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EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions

EBAG9 has been recently identified as an oestrogen responsive gene in MCF-7 human breast carcinoma cells. EBAG9 is identical to RCAS1, a cancer cell surface antigen possibly involved in immune escape. In this study, we examined the expression of EBAG9/RCAS1 in human breast carcinomas using immunohis...

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Detalles Bibliográficos
Autores principales: Suzuki, T, Inoue, S, Kawabata, W, Akahira, J, Moriya, T, Tsuchiya, F, Ogawa, S, Muramatsu, M, Sasano, H
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2001
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2363964/
https://www.ncbi.nlm.nih.gov/pubmed/11742495
http://dx.doi.org/10.1054/bjoc.2001.2176
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author Suzuki, T
Inoue, S
Kawabata, W
Akahira, J
Moriya, T
Tsuchiya, F
Ogawa, S
Muramatsu, M
Sasano, H
author_facet Suzuki, T
Inoue, S
Kawabata, W
Akahira, J
Moriya, T
Tsuchiya, F
Ogawa, S
Muramatsu, M
Sasano, H
author_sort Suzuki, T
collection PubMed
description EBAG9 has been recently identified as an oestrogen responsive gene in MCF-7 human breast carcinoma cells. EBAG9 is identical to RCAS1, a cancer cell surface antigen possibly involved in immune escape. In this study, we examined the expression of EBAG9/RCAS1 in human breast carcinomas using immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). EBAG9 immunoreactivity was also associated with various clinicopathological parameters, including intratumoural infiltration of inflammatory cells, to examine the biological significance of EBAG9 in human breast carcinomas. EBAG9 immunoreactivity was detected in the entire surface and cytoplasm of carcinoma cells in 82 out of 91 invasive ductal carcinomas (90.1%). In non-neoplastic mammary glands, EBAG9 immunoreactivity was weakly present on the luminal surface of epithelial cells. Results from RT-PCR (n = 7) were consistent with those of immunohistochemistry. EBAG9 immunoreactivity was significantly associated with estrogen receptor (ER) α labelling index (P = 0.0081), and inversely associated with the degree of intratumoural infiltration of mononuclear cells (P = 0.0020), or CD3(+) T lymphocytes (P = 0.0025). This study suggests that EBAG9 is produced via ER in carcinoma cells and inhibits the intratumoural infiltration of T lymphocytes in the context of a possible endocrine–immune interaction in human breast carcinomas. © 2001 Cancer Research Campaign http://www.bjcancer.com
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spelling pubmed-23639642009-09-10 EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions Suzuki, T Inoue, S Kawabata, W Akahira, J Moriya, T Tsuchiya, F Ogawa, S Muramatsu, M Sasano, H Br J Cancer Regular Article EBAG9 has been recently identified as an oestrogen responsive gene in MCF-7 human breast carcinoma cells. EBAG9 is identical to RCAS1, a cancer cell surface antigen possibly involved in immune escape. In this study, we examined the expression of EBAG9/RCAS1 in human breast carcinomas using immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). EBAG9 immunoreactivity was also associated with various clinicopathological parameters, including intratumoural infiltration of inflammatory cells, to examine the biological significance of EBAG9 in human breast carcinomas. EBAG9 immunoreactivity was detected in the entire surface and cytoplasm of carcinoma cells in 82 out of 91 invasive ductal carcinomas (90.1%). In non-neoplastic mammary glands, EBAG9 immunoreactivity was weakly present on the luminal surface of epithelial cells. Results from RT-PCR (n = 7) were consistent with those of immunohistochemistry. EBAG9 immunoreactivity was significantly associated with estrogen receptor (ER) α labelling index (P = 0.0081), and inversely associated with the degree of intratumoural infiltration of mononuclear cells (P = 0.0020), or CD3(+) T lymphocytes (P = 0.0025). This study suggests that EBAG9 is produced via ER in carcinoma cells and inhibits the intratumoural infiltration of T lymphocytes in the context of a possible endocrine–immune interaction in human breast carcinomas. © 2001 Cancer Research Campaign http://www.bjcancer.com Nature Publishing Group 2001-11 /pmc/articles/PMC2363964/ /pubmed/11742495 http://dx.doi.org/10.1054/bjoc.2001.2176 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
Suzuki, T
Inoue, S
Kawabata, W
Akahira, J
Moriya, T
Tsuchiya, F
Ogawa, S
Muramatsu, M
Sasano, H
EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions
title EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions
title_full EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions
title_fullStr EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions
title_full_unstemmed EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions
title_short EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions
title_sort ebag9/rcas1 in human breast carcinoma: a possible factor in endocrine–immune interactions
topic Regular Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2363964/
https://www.ncbi.nlm.nih.gov/pubmed/11742495
http://dx.doi.org/10.1054/bjoc.2001.2176
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