Genetics of nonmelanoma skin cancer.
Cancer is in essence a genetic disease characterized by genomic instability. Unlike classic genetic syndromes in which a single inherited mutation is often sufficient to determine the perturbed phenotype, most cancers, especially solid tumors, develop after an accumulation of multiple genetic lesions. Inherited mutations that predispose individuals to cancer formation are termed germline, while acquired mutations that contribute to tumor development are designated somatic. Bona fide hereditary cancers account for only a small proportion of all documented cancers. Most tumors result from mutations caused by inherent infidelities in DNA replication, carcinogens, or defects in the DNA reparative apparatus. When mutations occur in critical growth regulatory genes, variations in cellular proliferation and survival contribute to the selection of dominant tumor population(s). Furthermore, these mutations may alter the antigenic properties of the cancerous cell and encourage escape from the host response. Thus, cancer is evolution at the microscopic level.
Tsao
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Department of Dermatology, Massachusetts General Hospital, Barlett 622, 48 Blossom St, Boston, MA 02114, USA. tsao.hensin@mgh.harvard.edu
D003528:Carcinoma, Adenoid Cystic / Q000235:genetics; D002280:Basal Cell Carcinoma / Q000235:genetics*; D015266:Carcinoma, Merkel Cell / Q000235:genetics; D002294:Carcinoma, Squamous Cell / Q000235:genetics*; D018223:Dermatofibrosarcoma / Q000235:genetics; D006201:Hair Diseases / Q000235:genetics; D006801:Humans; D018296:Pilomatrixoma / Q000235:genetics; D012626:Sebaceous Gland Neoplasms / Q000235:genetics; D012878:Skin Neoplasms / Q000235:genetics*; D014983:Xeroderma Pigmentosum / Q000235:genetics*