ABSTRACT
I. INTRODUCTION The mechanism of carcinogenesis has always been a fascinating topic of discussion in cancer biology, although our knowledge of it is still incomplete. Numerous mechanisms have been proposed and are often inspired by new findings in cancer research. In the past century, hypotheses on the etiology of human cancer have shifted many times, from chemical to viral, back to chemical, and in a few cases, chemical and viral. The mechanisms proposed are mutations of cancer genes, activation of oncogenes, inactivation of tumor suppressor genes, enhanced cell proliferation and with various combinations. These processes can occur sequentially or concurrently. The progression of carcinogenesis was initially divided into initiation and promotion and later multistage. The number of stages is difficult to estimate experimentally, but results of cancer epidemiological studies suggested there could be three to seven stages, based on the age-dependent increase of cancer incidence in humans (1). Although carcinogenesis is a multifaceted process, the resultant cancer cells are always genetically altered with multiple mutations and chromosome alternations. Human cancer is thus firmly considered as a “genetic disease” (2).
