Genetic alterations in bladder cancer

Dalbagni, G.; Presti, J.; Fair, W.R.; Reuter, V.; Cordon-Cardo, C.

doi:10.1016/0140-6736(93)91595-d

Cited by 238Bladder and Urothelial Cancer TreatmentsUrinary and Genital Oncology StudiesCancer Genomics and Diagnostics

Genetic alterations in bladder cancer

Dalbagni, G., Presti, J., Fair, W.R., Reuter, V., Cordon-Cardo, C.·1993·The Lancet

DOI 10.1016/0140-6736(93)91595-d

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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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Mad2 is significantly increased in many bladder carcinomas compared with normal urothelium, particularly in more advanced tumours.
“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]
Rb inactivation is common in advanced bladder tumours.
“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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Self-citation

Authors: Dalbagni, G., Presti, J., Fair, W. R., Reuter, V., & Cordon-Cardo, C.
Affiliations: Memorial Sloan Kettering Cancer Center (US)
ORCID: Dalbagni, G.
Presti, J.
Reuter, V.
Venue: The Lancet
Publisher: Elsevier BV
Published: 1993-08
Volume: 342
Issue: 8869
Pages: 469-471
ISSN: 0099-5355 (ISSN-L)
0140-6736
DOI: 10.1016/0140-6736(93)91595-d
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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Genetic alterations in bladder cancer

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