Oncogenes and suppressor genes: their involvement in colon cancer.
Abnormalities in oncogenes, which are broadly classified into viral and cellular oncogenes, and suppressor genes appear critical for the development of colon cancer. Cellular oncogenes contribute to malignant transformation when they become activated by point mutation, translocation, amplification, or loss of regulator sequences. The properties of the oncoproteins, the proteins encoded by oncogenes which are essential for carcinogenesis, are unclear. Suppressor genes normally suppress the tumorigenic phenotype by keeping the growth of cells in check; it is their inactivation that contributes to malignant transformation. Development of colon cancer appears to take place by stepwise accumulation of multiple genetic alterations during the progression from normal colon to adenoma and carcinoma. Activation of ras, an early event in this sequence, is found in 50% of colon cancers; overexpression of c-myc is found in approximately 80%. Inactivation of suppressor genes, which occurs during later stages, is noted in greater than 70% of tumors. A current model of colonic tumorigenesis is presented.
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Division of Digestive Diseases, New York Hospital--Cornell Medical Center, NY 10021.
D003110:Colonic Neoplasms / Q000235:genetics*; D005786:Gene Expression Regulation / Q000502:physiology; D016147:Genes, Tumor Suppressor / Q000502:physiology*; D016259:Genes, myc; D011905:Genes, ras / Q000502:physiology; D006801:Humans; D009857:Oncogenes / Q000502:physiology*