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Expression of Rb2/p130 in breast and endometrial cancer: correlations with hormone receptor status

Rb2/p130 is a member of the retinoblastoma family of proteins, consisting of Rb, Rb2 and p107, which are important negative regulators of cell cycle progression and differentiation. While Rb2 downregulation was observed in several malignant tumours including endometrial cancer, the role of p130 in b...

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Autores principales: Milde-Langosch, K, Goemann, C, Methner, C, Rieck, G, Bamberger, A-M, Löning, T
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2001
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364100/
https://www.ncbi.nlm.nih.gov/pubmed/11506494
http://dx.doi.org/10.1054/bjoc.2001.1923
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author Milde-Langosch, K
Goemann, C
Methner, C
Rieck, G
Bamberger, A-M
Löning, T
author_facet Milde-Langosch, K
Goemann, C
Methner, C
Rieck, G
Bamberger, A-M
Löning, T
author_sort Milde-Langosch, K
collection PubMed
description Rb2/p130 is a member of the retinoblastoma family of proteins, consisting of Rb, Rb2 and p107, which are important negative regulators of cell cycle progression and differentiation. While Rb2 downregulation was observed in several malignant tumours including endometrial cancer, the role of p130 in breast carcinomas is still unknown. We investigated Rb2 protein expression in tumour tissue from 68 mammary and 41 endometrial carcinomas, 4 mammary cell lines, and normal tissue samples. Therefore, we performed Western blot experiments for Rb2, Rb, and the oestrogen and progesterone receptors (ER, PR-A, PR-B). Weak or absent Rb2 expression was more often found in endometrial (59%) than in mammary carcinomas (24%). We found significant positive correlations of Rb2 expression with Rb, ER, and PR-B in breast cancer samples, and of Rb2 with Rb, PR-A, PR-B, and younger age in endometrial carcinomas. No significant associations with histological grading, stage, nodal involvement, or Ki67 staining were detected. Rb2 mRNA expression was studied by semi-quantitative RT-PCR in 56 endometrial or mammary tissue samples and correlated significantly with Western blot results. Our results indicate that loss of Rb2 expression, mostly by transcriptional down-regulation, may be associated with the development and dedifferentiation of most endometrial and a subset of mammary carcinomas. © 2001 Cancer Research Campaign http://bjcancer.com
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spelling pubmed-23641002009-09-10 Expression of Rb2/p130 in breast and endometrial cancer: correlations with hormone receptor status Milde-Langosch, K Goemann, C Methner, C Rieck, G Bamberger, A-M Löning, T Br J Cancer Regular Article Rb2/p130 is a member of the retinoblastoma family of proteins, consisting of Rb, Rb2 and p107, which are important negative regulators of cell cycle progression and differentiation. While Rb2 downregulation was observed in several malignant tumours including endometrial cancer, the role of p130 in breast carcinomas is still unknown. We investigated Rb2 protein expression in tumour tissue from 68 mammary and 41 endometrial carcinomas, 4 mammary cell lines, and normal tissue samples. Therefore, we performed Western blot experiments for Rb2, Rb, and the oestrogen and progesterone receptors (ER, PR-A, PR-B). Weak or absent Rb2 expression was more often found in endometrial (59%) than in mammary carcinomas (24%). We found significant positive correlations of Rb2 expression with Rb, ER, and PR-B in breast cancer samples, and of Rb2 with Rb, PR-A, PR-B, and younger age in endometrial carcinomas. No significant associations with histological grading, stage, nodal involvement, or Ki67 staining were detected. Rb2 mRNA expression was studied by semi-quantitative RT-PCR in 56 endometrial or mammary tissue samples and correlated significantly with Western blot results. Our results indicate that loss of Rb2 expression, mostly by transcriptional down-regulation, may be associated with the development and dedifferentiation of most endometrial and a subset of mammary carcinomas. © 2001 Cancer Research Campaign http://bjcancer.com Nature Publishing Group 2001-08 /pmc/articles/PMC2364100/ /pubmed/11506494 http://dx.doi.org/10.1054/bjoc.2001.1923 Text en Copyright © 2001 Cancer Research Campaign https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Regular Article
Milde-Langosch, K
Goemann, C
Methner, C
Rieck, G
Bamberger, A-M
Löning, T
Expression of Rb2/p130 in breast and endometrial cancer: correlations with hormone receptor status
title Expression of Rb2/p130 in breast and endometrial cancer: correlations with hormone receptor status
title_full Expression of Rb2/p130 in breast and endometrial cancer: correlations with hormone receptor status
title_fullStr Expression of Rb2/p130 in breast and endometrial cancer: correlations with hormone receptor status
title_full_unstemmed Expression of Rb2/p130 in breast and endometrial cancer: correlations with hormone receptor status
title_short Expression of Rb2/p130 in breast and endometrial cancer: correlations with hormone receptor status
title_sort expression of rb2/p130 in breast and endometrial cancer: correlations with hormone receptor status
topic Regular Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364100/
https://www.ncbi.nlm.nih.gov/pubmed/11506494
http://dx.doi.org/10.1054/bjoc.2001.1923
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