PTEN expression in breast and endometrial cancer: correlations with steroid hormone receptor status.

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PTEN expression in breast and endometrial cancer: correlations with steroid hormone receptor status. / Kappes, H; Goemann, Christoph; Bamberger, A M; Löning, Thomas; Milde-Langosch, K.

In: PATHOBIOLOGY, Vol. 69, No. 3, 3, 2001, p. 136-142.

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

Harvard

Kappes, H, Goemann, C, Bamberger, AM, Löning, T & Milde-Langosch, K 2001, 'PTEN expression in breast and endometrial cancer: correlations with steroid hormone receptor status.', PATHOBIOLOGY, vol. 69, no. 3, 3, pp. 136-142. <http://www.ncbi.nlm.nih.gov/pubmed/11872959?dopt=Citation>

APA

Vancouver

Kappes H, Goemann C, Bamberger AM, Löning T, Milde-Langosch K. PTEN expression in breast and endometrial cancer: correlations with steroid hormone receptor status. PATHOBIOLOGY. 2001;69(3):136-142. 3.

Bibtex

@article{0998db861ac64bfe8e10e9d83d604adf,
title = "PTEN expression in breast and endometrial cancer: correlations with steroid hormone receptor status.",
abstract = "OBJECTIVE: The PTEN (MMAC1/TEP1) tumor suppressor gene is frequently mutated and homozygously deleted in human neoplasms, but there is only sparse information about PTEN protein expression in hormone-dependent female tumors. Therefore, we investigated PTEN expression in 68 breast and 43 endometrial carcinomas. METHODS: For PTEN protein detection, we used Western blot analysis followed by densitometry and compared these data with clinicopathologic parameters, the estrogen receptor (ER) and progesterone receptor (PR) status, HER2/neu and the proliferation marker Ki67. RESULTS: We were able to show significantly decreased PTEN protein expression in endometrial carcinomas compared with normal endometrial tissue samples, especially in the endometrioid histological subtype. In contrast, PTEN downregulation was found more rarely in breast cancer. Lower PTEN expression in breast cancer correlated significantly with high ER immunoreactivity (p = 0.008) and was weakly associated with PR expression (p = 0.055) and low histological grading (p = 0.081). No correlation with any of these parameters was observed in endometrial tumors. In both tumor types, no association of PTEN expression with any other analyzed parameter was found. CONCLUSIONS: These results suggest that PTEN expression plays different roles in the pathogenesis of endometrial carcinomas and breast cancer. In mammary carcinomas, loss of PTEN expression is mainly found in more differentiated tumors and is probably not a major event in carcinogenesis.",
author = "H Kappes and Christoph Goemann and Bamberger, {A M} and Thomas L{\"o}ning and K Milde-Langosch",
year = "2001",
language = "Deutsch",
volume = "69",
pages = "136--142",
journal = "PATHOBIOLOGY",
issn = "1015-2008",
publisher = "S. Karger AG",
number = "3",

}

RIS

TY - JOUR

T1 - PTEN expression in breast and endometrial cancer: correlations with steroid hormone receptor status.

AU - Kappes, H

AU - Goemann, Christoph

AU - Bamberger, A M

AU - Löning, Thomas

AU - Milde-Langosch, K

PY - 2001

Y1 - 2001

N2 - OBJECTIVE: The PTEN (MMAC1/TEP1) tumor suppressor gene is frequently mutated and homozygously deleted in human neoplasms, but there is only sparse information about PTEN protein expression in hormone-dependent female tumors. Therefore, we investigated PTEN expression in 68 breast and 43 endometrial carcinomas. METHODS: For PTEN protein detection, we used Western blot analysis followed by densitometry and compared these data with clinicopathologic parameters, the estrogen receptor (ER) and progesterone receptor (PR) status, HER2/neu and the proliferation marker Ki67. RESULTS: We were able to show significantly decreased PTEN protein expression in endometrial carcinomas compared with normal endometrial tissue samples, especially in the endometrioid histological subtype. In contrast, PTEN downregulation was found more rarely in breast cancer. Lower PTEN expression in breast cancer correlated significantly with high ER immunoreactivity (p = 0.008) and was weakly associated with PR expression (p = 0.055) and low histological grading (p = 0.081). No correlation with any of these parameters was observed in endometrial tumors. In both tumor types, no association of PTEN expression with any other analyzed parameter was found. CONCLUSIONS: These results suggest that PTEN expression plays different roles in the pathogenesis of endometrial carcinomas and breast cancer. In mammary carcinomas, loss of PTEN expression is mainly found in more differentiated tumors and is probably not a major event in carcinogenesis.

AB - OBJECTIVE: The PTEN (MMAC1/TEP1) tumor suppressor gene is frequently mutated and homozygously deleted in human neoplasms, but there is only sparse information about PTEN protein expression in hormone-dependent female tumors. Therefore, we investigated PTEN expression in 68 breast and 43 endometrial carcinomas. METHODS: For PTEN protein detection, we used Western blot analysis followed by densitometry and compared these data with clinicopathologic parameters, the estrogen receptor (ER) and progesterone receptor (PR) status, HER2/neu and the proliferation marker Ki67. RESULTS: We were able to show significantly decreased PTEN protein expression in endometrial carcinomas compared with normal endometrial tissue samples, especially in the endometrioid histological subtype. In contrast, PTEN downregulation was found more rarely in breast cancer. Lower PTEN expression in breast cancer correlated significantly with high ER immunoreactivity (p = 0.008) and was weakly associated with PR expression (p = 0.055) and low histological grading (p = 0.081). No correlation with any of these parameters was observed in endometrial tumors. In both tumor types, no association of PTEN expression with any other analyzed parameter was found. CONCLUSIONS: These results suggest that PTEN expression plays different roles in the pathogenesis of endometrial carcinomas and breast cancer. In mammary carcinomas, loss of PTEN expression is mainly found in more differentiated tumors and is probably not a major event in carcinogenesis.

M3 - SCORING: Zeitschriftenaufsatz

VL - 69

SP - 136

EP - 142

JO - PATHOBIOLOGY

JF - PATHOBIOLOGY

SN - 1015-2008

IS - 3

M1 - 3

ER -