Abstract
The boundary between promotion and progression in experimental carcinogenesis can be operationally defined as long as stable intermediate stages of tumor formation can be identified. Once operational definitions have been made, investigators can and should pursue questions of molecular mechanisms to explain phenotypic changes that occur during promotion and progression. This paper deals with the identification and characterization of molecular markers (i.e., differentially expressed cellular genes) that identify different stages of mouse skin tumor formation. These marker genes whose steady state levels of messenger are elevated at specific stages in skin tumor formation can serve to define the stages of promotion and progression. There is also the possibility that overexpression of one or a number of these genes actually plays a functional role in tumor formation.
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