A possible specific chromosome change in transitional cell carcinoma of the bladder

Gibas, Zenon; Prout, George R.; Pontes, J. Edson; Connolly, John G.; Sandberg, Avery A.

doi:10.1016/0165-4608(86)90051-8

Cited by 130 publications

(70 citation statements)

References 11 publications

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“…The alterations range from monosomies as sole cytogenetic abnormalities to allelic losses that were initially reported to be present in 67% of advanced bladder cancers (Gibas et al, 1984;Smeets et al, 1987;Vanni et al, 1988;Atkin and Baker 1985;Babu et al, 1987;Berger et al, 1986). Some studies have shown that allelic losses on 9q are the most frequent and appear in tumors of all histologic grades and stages (Olumi et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Superimposed histologic and genetic mapping of chromosome 9 in progression of human urinary bladder neoplasia: implications for a genetic model of multistep urothelial carcinogenesis and early detection of urinary bladder cancer

et al. 1999

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The evolution of alterations on chromosome 9, including the putative tumor suppressor genes mapped to the 9p21-22 region (the MTS genes), was studied in relation to the progression of human urinary bladder neoplasia by using whole organ superimposed histologic and genetic mapping in cystectomy specimens and was veri®ed in urinary bladder tumors of various pathogenetic subsets with longterm follow-up. The applicability of chromosome 9 allelic losses as non-invasive markers of urothelial neoplasia was tested on voided urine and/or bladder washings of patients with urinary bladder cancer. Although sequential multiple hits in the MTS locus were documented in the development of intraurothelial precursor lesions, the MTS genes do not seem to represent a major target for p21-23 deletions in bladder cancer. Two additional tumor suppressor genes involved in bladder neoplasia located distally and proximally to the MTS locus within p22-23 and p11-13 regions respectively were identi®ed. Several distinct putative tumor suppressor gene loci within the q12-13, q21-22, and q34 regions were identi®ed on the q arm. In particular, the pericentromeric q12-13 area may contain the critical tumor suppressor gene or genes for the development of early urothelial neoplasia. Allelic losses of chromosome 9 were associated with expansion of the abnormal urothelial clone which frequently involved large areas of urinary bladder mucosa. These losses could be found in a high proportion of urothelial tumors and in voided urine or bladder washing samples of nearly all patients with urinary bladder carcinoma.

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Section: Discussionmentioning

confidence: 99%

Superimposed histologic and genetic mapping of chromosome 9 in progression of human urinary bladder neoplasia: implications for a genetic model of multistep urothelial carcinogenesis and early detection of urinary bladder cancer

et al. 1999

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“…Until now, in spite of cytogenetic reports (Gibas et al, 1984;Atkin and Baker, 1985;Berger et al, 1986;Babu et al, 1987;Smeets et al, 1987) and comparative genomic hybridization or¯uorescent in situ hybridization studies (Wang et al, 1994;Kallioniemi et al, 1995) describing frequent chromosome 10 monosomies and deletions in bladder tumours, the role of chromosome 10 loss in bladder cancer has not been investigated in detail.…”

Section: Discussionmentioning

confidence: 99%

Frequent loss of heterozygosity on chromosome 10q in muscle-invasive transitional cell carcinomas of the bladder

et al. 1997

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Loss of heterozygosity (LOH) on chromosome 10 has been observed in several human cancers including glioblastomas, meningiomas, melanomas and endometrial and prostate carcinomas. We have investigated the incidence of LOH on chromosome 10 in 36 human transitional cell carcinomas (TCCs) of the bladder, three upper urinary tract TCCs and one lymph node metastasis, using a panel of 27 highly polymorphic markers spanning 10p (short arm) and 10q (long arm). Fourteen bladder tumours (39%), the three upper urinary tract tumours and the lymph node metastasis showed LOH for at least one locus on chromosome 10. Remarkably, LOH on chromosome 10 was observed mainly in muscle-invasive (P=0.01) and high grade tumours (P=0.03). For ®ve tumours and the lymph node metastasis, LOH was found at all informative loci, indicating monosomy or isodisomy of chromosome 10. The deletion mapping of the tumours with partial loss delineated two minimal regions of loss on chromosome 10q. One region, the most telomeric, was bounded by markers D10S214 and D10S169 and the other, the most proximal, was bounded by markers D10S222 and D10S531. Our results demonstrate that chromosome 10q LOH is common in muscle-invasive bladder cancers and that two potential tumour suppressor loci, at 10q24.1-q24.3 and 10q26.1-q26.2, may contribute to the malignant progression of these tumours. Localization of the smallest common regions of loss in bladder tumours provides a starting point for the identi®cation of the genes involved.

