Abstract
Recent advances in molecular biology have enabled oncologic researchers to probe the mechanisms of neoplasm at the level of individual gene expression. Current studies of oncogenesis suggest that specific genes may induce cancer and that normal resident genes, termed proto-oncogenes, required for cellular function can be converted to oncogenes by genetic mutation [1]. Alterations in the structure or expression of certain proto-oncogenes appear to occur through a variety of mechanisms, including point mutations within the gene, rearrangements within the coding sequence of the gene or within a noncoding but functionally effective segment, amplification or overexpression of the gene, and deletion of possible ‘antioncogenes.’ Each of these mechanisms may result in the activation of cellular proto-oncogenes and are found to be associated experimentally with human cancer [2]. While it has not been proven that these genetic anomalies are directly responsible for tumorigenesis, the frequency of their presence and/or expression in some oncologic diseases suggests a biologic importance in the transformation and growth of neoplastic cells [3, 4].
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