REVIEW

Genetic pathways to melanoma tumorigenesis

M R Hussein

Correspondence to:
Correspondence to:
Dr M R Hussein
Department of Pathology, Assiut University Hospitals, Assiut, Egypt; mrh17{at}swissnfo.org

The incidence of cutaneous malignant melanomas is growing faster than that of any other cancer and therefore posing a major heath threat worldwide. In melanocytic skin tumours, the feasibility of correlating a specific pathological stage with a corresponding genetic alteration provides a remarkable opportunity to study the multistep tumorigenesis model. This multistep melanoma tumorigenesis is best described as a continuum of transformation of the melanocytes, melanocytic dysplasia, and melanoma formation. These steps involve genotypic alterations including loss of tumour suppressor genes, microsatellite instability, and alterations of the mismatch repair system. This review seeks to examine melanoma tumorigenesis based on these genetic changes.

Abbreviations: BN, common acquired melanocytic naevus; CMM, primary melanoma; hMSH, human MutS homologue; HNPCC, human non-polyposis colorectal cancer; LOH, loss of heterozygosity; MDN, melanocytic dysplastic naevi; MMR, mismatch repair; MSI, microsatellite instability; MSI-H, high microsatellite instability; MSI-L, low microsatellite instability; RGP, radial growth phase; TSG, tumour suppressor gene; VGP, vertical growth phase

Keywords: melanoma; allelic loss; microsatellite instability

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