MOLECULAR EVENTS IN ONCOGENESIS - SOME MISSING LINKS - A PRELIMINARY HYPOTHESIS

At cellular level, cancer is an uncontrolled growth of cells, while at molecular level it results from the constitutive expression of those genes which promote cell doubling. Two gene families, oncogenes and an ti-oncogenes, have so far been identified to be directly associated wi th cancer. Hypothetically, normal mitotic cells should express cellula r oncogenes while in differentiated cells these genes should remain su ppressed. The reverse is the case of antioncogenes which should be sup pressed in mitotic cells and active in differentiated cells. This sugg ests the presence of a third set of genes regulating the antioncogenes depending on the differentiation stage of the cell. These novel genes could surprisingly connect normal and cancerous cell proliferation as well as directly initiate and maintain cancer. Alteration in a single gene of this family could bring about malignant transformation of a h igher magnitude in comparison to that of a single antioncogene or onco gene due to the multiplicity at each stage. This may also explain how cancer is established even when all the known oncogenes and antioncoge nes are structurally intact.