Cancer arises from the progressive accumulation of genetic lesions that are somatically acquired or, in certain instances, present in the genuline. Two major categories of genes including proto-oncogenes and suppressor genes, are affected. They can be distinguished according to positive or negative regulatory properties exerted on cell growth by their corresponding gene products. Genetic changes converting proto-oncogenes to oncogenes result in constitutive gain of function of the gene product and consequently exert a dominant effect on phenotype. Mutations resulting in loss of function of suppressor genes determine phenotype usually in a recessive manner but can sometimes gain dominant properties. Proto-oncogene activation and inactivation of suppressor gene function both contribute to the lack of growth control and unrestrained proliferation characteristic of tumor cells [1, 2]. Direct corroboration of the genetic basis of cancer originated from observations emerging from studies of acute transforming retroviruses, which led to the identification of oncogenes. The normal counterparts of oncogenes comprise a limited number of evolutionarily conserved molecules (ie, proto-oncogenes) that are frequently activated as cellular oncogenes (c-onc) independent of retroviruses in spontaneous human cancer. Proto-oncogenes encode proteins residing at decisive checkpoints within a complex cellular signaling network controlling growth and proliferation. Under physiologic conditions, they integrate growth programs of a cell in response to extracellular signals and thereby exert control on the homeostasis of metazoan organisms. Subversion of their physiologic control function by activation to cellular oncogenes represents an intricate component in the pathogenesis of cancer .
KeywordsEpidermal Growth Factor Receptor Gene Rearrangement Epidermal Growth Factor Receptor Gene Familial Medullary Thyroid Carcinoma Cellular Oncogene
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