Chapter Summary

Cancer is the second leading cause of death in the United States in both adults and children. In men, the sites with the highest new cancer rates are (in order of decreasing frequency): prostate, lung and bronchus, and colon and rectum. These same sites have the highest mortality rate, although lung and bronchus cancers more commonly cause death than prostate cancer. In women, the sites with the highest new cancer rate are (in order of decreasing frequency): breast, lung and bronchus, and colon and rectum. These same sites have the highest mortality rate, although lung and bronchus cancers more commonly cause death than breast cancer.

The incidence of different cancers can vary with geographic site, racial factors, occupational exposures, age, hereditary predisposition, and acquired preneoplastic disorders.

A variety of chemical carcinogens have been identified that can act as initiators or promoters of specific cancers. Ultraviolet light and ionizing radiation are also carcinogenic. A relatively small number of cancers have been linked to infection with specific viruses. Patients with immune system dysfunction also have an increased number of neoplasms.

Carcinogenesis is a multistep process requiring the accumulation of multiple genetic changes as the result of either inherited germ-line mutations or acquired mutations, leading to the monoclonal expansion of a mutated cell.

Cancer growth can involve either activation of growth promoting oncogenes or inactivation of tumor suppressor genes.

Activated oncogenes lack regulatory control and are overexpressed, resulting in unregulated cellular proliferation. Examples of clinically important oncogenes include erb, ras, and myc

Tumor suppressor genes encode proteins that regulate and suppress cell proliferation by inhibiting progression of the cell through the cell cycle. Inactivation of these genes leads to uncontrolled cellular proliferation with tumor formation. Examples of clinically important tumor suppressor genes include VHL p53, Rb, APC, DCC, and NF-1.

Cancers can also develop if apoptosis (programmed cell death) is prevented by mutations in genes such as bcl-2, bax, bad, and bcl-xS.

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