Calpain system protein expression in basal-like and triple-negative invasive breast cancer

Background: Basal-like and triple-negative breast tumours encompass an important clinical subgroup and biomarkers that can prognostically stratify these patients are required. Materials and methods: We investigated two breast cancer tissue microarrays for the expression of calpain-1, calpain-2 an...

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Main Authors: Storr, Sarah J., Lee, K.W., Woolston, Caroline M., Safuan, Sabreena, Green, A.R., Macmillan, R.D., Benhasouna, A., Parr, T., Ellis, I.O., Martin, Stewart G.
Format: Article
Published: Oxford University Press 2012
Online Access:https://eprints.nottingham.ac.uk/2787/
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author Storr, Sarah J.
Lee, K.W.
Woolston, Caroline M.
Safuan, Sabreena
Green, A.R.
Macmillan, R.D.
Benhasouna, A.
Parr, T.
Ellis, I.O.
Martin, Stewart G.
author_facet Storr, Sarah J.
Lee, K.W.
Woolston, Caroline M.
Safuan, Sabreena
Green, A.R.
Macmillan, R.D.
Benhasouna, A.
Parr, T.
Ellis, I.O.
Martin, Stewart G.
author_sort Storr, Sarah J.
building Nottingham Research Data Repository
collection Online Access
description Background: Basal-like and triple-negative breast tumours encompass an important clinical subgroup and biomarkers that can prognostically stratify these patients are required. Materials and methods: We investigated two breast cancer tissue microarrays for the expression of calpain-1, calpain-2 and calpastatin using immunohistochemistry. The first microarray was comprised of invasive tumours from 1371 unselected patients, and the verification microarray was comprised of invasive tumours from 387 oestrogen receptor (ER)-negative patients. Results: The calpain system contains a number of proteases and an endogenous inhibitor, calpastatin. Calpain activity is implicated in important cellular processes including cytoskeletal remodelling, apoptosis and survival. Our results show that the expression of calpastatin and calpain-1 are significantly associated with various clinicopathological criteria including tumour grade and ER expression. High expression of calpain-2 in basal-like or triple-negative disease was associated with adverse breast cancer-specific survival (P = 0.003 and <0.001, respectively) and was verified in an independent cohort of patients. Interestingly, those patients with basal-like or triple-negative disease with a low level of calpain-2 expression had similar breast cancer-specific survival to non-basal- or receptor- (oestrogen, progesterone or human epidermal growth factor receptor 2 (HER2)) positive disease. Conclusions: Expression of the large catalytic subunit of m-calpain (calpain-2) is significantly associated with clinical outcome of patients with triple-negative and basal-like disease.
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spelling nottingham-27872024-08-15T15:13:51Z https://eprints.nottingham.ac.uk/2787/ Calpain system protein expression in basal-like and triple-negative invasive breast cancer Storr, Sarah J. Lee, K.W. Woolston, Caroline M. Safuan, Sabreena Green, A.R. Macmillan, R.D. Benhasouna, A. Parr, T. Ellis, I.O. Martin, Stewart G. Background: Basal-like and triple-negative breast tumours encompass an important clinical subgroup and biomarkers that can prognostically stratify these patients are required. Materials and methods: We investigated two breast cancer tissue microarrays for the expression of calpain-1, calpain-2 and calpastatin using immunohistochemistry. The first microarray was comprised of invasive tumours from 1371 unselected patients, and the verification microarray was comprised of invasive tumours from 387 oestrogen receptor (ER)-negative patients. Results: The calpain system contains a number of proteases and an endogenous inhibitor, calpastatin. Calpain activity is implicated in important cellular processes including cytoskeletal remodelling, apoptosis and survival. Our results show that the expression of calpastatin and calpain-1 are significantly associated with various clinicopathological criteria including tumour grade and ER expression. High expression of calpain-2 in basal-like or triple-negative disease was associated with adverse breast cancer-specific survival (P = 0.003 and <0.001, respectively) and was verified in an independent cohort of patients. Interestingly, those patients with basal-like or triple-negative disease with a low level of calpain-2 expression had similar breast cancer-specific survival to non-basal- or receptor- (oestrogen, progesterone or human epidermal growth factor receptor 2 (HER2)) positive disease. Conclusions: Expression of the large catalytic subunit of m-calpain (calpain-2) is significantly associated with clinical outcome of patients with triple-negative and basal-like disease. Oxford University Press 2012-09-09 Article PeerReviewed Storr, Sarah J., Lee, K.W., Woolston, Caroline M., Safuan, Sabreena, Green, A.R., Macmillan, R.D., Benhasouna, A., Parr, T., Ellis, I.O. and Martin, Stewart G. (2012) Calpain system protein expression in basal-like and triple-negative invasive breast cancer. Annals of Oncology, 23 (9). pp. 2289-2296. ISSN 0923-7534 http://annonc.oxfordjournals.org/content/23/9/2289.full doi:10.1093/annonc/mds176 doi:10.1093/annonc/mds176
spellingShingle Storr, Sarah J.
Lee, K.W.
Woolston, Caroline M.
Safuan, Sabreena
Green, A.R.
Macmillan, R.D.
Benhasouna, A.
Parr, T.
Ellis, I.O.
Martin, Stewart G.
Calpain system protein expression in basal-like and triple-negative invasive breast cancer
title Calpain system protein expression in basal-like and triple-negative invasive breast cancer
title_full Calpain system protein expression in basal-like and triple-negative invasive breast cancer
title_fullStr Calpain system protein expression in basal-like and triple-negative invasive breast cancer
title_full_unstemmed Calpain system protein expression in basal-like and triple-negative invasive breast cancer
title_short Calpain system protein expression in basal-like and triple-negative invasive breast cancer
title_sort calpain system protein expression in basal-like and triple-negative invasive breast cancer
url https://eprints.nottingham.ac.uk/2787/
https://eprints.nottingham.ac.uk/2787/
https://eprints.nottingham.ac.uk/2787/