AI Article Synopsis
- The genetic mechanisms behind ocular melanoma are not well understood compared to skin melanoma, with research suggesting that it may arise from genetic changes in normal melanocytes.
- Genetic alterations linked to choroidal melanoma include deletions and amplifications on several chromosomes (3, 6, 8, 9, 11, and 18) along with point mutations that lead to monosomy or loss of heterozygosity.
- These genetic changes can produce faulty proteins, such as p16 and p14, which normally help suppress cancer development; defects in these proteins may contribute to the formation of melanoma.
Article Abstract
Genetic mechanisms underlying formation of ocular and skin melanoma differ in many aspects, the former being still poorly understood. It has been suggested that choroidal melanoma can develop due to accumulation of genetic alterations in the DNA of normal melanocytes. Neoplastic transformation in the choroid can be triggered as a consequence of the following genetic alterations: --deletions and/or amplifications in the genetic material, usually in the chromosome 3, 6, 8, 9, 11, and 18; --point mutations, especially within some egzones, which leads to monosomia or loss of heterozygosity of the chromosome. As a consequence of the above alterations a number of false codons can appear resulting in formation of defective enzymatic proteins. Some of these proteins, like p16 and p14, normally play a role of suppressors of oncogenesis and defects in their structure may result in melanoma formation.
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