tailieunhanh - Ebook Manual of clinical oncology (8/E): Part 2

Part 2 book “Manual of clinical oncology” has contents: Skin cancers, miscellaneous neoplasms, chronic leukemias, chronic leukemias, acute leukemia and myelodysplastic syndromes, metabolic complications, thoracic complications, cutaneous complications, abdominal complications, renal complications, neuromuscular complications, and other contents. | 17 Skin Cancers Bartosz Chmielowski, Richard Wagner Jr, and Antoni Ribas F. Malignant Melanoma I. EPIDEMIOLOGY AND ETIOLOGY A. Incidence. Malignant melanoma accounts for about 2% of all skin cancers, but it is responsible for 80% of deaths. The incidence of melanoma in the United States has been rising for the last 40 years. Before the age of 45, women have a higher risk than men, but after the age of 60, the risk for men is twice as high as for women. The estimated number of new cases in the United States in 2016 is 76,380, and 10,130 patients would die of melanoma. The incidence of melanoma rose rapidly in the 1970s at about 6% per year; it continues to rise but at a lower rate of per year from 2006 to 2010. White people have a lifetime risk for the development of melanoma and African Americans , but melanoma is diagnosed among all races. B. Risk factors. The strongest risk factors for melanoma are a family history of melanoma, multiple benign or atypical nevi, and a previous melanoma. The list of additional risk factors includes immunosuppression, sun sensitivity, and exposure to ultraviolet (UV) radiation. 1. Familial factors. Approximately 10% of melanomas are familial. The higher risk of melanoma in these families may be attributed to both shared susceptibility genes and shared environment. a. High-penetrance susceptibility genes. Two genes, CDKN2A and CDK4, are associated with high-penetrance susceptibility. Mutated CDKN2A is the most prevalent gene in families with 641 melanoma. It is located on chromosome 9p21, and it encodes cyclin-dependent kinase inhibitor 2A (p16INK4a). CDK4 encodes cyclin-dependent kinase 4, which is one of the binding partners of p16INK4a. Mutations in CDK4 are found much less frequently than in CDKN2A. Other less common high-penetrance genes are BAP1, TERT, XP (various genes mutated in individuals with xeroderma pigmentosum). The higher the number of family members with melanoma, the higher the probability of .