Nonrandom changes of chromosome 10 in bladder cancer

Wang, Ming-Rong; Perissel, B; Taillandier, J.; Kémény, Jean-Louis; Fonck, Y; Lautier, A; Benkhalifa, Moncef; Malet, P

doi:10.1016/0165-4608(94)90175-9

Cited by 15 publications

(12 citation statements)

References 5 publications

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“…Recently, loss of heterozygosity (LOH) of 10q has been reported in bladder tumours (Cappellen et al, 1997;Kagan et al, 1998), confirming previous cytogenetic reports of monosomy 10 and 10q deletion (Gibas et al, 1984;Atkin and Baker, 1985;Berger et al, 1986;Babu et al, 1987;Smeets et al, 1987) and comparative genomic hybridization and fluorescence in situ hybridization studies (Kallioniemi et al, 1992;Wang et al, 1994). A critical region of deletion defined in these studies is coincident with the major region mapped in other tumour types.…”

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confidence: 72%

Somatic mutation of PTEN in bladder carcinoma

et al. 1999

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SummaryThe tumour suppressor gene PTEN/MMAC1, which is mutated or homozygously deleted in glioma, breast and prostate cancer, is mapped to a region of 10q which shows loss of heterozygosity (LOH) in bladder cancer. We screened 123 bladder tumours for LOH in the region of PTEN. In 53 informative muscle invasive tumours (≥ pT2), allele loss was detected in 13 (24.5%) and allelic imbalance in four tumours (overall frequency 32%). LOH was found in four of 60 (6.6%) informative, non-invasive tumours (pTa/pT1). We screened 63 muscle invasive tumours for PTEN mutations by single-strand conformation polymorphism (SSCP) analysis and for homozygous deletion by duplex quantitative polymerase chain reaction (PCR). Two homozygous deletions were identified but no mutations. Of 15 bladder tumour cell lines analysed, three showed homozygous deletion of all or part of the PTEN gene, but none had mutations detectable by SSCP analysis. Our results indicate that PTEN is involved in the development of some bladder tumours. The low frequency of mutation of the retained allele in tumours with 10q23 LOH suggests that there may be another predominant mechanism of inactivation of the second allele, for example small intragenic deletions, that hemizygosity may be sufficient for phenotypic effect, or that there is another target gene at 10q23.

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confidence: 72%

Somatic mutation of PTEN in bladder carcinoma

et al. 1999

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“…LOH on the long arm of chromosome 10 has also been found in the progression of other tumor types, e.g., glioblastomas (Leon et al 1994), malignant meningiomas (Rempel et al 1993), malignant melanomas (Isshiki et al 1993), and bladder carcinomas (Wang et al 1994). In an earlier paper, we touched upon an interesting finding of an aggressive follicular thyroid carcinoma in a young girl with a constitutional ring chromosome, most likely lacking genetic material at the distal part of chromosome lOq (Sparkes et al 1978;Tommerup and Lothe 1992).…”

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confidence: 99%

Deletions of the long arm of chromosome 10 in progression of follicular thyroid tumors

et al. 1996

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Previous studies of follicular thyroid tumors have shown loss of heterozygosity (LOH) on the short arm of chromosome 3 in carcinomas, and on chromosome 10 in atypical adenomas and carcinomas, but not in common adenomas. We studied LOH on these chromosomal arms in 15 follicular thyroid carcinomas, 19 atypical follicular adenomas and 6 anaplastic (undifferentiated) carcinomas. Deletion mapping of chromosome 10 using 15 polymorphic markers showed that 15 (37.5%) of the tumors displayed LOH somewhere along the long arm. Thirteen of these tumors showed deletions involving the telomeric part of chromosome lOq, distal to D10S187. LOH on chromosome 3p was found in 8 (20%) cases. Seven of these also showed LOH on chromosome lOq. In eight cases LOH was seen on chromosome lOq but not 3p. In comparison, the retinoblastoma gene locus at chromosome 13q showed LOH in 22% of the tumors. Most of these also had deletions on chromosome lOq. The results indicate that a region at the telomeric part of 1 Oq may be involved in progression of follicular thyroid tumors.

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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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Nonrandom changes of chromosome 10 in bladder cancer

Cited by 15 publications

References 5 publications

Somatic mutation of PTEN in bladder carcinoma

Somatic mutation of PTEN in bladder carcinoma

Deletions of the long arm of chromosome 10 in progression of follicular thyroid tumors

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

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