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“…Early karyotyping studies identified deletions and amplifications of both arms of chromosome 5, suggesting the involvement of several genes in human bladder carcinogenesis (Atkin and Fox, 1990;Gibas et al, 1986;Klingelhutz et al, 1991). More recent studies using comparative genomic hybridization and hypervariable markers have identified three distinct regions on chromosome 5 as being involved in the progression of urinary bladder cancer (Bohm et al, 1997;Koo et al, 1999;von Knobloch et al, 2000;Voorter et al, 1995).…”

Section: Kram Et Almentioning

confidence: 99%

Mapping and Genome Sequence Analysis of Chromosome 5 Regions Involved in Bladder Cancer Progression

Kram

Zhang

et al. 2001

Laboratory Investigation

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SUMMARY:We studied the evolution of allelic losses on chromosome 5 by whole-organ histologic and genetic mapping in 234 mucosal DNA samples of 5 cystectomy specimens with invasive bladder cancer and preneoplastic changes in adjacent urothelium. The frequency of alterations in individual loci was verified on 32 tumors and 29 voided urine samples from patients with bladder cancer. Finally, deleted regions on chromosome 5 were integrated with the human genome contigs and sequence-based databases. Deleted regions on chromosome 5 involved in intraurothelial phases of bladder neoplasia defined by their nearest flanking markers and predicted size were identified as follows: q13.3-q22 (D5S424-D5S656; 38.8 centimorgan [cM]); q22-q31.1 (D5S656-D5S808; 19.2 cM), q31.1-q32 (D5S816-SPARC; 11.5 cM), and q34 (GABRA1-D5S415; 6.4 cM). The two most frequently deleted neighbor markers (D5S2055 and D5S818) mapping to q22-q31.1 defined a 9 cM region, which may contain genes that play an important role in early phases of urinary bladder carcinogenesis. Human genome database analysis provided an accurate map of deleted regions with positions of 138 known genes and revealed several smaller gene-rich areas representing putative targets for further mapping. The strategic approach presented here, which combines whole-organ histologic and genetic mapping with analysis of the rapidly emerging human genome sequence database, facilitates identification of genes potentially involved in early phases of bladder carcinogenesis. (Lab Invest 2001, 81:1039 -1048.C ancer develops via multiple, cumulative steps, many of which precede the development of clinically and even microscopically recognizable disease. Mapping and human genome sequence analysis of chromosomal regions involved in clinically occult preinvasive phases of neoplasia may provide valuable clues for more specific studies of early events in human carcinogenesis and could lead to the development of novel early detection markers as well as preventive strategies.We have previously reported the identification of several putative tumor suppressor gene loci involved in early preinvasive phases of human urinary bladder carcinogenesis (Chaturvedi et al, 1997;Czerniak et al, 1999Czerniak et al, , 2000. Bladder tumors were used as a common model of human cancer, which develops by progression of microscopically recognizable in situ precursor conditions, and are easily accessible by various minimally invasive or noninvasive techniques (Gazdar and Czerniak, 2001;Greenlee et al, 2000). The entire mucosal surface of the bladder can be examined by cystoscopy and biopsies with minimal risk for the patient, and exfoliated urothelial cells can be repeatedly tested for various alterations in voided urine at no risk at all (Gazdar and Czerniak, 2001). Moreover, the simple anatomy and appropriate size of the bladder permit the histologic and genetic mapping studies of invasive cancer and preneoplastic lesions in the entire mucosa of cystectomy specimens. The whole-organ histologic and genetic mapping combine...

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A possible specific chromosome change in transitional cell carcinoma of the bladder

Cited by 130 publications

References 11 publications

Superimposed histologic and genetic mapping of chromosome 9 in progression of human urinary bladder neoplasia: implications for a genetic model of multistep urothelial carcinogenesis and early detection of urinary bladder cancer

Superimposed histologic and genetic mapping of chromosome 9 in progression of human urinary bladder neoplasia: implications for a genetic model of multistep urothelial carcinogenesis and early detection of urinary bladder cancer

Frequent loss of heterozygosity on chromosome 10q in muscle-invasive transitional cell carcinomas of the bladder

Mapping and Genome Sequence Analysis of Chromosome 5 Regions Involved in Bladder Cancer Progression

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