Aims: To determine whether basal-like phenotype and vimentin and/or laminin are related in both sporadic/familial (BRCA1 or BRCA2 mutated) tumours.
Methods: 230 non-familial and 28 hereditary node-negative invasive breast carcinomas were immunohistochemically analysed for oestrogen receptors (ER), progesterone receptors (PR), cytokeratin 5/6 (CK5/6), epidermal growth factor receptors (EGFR), Ki67, p53, vimentin and laminin, using tissue microarrays. Tumours were considered to have basal-like phenotype if they were ER negative and HER2 negative, but positive for CK5/6 and/or EGFR.
Results: In sporadic tumours, vimentin expression was found in 77.8% cases with basal-like phenotype and 15.5% of non-basal cases (p<0.001). In familial cases, vimentin was expressed in 83.3% basal-like cancers and 16.7% of non-basal tumours (p<0.001). Vimentin expression was more frequent in BRCA1 than BRCA2 mutation carriers. Vimentin expressing tumours were associated with poor prognosis (p = 0.012) among patients not receiving adjuvant chemotherapy and showed a trend for local recurrence or visceral but not bone metastasis (p = 0.021). Laminin expression was also related to basal-like phenotype in both sporadic/familial cases (p<0.001 and p = 0.007, respectively), but neither with prognosis nor recurrence pattern in sporadic cancers.
Conclusions: Vimentin and laminin expression is associated with basal-like phenotype in breast cancer. Expression of vimentin and laminin is characteristic of BRCA1 associated tumours. Since vimentin and laminin staining is widely used by pathologists for diagnostic purposes, thus demonstrating the robustness of their specific antibodies, the immunohistochemical evaluation of these two molecules could be used in identification of basal-like breast tumours in both sporadic/familial cases.
- EGFR, epidermal growth factor receptor
- ER, oestrogen receptor
- PR, progesterone receptor
- basal-like phenotype
- node-negative breast carcinomas
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Published Online First 14 November 2006
Funding: This study was supported by the Spanish Ministry of Education and Science (SAF2004-08258-C02-01) and the Instituto de Salud Carlos III (PI051890). Socorro María Rodríguez-Pinilla is the recipient of a research grant from the Fondo de Investigación Sanitaria, Spain. Emiliano Honrado is funded by the Foundation of the Spanish Association against Cancer (AECC). Gema Moreno Bueno is a junior investigator of the Ramón y Cajal Programme (2004).
Competing interests: None declared.