[p53 in urogenital tumors:analysis of expression and mutation]

Standard

[p53 in urogenital tumors:analysis of expression and mutation]. / Löning, Thomas; Schlechte, H; Friedrichs, K; Schnoor, D; Ditscherlein, G; Bommer, G; Löning, S.

In: Verh Dtsch Ges Pathol, Vol. 77, 1993, p. 117-118.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Löning, T, Schlechte, H, Friedrichs, K, Schnoor, D, Ditscherlein, G, Bommer, G & Löning, S 1993, '[p53 in urogenital tumors:analysis of expression and mutation]', Verh Dtsch Ges Pathol, vol. 77, pp. 117-118. <http://www.ncbi.nlm.nih.gov/pubmed/7511267?dopt=Citation>

APA

Löning, T., Schlechte, H., Friedrichs, K., Schnoor, D., Ditscherlein, G., Bommer, G., & Löning, S. (1993). [p53 in urogenital tumors:analysis of expression and mutation]. Verh Dtsch Ges Pathol, 77, 117-118. http://www.ncbi.nlm.nih.gov/pubmed/7511267?dopt=Citation

Vancouver

Löning T, Schlechte H, Friedrichs K, Schnoor D, Ditscherlein G, Bommer G et al. [p53 in urogenital tumors:analysis of expression and mutation]. Verh Dtsch Ges Pathol. 1993;77:117-118.

Bibtex

@article{61f7f1f338674feb8e57934f3f24103c,
title = "[p53 in urogenital tumors:analysis of expression and mutation]",
abstract = "DNA and paraffin material of more than 100 tumors of prostate, bladder and female genital organs were analyzed for p53 aberrations and compared with normal tissues by immunohistochemistry, PCR of p53 exons 5-8 and TGGE. While normal tissues, precancerous and borderline lesions, and well differentiated carcinomas usually showed wild type p53 and negative immunostaining, high grade and/or high stage carcinomas often revealed mutant p53 (rate of mutation in exon 8 >> 7 >> 6 >> 5) and/or p53 accumulation. Accumulation of p53 protein in the absence of detectable mutant p53 was recognized more often in prostate cancer than in any other tumor examined. Although p53 aberration probably represents a late molecular event in cancerogenesis, its detection may be of clinical interest as genetic footprint in recurrent and metastatic disease.",
author = "Thomas L{\"o}ning and H Schlechte and K Friedrichs and D Schnoor and G Ditscherlein and G Bommer and S L{\"o}ning",
year = "1993",
language = "Deutsch",
volume = "77",
pages = "117--118",

}

RIS

TY - JOUR

T1 - [p53 in urogenital tumors:analysis of expression and mutation]

AU - Löning, Thomas

AU - Schlechte, H

AU - Friedrichs, K

AU - Schnoor, D

AU - Ditscherlein, G

AU - Bommer, G

AU - Löning, S

PY - 1993

Y1 - 1993

N2 - DNA and paraffin material of more than 100 tumors of prostate, bladder and female genital organs were analyzed for p53 aberrations and compared with normal tissues by immunohistochemistry, PCR of p53 exons 5-8 and TGGE. While normal tissues, precancerous and borderline lesions, and well differentiated carcinomas usually showed wild type p53 and negative immunostaining, high grade and/or high stage carcinomas often revealed mutant p53 (rate of mutation in exon 8 >> 7 >> 6 >> 5) and/or p53 accumulation. Accumulation of p53 protein in the absence of detectable mutant p53 was recognized more often in prostate cancer than in any other tumor examined. Although p53 aberration probably represents a late molecular event in cancerogenesis, its detection may be of clinical interest as genetic footprint in recurrent and metastatic disease.

AB - DNA and paraffin material of more than 100 tumors of prostate, bladder and female genital organs were analyzed for p53 aberrations and compared with normal tissues by immunohistochemistry, PCR of p53 exons 5-8 and TGGE. While normal tissues, precancerous and borderline lesions, and well differentiated carcinomas usually showed wild type p53 and negative immunostaining, high grade and/or high stage carcinomas often revealed mutant p53 (rate of mutation in exon 8 >> 7 >> 6 >> 5) and/or p53 accumulation. Accumulation of p53 protein in the absence of detectable mutant p53 was recognized more often in prostate cancer than in any other tumor examined. Although p53 aberration probably represents a late molecular event in cancerogenesis, its detection may be of clinical interest as genetic footprint in recurrent and metastatic disease.

M3 - SCORING: Zeitschriftenaufsatz

VL - 77

SP - 117

EP - 118

ER -