Isozyme alterations, gene regulation and the neoplastic transformation
Abstract
Studies of isozyme composition in the rat liver-hepatocellular carcinoma model system have revealed wide-ranging abnormalities of gene expression. Isozymes geared for adult liver function are lost in tumors to varying degrees, depending on growth rate and degree of tumor dedifferentiation; whereas isozymes low or absent in normal adult liver become predominant or sole forms in fast growing, poorly differentiated hepatic tumors. The prevailing pattern is a switch from the adult to fetal forms, thereby indicating that genes coding for adult isozymes are suppressed in liver neoplasms, while genes active in fetal stages but inactivated during normal embryonic development become re-activated in cancer. These isozyme alterations not only are a key to neoplastic behavior, but are a striking example, among many, of pervasive abnormalities of gene expression involving virtually every means of identification of gene products; for example, the expression in tumors of fetal antigens, growth factors, angiogenesis factors, membrane components, and ectopic polypeptide hormones. Most important is the recently discovered activation of normally silent host oncogenes associated with and probably causally related to viral or chemical carcinogenesi...Continue Reading
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Plasminogen activator in early embryogenesis: enzyme production by trophoblast and parietal endoderm
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