Abstract
Malignant melanoma is a disease with high metastatic potential and poor clinical response to current therapeutic measures1. It represents a significant health crisis given its high rate of increase in incidence; by year 2000, one in 76 Americans will develop melanoma2. Although the molecular pathogenesis of this disease is poorly understood, predisposition to melanoma appears to have a strong genetic component. Tumor surveys and kindred analyses have uncovered several potential chromosomal “hot spots” including frequent loss of 6q and 10q, non-random karyotypic alterations of chromosome 1, and 9p21-associated deletion/mutation1. The latter appears to be the most compelling etiological link to melanoma in that cytogenetic, linkage and molecular analyses have documented a high incidence of 9p21 germline and somatic mutations in both familial and sporadic melanomas3–6.
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Pomerantz, J. et al. (1998). The Role for ink4a in Melanoma Pathogenesis. In: Mihich, E., Croce, C. (eds) The Biology of Tumors. Pezcoller Foundation Symposia, vol 9. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1352-4_1
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DOI: https://doi.org/10.1007/978-1-4899-1352-4_1
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