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Low expression of β 1 , α 2 and α 3 subunits of VLA integrins in malignant mammary tumours
Author(s) -
Pignatelli Massimo,
Hanby Andrew M.,
Stamp Gordon W. H.
Publication year - 1991
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711650106
Subject(s) - myoepithelial cell , biology , immunoperoxidase , pathology , extracellular matrix , cancer research , immunohistochemistry , epithelium , cytokeratin , tenascin , integrin , cell , fibronectin , monoclonal antibody , antibody , medicine , microbiology and biotechnology , immunology , genetics
The Very Late Antigens (VLAs) are αβ heterodimeric transmembrane proteins mediating cell–substratum as well as cell–cell interactions. Changes in their expression and/or function seem to occur in a number of invasive carcinomas and may at least in part explain their abnormal patterns of growth and differentiation. Using monoclonal antibodies to the β 1 (DH12, A1A‐5), α 2 (B1.515) and α 3 (E1.56) chains, VLA‐2 (α 2 β 1 ) and VLA‐3 (α 3 β 1 ) were studied on cryostat sections of three fibroadenomas and 43 invasive breast carcinomas (29 ductal, 14 lobular) by the avidin–biotin complex immunoperioxidase technique. In non‐neoplastic breast tissue and in fibroadenomas VLA‐2 and VLA‐3 were expressed by myoepithelial cells and on the basolateral surface of the luminal cells. There was weak or absent expression of α 2 , α 3 and the common β 1 chain in the majority of invasive carcinomas compared to the adjacent normal breast epithelium and preinvasive ( in‐situ ) carcinomas. In addition, the expression of the α 2 chain of VLA‐2 was reduced significantly ( P < 0.005) in the poorly differentiated ductal breast carcinomas (Grade III) compared to the well (Grade I) and moderately (Grade II) differentiated ductal tumours. These data give further evidence that loss or down‐regulation of VLA‐2 and VLA‐3 occur relatively frequently in invasive cancers, and, at least in the invasive ductal breast carcinomas. Loss of an extracellular matrix receptor controlling growth and differentiation seems to be one of the abnormalities underlying the progression towards an undifferentiated morphology.