Laminin α2 chain (merosin M chain) distribution and VEGF, FGF2, and TGFβ1 gene expression in angiogenesis of supraglottic, lung, and breast carcinomas

The prognostic significance of vessel quantification in human solid tumours is still debated, due to the presence of multiple factors modulating neoangiogenesis and the invasiveness of neoplastic cells. This study examined ten supraglottic squamous carcinomas, ten non‐small cell lung carcinomas (three squamous, five bronchioloalveolar, two adenocarcinomas), and nine classic (NOS) invasive ductal breast carcinomas. The properties studied in these tumours were vascularity; the immunohistochemical distribution of adhesion molecules such as α2β1, α3β1, α4β1, α5β1, α6β4, and ICAM‐1 in endothelial cells; extracellular matrix proteins (ECMPs) and laminin α2 chain (merosin M chain) in basal membranes of vessels; and gene expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF2), and transforming growth factor β1 (TGFβ1), by in situ hybridization. Independently of tumour type and vascularity, laminin α2 chain expression was observed in the basal membranes of a limited proportion of vessels. In vitro experiments demonstrated laminin α2 chain expression mainly in early endothelial cell cultures, suggesting that laminin α2 chain expression in vivo can be considered a marker of early angiogenesis. Stromal and parenchymal vascularity was associated with laminin α2 chain expression in supraglottic carcinomas, whereas in the other tumours, laminin α2 chain‐positive vessels were observed only in the stroma. In supraglottic carcinomas, VEGF‐positive cells were mainly represented by neoplastic cells, whereas in the other tumours, the great majority of VEGF‐positive cells were macrophages and fibroblasts. FGF2‐ and TGFβ1‐positive cells were macrophages and fibroblasts in all tumours. These observations suggest that in addition to the quantification and distribution of vessels, evaluation of their maturation may contribute to a better understanding of the role of angiogenesis in the growth and spread potential of solid tumours. In this regard, in supraglottic carcinomas, parenchymal angiogenesis seems to be regulated mainly by neoplastic cells, which may help to explain their high metastatic potential; in solid tumours of different histogenesis, different cells might be responsible for modulating tumour angiogenesis. Copyright © 2001 John Wiley & Sons, Ltd.