 |
|
Genetics of Nonmelanoma Skin Cancer
Hensin Tsao, MD, PhD
Arch Dermatol. 2001;137:1486-1492.
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.
From the Department of Dermatology, Massachusetts General Hospital Melanoma Center, Massachusetts General Hospital, Boston.
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Single nucleotide polymorphisms in DNA repair genes and basal cell carcinoma of skin
Thirumaran et al.
Carcinogenesis 2006;27:1676-1681.
ABSTRACT
| FULL TEXT
Non-melanoma skin cancer: what drives tumor development and progression?
Boukamp
Carcinogenesis 2005;26:1657-1667.
ABSTRACT
| FULL TEXT
Alterations of {beta}-Catenin Pathway in Non-Melanoma Skin Tumors: Loss of {alpha}-ABC Nuclear Reactivity Correlates with the Presence of {beta}-Catenin Gene Mutation
Doglioni et al.
Am. J. Pathol. 2003;163:2277-2287.
ABSTRACT
| FULL TEXT
|
