Tumors can best be defined as diseases in which a single cell acquires the ability to proliferate abnormally, resulting in an accumulation of progeny. Cancers are those tumors which have acquired the ability to invade through surrounding normal tissues. The most advanced form of this invasive process is metastasis, a state in which cancer cells escape from their original location, travel by hematogenous or lymphogenous channels, and take up residence in distant sites. The only difference between a malignant tumor (a.k.a. cancer) and a benign tumor is the capacity of the former to invade. Both benign and malignant tumors can achieve large sizes, but benign tumors are circumscribed and therefore generally can be removed surgically. Malignant tumors often have invaded surrounding or distant tissues prior to their detection, precluding surgical excision of the entire tumor cell population. It is the ability of cancers to destroy other tissues through invasion that makes them lethal.
There are as many tumor types as there are cell types in the human body. Cancers thus represent not a single disease but a group of heterogeneous diseases that share certain biological properties (in particular, clonal cell growth and invasive ability). Cancers can be classified in various ways. Most common cancers of adults are carcinomas, representing cancers derived from epithelial cells. Leukemias and lymphomas are derived from blood-forming cells and lymphoid cells, respectively. Sarcomas are derived from mesenchymal tissues. Melanomas are derived from melanocytes, and retinoblastomas, neuroblastomas, and glioblastomas are derived from stem cells of the retina, neurons, and glia, respectively.
Twenty years ago it could not have been predicted that all these different cancers share common molecular pathogeneses in addition to common biological properties. The cancer research revolution has demonstrated that they do: All result from defects in oncogenes and tumor suppressor genes. Each specific cancer arises through characteristic mutations in specific genes. Although dozens of human oncogenes and tumor suppressor genes have been described in the literature, these genes' products appear to converge on a relatively small number of growth-controlling pathways. In some cases, the same gene is involved in multiple cancers. For example, p53 mutations commonly occur in cancers of the brain, colon, breast, stomach, bladder, and pancreas. In other cases, a defective gene appears to be associated with a single tumor type, such as the WT1 gene in childhood kidney cancers (see Chap. 38).