In this paper we present a new multiple-pathway stochastic model of carcinogenesis with potential of predicting individual incidence risks on the basis of biomedical measurements.
Considering this information, we have summarized the latest experimental evidence and relevant literature to provide an up-to-date view of the cellular origin of ICC, which will contribute to establishment of a hierarchical model of carcinogenesis and allow for improvement of the anatomical-based classification of ICC.
The vast majority of tumors were detected in the descending colon, which is typical for this model of carcinogenesis [32].
First, an evolutionary model of carcinogenesis predicts that advanced disease states are more likely to depict heterogeneity [1].
This genetic model of carcinogenesis (referred to here as V theory) is augmented by the elegant description of major cancer features by Weinberg et al which is recognized as a seminal and most comprehensive molecular definition of cancer [3], [6].
More recently, it was reported that podoplanin, a plasma membrane glycoprotein, induces tumor cell migration and invasion without disrupting E-cadherin-mediated cell-cell junction both in vitro and in a transgenic model of carcinogenesis in vivo [12].
The simple multistage model of carcinogenesis is outlined.
In the sequential multistep model of carcinogenesis (Vogelstein), may the order of oncogenic events vary?
Students in this class constructed synthesis maps as visual representations of their model of carcinogenesis.
Recently, a non-linear, chaodynamic model of carcinogenesis has been suggested by others.
Both of these observations can be explained by a multistep/multigene model of carcinogenesis.
