Breast Cancer Research

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Basal cytokeratins in breast tumours among BRCA1, BRCA2 and mutation-negative breast cancer families

Hannaleena Eerola1,2*, Mira Heinonen3,4, Päivi Heikkilä5, Outi Kilpivaara2, Anitta Tamminen2, Kristiina Aittomäki6, Carl Blomqvist1, Ari Ristimäki3,4 and Heli Nevanlinna2

Author Affiliations

1 Department of Oncology, Helsinki University Central Hospital, Haartmaninkatu, 00029 HUS, Helsinki Finland

2 Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Haartmaninkatu, 00029 HUS, Helsinki, Finland

3 Department of Pathology/HUSLAB and Haartman Institute, Helsinki University Central Hospital, Haartmaninkatu,00029 HUS, Helsinki, Finland

4 Genome-Scale Biology Program, Biomedicum Helsinki, University of Helsinki, Haartmaninkatu, 00014 Helsinki, Finland

5 Department of Pathology, Helsinki University Central Hospital, Haartmaninkatu,00029 HUS, Helsinki, Finland

6 Department of Clinical Genetics, Helsinki University Central Hospital, Haartmaninkatu,00029 HUS, Helsinki, Finland

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Breast Cancer Research 2008, 10:R17 doi:10.1186/bcr1863

Published: 14 February 2008

Abstract

Introduction

Finding new immunohistochemical markers that are specific to hereditary breast cancer could help us to select candidates for BRCA1/BRCA2 mutation testing and to understand the biological pathways of tumour development.

Methods

Using breast cancer tumour microarrays, immunohistochemical expression of cytokeratin (CK)-5/6, CK-14 and CK-17 was evaluated in breast tumours from BRCA1 families (n = 46), BRCA2 families (n = 40), non-BRCA1/BRCA2 families (n = 358) and familial breast cancer patients with one first-degree relative affected by breast or ovarian cancer (n = 270), as well as from patients with sporadic breast cancer (n = 364). Staining for CK-5/6, CK-14 and CK-17 was compared between these groups and correlated with other clinical and histological factors.

Results

CK-5/6, CK-14 and CK-17 were detected mostly among oestrogen receptor (ER)-negative, progesterone receptor (PR)-negative and high-grade tumours. We found the highest percentages of samples positive for these CKs among ER-negative/HER2-negative tumours. In univariate analysis, CK-14 was significantly associated with tumours from BRCA1 (39%; P < 0.0005), BRCA2 (27%; P = 0.011), and non-BRCA1/BRCA2 (21%; P < 0.005) families, as compared with sporadic tumours (10%). However, in multivariate analysis, CKs were not found to be independently associated with BRCA1 or BRCA2 mutation status, and the most effective predictors of BRCA1 mutations were age at onset, HER2 status, and either ER or PR status.

Conclusion

Although our study confirms that basal CKs can help to identify BRCA1 mutation carriers, this effect was weaker than previously suggested and CKs did not independently predict BRCA1 mutation either from sporadic or familial breast cancer cases. The most effective, independent predictors of BRCA1 mutations were age at onset, HER2 status, and either ER or PR status, as compared with sporadic or non-BRCA1/BRCA2 cancers.