Cancer arises from an accumulation of genetic or epigenetic derangements within the cell, accompanied by a progressive loss of growth regulation. Most cancers are extensively aneuploid, and the aneuploidy becomes more severe the later the stage of tumor progression. Tumorigenesis is a multistep process, whereby multiple genetic events govern the initiation, promotion and progression of human (and presumably companion animal) tumors. Each step in multistep carcinogenesis represents a physiologic barrier that must be overcome for a cell to progress further toward the endpoint of malignancy. During this process, the normal cell population undergoes a series of genetic or epigenetic changes giving rise to an altered or transformed cell population with growth advantages over the normal cellular counterparts. For some tumors, these altered cells may be recognized as precancers, e.g., hyperplastic alveolar nodules or ductular dysplasia of the mammary gland, myelodysplasia, carcinoma in situ, colonic adenomas, and others.  

Tumor progression is thought to occur when variant cells that have selective growth characteristics arise within a cell population. For example, some of the genetic events associated with colon cancer have been identified, and there are data to suggest that similar multistep mechanisms are operative in other tumor types including those affecting the lung, breast, urinary bladder and brain. In colon cancer, the prototype model, tumorigenesis proceeds through a series of histologic abnormalities that include the sequential accumulation of genetic aberrations, leading to uncontrolled proliferative capacity (induction of immortality), oncogene activation, and inactivation of tumor suppressor genes. Each of these discrete steps must accumulate in a single cell - the precise number of mutations required for the initiation of malignancy probably being dependent upon the tumor type and whether the tumor is sporadic or familial.