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Titolo:
Genetic mapping and DNA sequence-based analysis of deleted regions on chromosome 16 involved in progression of bladder cancer from occult preneoplastic conditions to invasive disease
Autore:
Yoon, DS; Li, L; Zhang, RD; Kram, A; Ro, JY; Johnston, D; Grossman, HB; Scherer, S; Czerniak, B;
Indirizzi:
Univ Texas, MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 c Ctr, Dept Pathol, Houston, TX 77030 USA Univ Texas, MD Anderson Canc Ctr, Dept Biomath, Houston, TX 77030 USA UnivTexas Houston TX USA 77030 Ctr, Dept Biomath, Houston, TX 77030 USA Univ Texas, MD Anderson Canc Ctr, Dept Urol, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 anc Ctr, Dept Urol, Houston, TX 77030 USA Baylor Coll Med, Human Genome Sequencing Ctr, Dept Mol & Human Genet, Houston, TX 77030 USA Baylor Coll Med Houston TX USA 77030 & Human Genet, Houston, TX 77030 USA
Titolo Testata:
ONCOGENE
fascicolo: 36, volume: 20, anno: 2001,
pagine: 5005 - 5014
SICI:
0950-9232(20010816)20:36<5005:GMADSA>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-BREAST-CARCINOMA; URINARY-BLADDER; MICROSATELLITE ANALYSIS; PROSTATE-CANCER; ALLELIC LOSS; E-CADHERIN; EXPRESSION; CARCINOGENESIS; HETEROZYGOSITY; ALLELOTYPE;
Keywords:
tumor suppressor gene loci; chromosome 16; bladder cancer;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Czerniak, B Univ Texas, MD Anderson Canc Ctr, Dept Pathol, 1515 Holcombe Blvd, Houston, TX 77030 USA Univ Texas 1515 Holcombe Blvd Houston TX USA 77030 X 77030 USA
Citazione:
D.S. Yoon et al., "Genetic mapping and DNA sequence-based analysis of deleted regions on chromosome 16 involved in progression of bladder cancer from occult preneoplastic conditions to invasive disease", ONCOGENE, 20(36), 2001, pp. 5005-5014

Abstract

Histologic and genetic mapping with 30 hypervariable markers mapped to chromosome 16 were performed on 234 DNA samples of five cystectomy specimens from patients with invasive bladder cancer. Allelic losses of individual markers were related to microscopically identified precursor conditions in theentire bladder mucosa and invasive cancer. Their significance for the development and progression of neoplasia from in situ preneoplastic conditions to invasive disease was analysed by the nearest neighbor algorithm and binomial maximum likelihood analysis. Using this approach we identified five distinct regions of allelic losses defined by their flanking markers and predicted size as follows. p13.3(D16S418-D16S406, 1.2 cM), p13.1(D16S748-D16S287, 12.9 cM), q12 1(D16S409-D16S514, 24.0 cM), q22.1 (D16S496-D16S515, 5.4 cM), and q24 (D16S507-D16S511, 5.9 cM and D16S402-D16S413, 17.4 cM). The regions mapping to p13.1 and q24 were involved in early intraurothelial phasesof bladder neoplasia such as mild to moderate dysplasia. On the other handthe deleted region mapping to p13.3 was involved in progression of severe dysplasia/carcinoma in situ to invasive bladder cancer. Testing of markers that exhibited statistically significant LOH in relation to progression of neoplasia from precursor conditions to invasive cancer on 28 tumors and voided urine samples from 25 patients with bladder cancer revealed that q12.1 showed LOH in 46.4% of tumor and 32.0% of voided urine samples. The LOH of a single marker D16S541 could be detected in approximately 28% of tumors and 20% of voided urine samples of patients with bladder cancer. These data imply that the deleted region centered around marker D16S541 spanning approximately 10 cM and flanked by D16S409 and D16S415 contains a novel putative tumor suppressor gene or genes playing an important role in the developmentof human bladder cancer. To facilitate more precise positional mapping andidentification of pathogenetically relevent genes, we analysed of human genome contig and sequence databases spanning the deleted regions. Multiple known candidate genes and several smaller gene-rich areas mapping to the target regions of chromosome 16 were identified Oncogene (2001) 20, 5005-5014.

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Documento generato il 28/03/20 alle ore 14:11:27