedgehog Signaling Regulates Bladder Cancer Growth and Tumorigenicity
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Genetic aspects of prostate cancer
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Metadata
- Authors
- Dalbagni, G., Presti, J., Fair, W. R., Reuter, V., & Cordon-Cardo, C.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 1993-08
- Volume
- 342
- Issue
- 8869
- Pages
- 469-471
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- OpenAlex
- W2039609330
- Cited by
- 238
- References
- 9
- Citations by year
- 2025: 1 · 2024: 4 · 2020: 2 · 2019: 1 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 6 · 2014: 4 · 2013: 6 · 2012: 7
- FWCI
- 18.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (NCI CA-47538)
- Topics
- Health Sciences › Medicine › Surgery › Bladder and Urothelial Cancer Treatments
- Health Sciences › Medicine › Surgery › Urinary and Genital Oncology Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- bladder cancer, loss of heterozygosity, tumor suppressor, 9q deletion, muscle-invasive bladder cancer, tumor progression, chromosomal abnormalities, 3p deletion, 5q deletion, 17p deletion, clinical outcomes
- MeSH terms
- Alleles, Urinary Bladder Neoplasms, Chromosome Deletion, Chromosomes, Human, Pair 13, Chromosomes, Human, Pair 17, Chromosomes, Human, Pair 3, Chromosomes, Human, Pair 5, Chromosomes, Human, Pair 9, Genotype, Heterozygote, Humans, Neoplasm Invasiveness, Neoplasm Staging, Prognosis, Genes, Tumor Suppressor
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