Two-Dimensional Polyacrylamide Gel Electrophoresis of Cancer-Associated Proteins

It is generally accepted that cancer development is a multistage process involving a variety of cell types (Farber and Cameron 1980). Over the last 20 years considerable effort has been made to define the genetic events involved in the etiology of cancer development. Indeed, molecular genetics has been highly successful in the demonstration that development of certain forms of human cancers, in particular, colorectal, lung, and breast, may arise following a series of four to six distinct genetic alterations in specific target tissues (Fearon and Vogelstein 1990). These mutations may involve either the activation of one or more cellular protooncogene(s) and/or inactivation of one or more tumor suppressor gene(s) and are thought to initiate a cascade of biochemical events that culminate in the dysregulation of normal control mechanisms governing cellular growth and differentiation (Weinberg 1989; Hunter 1991). Regardless of the nature of the oncogenic agent, the observed phenotypic effects on the host cells are remarkably similar. These include characteristic alterations in cellular morphology, adhesiveness and motility, and cell-to-cell communication, as well as dysregulation of cellular growth and differentiation, including loss of contact growth inhibition in vitro, acquisition of anchorage-independent growth in soft agar, and tumorigenicity in susceptible animals.