A Millimeter Too Far: Metastatic Melanoma

1106 words - 4 pages

Metastatic Melanoma is defined as the transformation of normal melanocytes due to unregulated growth factors involved in normal cell proliferation. Identifying the altered genes via mutation, deletion or amplification will enable us to find a treatment that is tailored to correct that particular gene.
Melanoma determines skin pigmentation. Neural crest cells give rise to Melanocytes which transfer to the skin and hair follicles during embryonic progression. There are 5 phases in which melanoma develops, firstly nevus, then dysplastic nevus, next radial-growth phase, after that vertical growth phase and finally metastatic melanoma. The most important transition is RGP to VGP because this is where keratinocyte mediated growth control is lost, related with tumour thickness being a forecaster of metastatic melanoma.
Risk factors are environmental and genetic; exposure to ultraviolet radiation causes melanocytes to produce melanin, which is taken up by keratinocytes and hereditary mutations create susceptibility to developing melanoma. Symptoms are small dark spot, with irregular borders or a change in an existing mole. However, tests such as skin biopsy are carried out to verify whether the mole is a tumour or not. At the early stage, melanoma is excised with low chance of it reoccurring, but with metastatic melanomas an aggressive form of treatment would be needed such as chemotherapy and radiotherapy. Protective clothing, sun screen and early detection prevent melanoma from developing.
Genes Altered In Metastatic Melanoma
The development of melanoma is the attainment of mutations in regulatory genes. Three pathways have been found to be deregulated in melanocytic tumours, including the RAS-RAF-MEK-ERK pathway, the p16INK4A-CDK4-RB pathway and the ARF-p53 pathway. Other pathways include PI3K-AKT pathway and the Wnt signalling pathway (Dahl and Guldberg, 2007).
NRAS is a gene involved in signal transduction which triggers cellular proliferation and transformation. This gene is altered by point mutations which cause the protein product to be unresponsive to GTPase activating proteins that silence RAS, leading to melanoma. RAS production is mediated by helicase HAGE led to a significant decrease in RAS protein expression with a decrease in activation of the AKT and ERK signalling pathways implicated to play an important role in melanoma progression (Linley et al., 2012).
p16INK4A-CDK4-RB pathway
CDKN2A is a tumour suppressor gene; it regulates cell cycle which consists of pRb, cdk4 and cyclin D1. Therefore deletions and mutations in this gene increase the risk of developing melanoma. Cyclin-dependent kinases cause cell proliferation due to loss of CDK inhibitors such as p16INK4a and p27IP1, and up regulation of cyclin D1, cyclin A and cyclin E. CDK inactivates pRb, p107 and p130 which releases E2F transcription factors, which in turn expresses genes involved in cell cycle development (Halaban...

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