Controversies about the genetic model of colorectal tumorigenesis.
According to the genetic model, intestinal tumorigenesis is a result of the ordered in time inactivation of tumor suppressor genes and the activation of oncogenes. A tacit assumption is that both genes involved in the regulation of proliferation and growth factor-inducible genes, although inactivated, would not be changed during that process. The model requires that cancer cell population is homogenous, exists in a deterministic environment, and develops in a teleological manner. Meanwhile, tumorigenesis is rather a combination of both deterministic and stochastic molecular phenomena. Therefore, a novel notion of bifurcating point genes is defined as a generalization of the idea of tumor suppressor genes and oncogenes. Alternative stochastic mechanisms of tumorigenesis are discussed such as a decreased expression of intestinal-specific genes in cancer cells, most likely reflecting adaptation to survival within a heterogeneous, and non-equilibrated cellular population.
Waliszewski
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Department of Urology, University of Oklahoma HSC, Oklahoma City 73104, USA. Przemko-Waliszewski@uokhsc.edu
D015179:Colorectal Neoplasms / Q000209:etiology* / Q000235:genetics*; D006801:Humans; D008957:Models, Genetic