Microsatellite alterations at chromosomes 9p, 13q, and 17p in nonmuscle-invasive transitional cell carcinomas of the urinary bladder.

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Microsatellite alterations at chromosomes 9p, 13q, and 17p in nonmuscle-invasive transitional cell carcinomas of the urinary bladder. / Erbersdobler, A; Friedrich, Martin; Schwaibold, H; Henke, R P; Huland, H.

In: ONCOL RES, Vol. 10, No. 8, 8, 1998, p. 415-420.

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@article{8b7c79f42b194400a8115a30378382d4,
title = "Microsatellite alterations at chromosomes 9p, 13q, and 17p in nonmuscle-invasive transitional cell carcinomas of the urinary bladder.",
abstract = "The clinical behavior of bladder cancer is difficult to predict and prognostic markers applicable to routinely processed tumor specimens clearly are needed. We screened 40 primary Ta and T1 bladder cancers for microsatellite alterations at 9p, 13q, and 17p with PCR, using nine polymorphic microsatellite markers. DNA was prepared after microdissection of paraffin-embedded transurethral resection specimens. PCR products were separated on sequencing gels, and allelic loss as well as band shifts was assessed by comparing alleles of control and tumor tissue. The results were correlated with grade, stage, and clinically documented tumor recurrence. Overall, allelic loss at 9p, 13q, and 17p was present in 35.1%, 25%, and 27.5% of cases, respectively. Whereas the frequency of allelic loss at 9p was nearly equally distributed throughout all tumor grades and stages, the occurrence of allelic loss at 13q and 17p correlated statistically significantly with higher grades and stage. Band shifts were observed in three cases. Of the 40 patients, 16 had tumor recurrence during a follow-up period of 3-49 months (median, 23 months). Kaplan-Meier analysis did not show any statistically significant correlation between allelic loss at either locus and tumor recurrence. The results confirm the role of alterations at 13q and 17p in the progression of bladder cancer. Allelic loss at 9p seems to be an early event in tumor development. However, the detection of alterations at the three chromosomal loci studied did not have any prognostic value regarding tumor recurrence in this group of patients.",
author = "A Erbersdobler and Martin Friedrich and H Schwaibold and Henke, {R P} and H Huland",
year = "1998",
language = "Deutsch",
volume = "10",
pages = "415--420",
journal = "ONCOL RES",
issn = "0965-0407",
publisher = "Cognizant Communication Corporation",
number = "8",

}

RIS

TY - JOUR

T1 - Microsatellite alterations at chromosomes 9p, 13q, and 17p in nonmuscle-invasive transitional cell carcinomas of the urinary bladder.

AU - Erbersdobler, A

AU - Friedrich, Martin

AU - Schwaibold, H

AU - Henke, R P

AU - Huland, H

PY - 1998

Y1 - 1998

N2 - The clinical behavior of bladder cancer is difficult to predict and prognostic markers applicable to routinely processed tumor specimens clearly are needed. We screened 40 primary Ta and T1 bladder cancers for microsatellite alterations at 9p, 13q, and 17p with PCR, using nine polymorphic microsatellite markers. DNA was prepared after microdissection of paraffin-embedded transurethral resection specimens. PCR products were separated on sequencing gels, and allelic loss as well as band shifts was assessed by comparing alleles of control and tumor tissue. The results were correlated with grade, stage, and clinically documented tumor recurrence. Overall, allelic loss at 9p, 13q, and 17p was present in 35.1%, 25%, and 27.5% of cases, respectively. Whereas the frequency of allelic loss at 9p was nearly equally distributed throughout all tumor grades and stages, the occurrence of allelic loss at 13q and 17p correlated statistically significantly with higher grades and stage. Band shifts were observed in three cases. Of the 40 patients, 16 had tumor recurrence during a follow-up period of 3-49 months (median, 23 months). Kaplan-Meier analysis did not show any statistically significant correlation between allelic loss at either locus and tumor recurrence. The results confirm the role of alterations at 13q and 17p in the progression of bladder cancer. Allelic loss at 9p seems to be an early event in tumor development. However, the detection of alterations at the three chromosomal loci studied did not have any prognostic value regarding tumor recurrence in this group of patients.

AB - The clinical behavior of bladder cancer is difficult to predict and prognostic markers applicable to routinely processed tumor specimens clearly are needed. We screened 40 primary Ta and T1 bladder cancers for microsatellite alterations at 9p, 13q, and 17p with PCR, using nine polymorphic microsatellite markers. DNA was prepared after microdissection of paraffin-embedded transurethral resection specimens. PCR products were separated on sequencing gels, and allelic loss as well as band shifts was assessed by comparing alleles of control and tumor tissue. The results were correlated with grade, stage, and clinically documented tumor recurrence. Overall, allelic loss at 9p, 13q, and 17p was present in 35.1%, 25%, and 27.5% of cases, respectively. Whereas the frequency of allelic loss at 9p was nearly equally distributed throughout all tumor grades and stages, the occurrence of allelic loss at 13q and 17p correlated statistically significantly with higher grades and stage. Band shifts were observed in three cases. Of the 40 patients, 16 had tumor recurrence during a follow-up period of 3-49 months (median, 23 months). Kaplan-Meier analysis did not show any statistically significant correlation between allelic loss at either locus and tumor recurrence. The results confirm the role of alterations at 13q and 17p in the progression of bladder cancer. Allelic loss at 9p seems to be an early event in tumor development. However, the detection of alterations at the three chromosomal loci studied did not have any prognostic value regarding tumor recurrence in this group of patients.

M3 - SCORING: Zeitschriftenaufsatz

VL - 10

SP - 415

EP - 420

JO - ONCOL RES

JF - ONCOL RES

SN - 0965-0407

IS - 8

M1 - 8

ER -