Research ExplorerPublicationsPatterns of chromosomal imbalances in muscle invasive bladde...

Patterns of chromosomal imbalances in muscle invasive bladder cancer.

Standard

Patterns of chromosomal imbalances in muscle invasive bladder cancer. / Simon, Ronald; Burger, H; Semjonow, A; Hertle, L; Terpe, H J; Bocker, W.

In: INT J ONCOL, Vol. 17, No. 5, 5, 2000, p. 1025-1029.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Simon, R, Burger, H, Semjonow, A, Hertle, L, Terpe, HJ & Bocker, W 2000, 'Patterns of chromosomal imbalances in muscle invasive bladder cancer.', INT J ONCOL, vol. 17, no. 5, 5, pp. 1025-1029. <http://www.ncbi.nlm.nih.gov/pubmed/11029508?dopt=Citation>

APA

Simon, R., Burger, H., Semjonow, A., Hertle, L., Terpe, H. J., & Bocker, W. (2000). Patterns of chromosomal imbalances in muscle invasive bladder cancer. INT J ONCOL, 17(5), 1025-1029. [5]. http://www.ncbi.nlm.nih.gov/pubmed/11029508?dopt=Citation

Vancouver

Simon R, Burger H, Semjonow A, Hertle L, Terpe HJ, Bocker W. Patterns of chromosomal imbalances in muscle invasive bladder cancer. INT J ONCOL. 2000;17(5):1025-1029. 5.

Bibtex

@article{389e0e4f3a7b4f3e881a41f4e2bfedc0,
title = "Patterns of chromosomal imbalances in muscle invasive bladder cancer.",
abstract = "Cytogenetic investigations of bladder cancer suggested that development and progression is characterized by specific chromosomal aberrations. In order to identify genetic changes linked to muscle invasive tumors and metastatic growth we analyzed 67 bladder carcinomas (30 pT1 and 37 pT2-4) by means of comparative genomic hybridization (CGH). The most frequent changes were gains of chromosome 1q (54%), 8q (54%), 17q (49%), 2p (30%), 12 (30%), 5p (25%), 3q (24%) and 6p (24%) as well as losses of 11p (43%), 8p (42%), 9p (36%), 11q (34%), 2q, 4q, 5q (30% each), 9q (27%) and 10q (27%). Previously not described amplifications were found at 5p11-p13, 7q21-q31, 9p24 and 17q24-q25. Gains of 3q, 7p, and 18p were markedly more frequent in pT2-4 in comparison to pT1 carcinomas but the difference did not reach statistical significance. Non-metastatic tumors showed more aberrations on average than metastatic carcinomas, although no particular change was found to be predominating in either group. Our data confirm previous findings of strong genetic similarities between minimally and deeply invasive bladder carcinomas but argue for differences between metastatic and non-metastatic disease.",
author = "Ronald Simon and H Burger and A Semjonow and L Hertle and Terpe, {H J} and W Bocker",
year = "2000",
language = "Deutsch",
volume = "17",
pages = "1025--1029",
journal = "INT J ONCOL",
issn = "1019-6439",
publisher = "Spandidos Publications",
number = "5",

}

RIS

TY - JOUR

T1 - Patterns of chromosomal imbalances in muscle invasive bladder cancer.

AU - Simon, Ronald

AU - Burger, H

AU - Semjonow, A

AU - Hertle, L

AU - Terpe, H J

AU - Bocker, W

PY - 2000

Y1 - 2000

N2 - Cytogenetic investigations of bladder cancer suggested that development and progression is characterized by specific chromosomal aberrations. In order to identify genetic changes linked to muscle invasive tumors and metastatic growth we analyzed 67 bladder carcinomas (30 pT1 and 37 pT2-4) by means of comparative genomic hybridization (CGH). The most frequent changes were gains of chromosome 1q (54%), 8q (54%), 17q (49%), 2p (30%), 12 (30%), 5p (25%), 3q (24%) and 6p (24%) as well as losses of 11p (43%), 8p (42%), 9p (36%), 11q (34%), 2q, 4q, 5q (30% each), 9q (27%) and 10q (27%). Previously not described amplifications were found at 5p11-p13, 7q21-q31, 9p24 and 17q24-q25. Gains of 3q, 7p, and 18p were markedly more frequent in pT2-4 in comparison to pT1 carcinomas but the difference did not reach statistical significance. Non-metastatic tumors showed more aberrations on average than metastatic carcinomas, although no particular change was found to be predominating in either group. Our data confirm previous findings of strong genetic similarities between minimally and deeply invasive bladder carcinomas but argue for differences between metastatic and non-metastatic disease.

AB - Cytogenetic investigations of bladder cancer suggested that development and progression is characterized by specific chromosomal aberrations. In order to identify genetic changes linked to muscle invasive tumors and metastatic growth we analyzed 67 bladder carcinomas (30 pT1 and 37 pT2-4) by means of comparative genomic hybridization (CGH). The most frequent changes were gains of chromosome 1q (54%), 8q (54%), 17q (49%), 2p (30%), 12 (30%), 5p (25%), 3q (24%) and 6p (24%) as well as losses of 11p (43%), 8p (42%), 9p (36%), 11q (34%), 2q, 4q, 5q (30% each), 9q (27%) and 10q (27%). Previously not described amplifications were found at 5p11-p13, 7q21-q31, 9p24 and 17q24-q25. Gains of 3q, 7p, and 18p were markedly more frequent in pT2-4 in comparison to pT1 carcinomas but the difference did not reach statistical significance. Non-metastatic tumors showed more aberrations on average than metastatic carcinomas, although no particular change was found to be predominating in either group. Our data confirm previous findings of strong genetic similarities between minimally and deeply invasive bladder carcinomas but argue for differences between metastatic and non-metastatic disease.

M3 - SCORING: Zeitschriftenaufsatz

VL - 17

SP - 1025

EP - 1029

JO - INT J ONCOL

JF - INT J ONCOL

SN - 1019-6439

IS - 5

M1 - 5

ER -