A Millimeter Too Far: Metastatic Melanoma Essays -- Disease, Disorder

Summary 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. Introduction 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-ER... ...l autonomous growth: the Rb/E2F pathway. Cancer Metastasis Rev. 18 (3), 333-43. 5. Linley AJ, Mathieu MG, Miles AK, Rees RC, McArdle SE, Regad T. (2012). The helicase HAGE expressed by malignant melanoma-initiating cells is required for tumor cell proliferation In Vivo. The journal of biological chemistry. DOI: 10.1074/jbc.M111.308973. 6. Maelandsmo GM, Flà ¸renes VA, Hovig E, Oyjord T, Engebraaten O, Holm R, Bà ¸rresen AL, Fodstad O. (1996). Involvement of the pRb/p16/cdk4/cyclin D1 pathway in the tumorigenesis of sporadic malignant melanomas. Br J Cancer. 73 (8), 909-16. 7. Melnikova VO, Bolshakov SV, Walker C, Ananthaswamy HN. (2004). Genomic alterations in spontaneous and carcinogen-induced murine melanoma cell lines. Oncogene. 23 (13), 2347-56. 8. Pà ³pulo H, Lopes JM, Soares P. (2012). The mTOR Signalling Pathway in Human Cancer. Int J Mol Sci. 13 (2), 1886-918.