Studies have continued on the role of derangements in tropomyosin (TM) expression and utilization in neoplastic transformation. Neoplastic transformation secondary to expression of retroviral oncogenes is correlated with the production of TM-deficient, structurally defective, microfilaments in both fibroblasts and epithelial cells. This may be a basic structural and functional lesion which is conducive to expression of components of the transformed phenotype. The derangement results either from suppression of synthesis and utilization of TM (fibroblasts), or from relative over-expression of actin (epithelial cells). TM suppression in fibroblasts transformed by retroviral oncogenes may be due to the action of alpha-transforming growth factor produced as a consequence of oncogene expression. TM expression was also studied in a panel of established human breast cancer lines. Consistent abnormalities in tropomyosin expression were observed in the tumor cell lines, suggesting that derangement of TM supression may be a frequent event in human mammary neoplasia.
