Fair- and red-haired people, persons with multiple atypical nevi or dysplastic nevi and persons born with giant congenital melanocytic nevi are at increased risk. [38] The risk of melanoma increases as people age. The average age of people when the disease is diagnosed is 63. [157] History [ edit ]

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Yeh I, Tee MK, Botton T, Shain AH, Sparatta AJ, Gagnon A, etal. (November 2016). "NTRK3 kinase fusions in Spitz tumours". The Journal of Pathology. 240 (3): 282–290. doi: 10.1002/path.4775. PMC 5071153. PMID 27477320. {{ cite journal}}: CS1 maint: overridden setting ( link) Other mutations confer lower risk, but are more common in the population. People with mutations in the MC1R gene are two to four times more likely to develop melanoma than those with two wild-type (typical unaffected type) copies. MC1R mutations are very common, and all red-haired people have a mutated copy. [ citation needed] Mutation of the MDM2 SNP309 gene is associated with increased risks for younger women. [37] Melanocytes house melanin in cells called melanosomes. The amount of melanin in the skin is a result of the quantity and distribution of melanocytes.Melanoma is a type of neuroectodermal neoplasm. [81] There are four main types of melanoma: [82] SN Can we get skin cancer from tanning beds?". CuradermBCC. 1 September 2022. Archived from the original on 3 September 2022 . Retrieved 3 September 2022. Ongoing research is looking at treatment by adoptive cell transfer. [137]Adoptive cell transfer refers to the application of pre-stimulated, modified T cells or dendritic cells and is presently used to minimize complications from graft-versus-host disease. [134] [138]

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a b c d e Gershenwald JE, Scolyer RA, Hess KR, Sondak VK, Long GV, Ross MI, etal. (November 2017). "Melanoma staging: Evidence-based changes in the American Joint Committee on Cancer eighth edition cancer staging manual". CA: A Cancer Journal for Clinicians. 67 (6): 472–492. doi: 10.3322/caac.21409. PMC 5978683. PMID 29028110. {{ cite journal}}: CS1 maint: overridden setting ( link), citingpeople in the United States were diagnosed with melanomas of the skin, including 42,430 men and 29,513 women. Kirkwood JM, Strawderman MH, Ernstoff MS, Smith TJ, Borden EC, Blum RH (January 1996). "Interferon alfa-2b adjuvant therapy of high-risk resected cutaneous melanoma: the Eastern Cooperative Oncology Group Trial EST 1684". Journal of Clinical Oncology. 14 (1): 7–17. doi: 10.1200/JCO.1996.14.1.7. PMID 8558223. S2CID 24020903. A number of treatments improve survival over traditional chemotherapy. [124] Biochemotherapy (chemotherapy with cytokines IL-2 and IFN-α) combined with BRAF inhibitors improved survival for people with BRAF positive melanoma. [124] Biochemotherapy alone did not improve overall survival and had higher toxicity than chemotherapy. [124] Combining multiple chemotherapy agents (polychemotherapy) did not improve survival over monochemotherapy. [124] Targeted therapies result in relatively short progression-free survival (PFS) times. The therapy combination of dabrafenib and trametinib has a 3-year PFS of 23%, and 5-year PFS of 13%. [131] Immunotherapy [ edit ] a b Vos T, Allen C, Arora M, Barber RM, Bhutta ZA, Brown A, etal. (GBD 2015 Mortality Causes of Death Collaborators) (October 2016). "Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1459–1544. doi: 10.1016/s0140-6736(16)31012-1. PMC 5388903. PMID 27733281. Bhoumik A, Singha N, O'Connell MJ, Ronai ZA (June 2008). "Regulation of TIP60 by ATF2 modulates ATM activation". The Journal of Biological Chemistry. 283 (25): 17605–14. doi: 10.1074/jbc.M802030200. PMC 2427333. PMID 18397884.

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Vlahopoulos SA, Logotheti S, Mikas D, Giarika A, Gorgoulis V, Zoumpourlis V (April 2008). "The role of ATF-2 in oncogenesis". BioEssays. 30 (4): 314–27. doi: 10.1002/bies.20734. PMID 18348191. S2CID 678541. It is possible for a person to produce too much melanin within the body. Experts call it hyperpigmentation. It can occur due to certain conditions or the presence of excess melanocyte-stimulating hormone. Pharmacotherapy research for un-resectable or metastatic malignant melanoma is ongoing. [168] Targeted therapies [ edit ] F18-FDG PET/CT in a melanoma patient showing multiple lesions, most likely metastases Laboratory [ edit ] Davies MA, Samuels Y (October 2010). "Analysis of the genome to personalize therapy for melanoma". Oncogene. 29 (41): 5545–55. doi: 10.1038/onc.2010.323. PMC 3169242. PMID 20697348.In the European Union, interferon is usually not used outside the scope of clinical trials. [122] [123] Chemotherapy [ edit ] UV radiation causes damage to the DNA of cells, typically thymine dimerization, which when unrepaired can create mutations in the cell's genes. This strong mutagenic factor makes cutaneous melanoma the tumor type with the highest number of mutations. [53] When the cell divides, these mutations are propagated to new generations of cells. If the mutations occur in protooncogenes or tumor suppressor genes, the rate of mitosis in the mutation-bearing cells can become uncontrolled, leading to the formation of a tumor. Data from patients suggest that aberrant levels of activating transcription factor in the nucleus of melanoma cells are associated with increased metastatic activity of melanoma cells; [54] [55] [56] studies from mice on skin cancer tend to confirm a role for activating transcription factor-2 in cancer progression. [57] [58] Melanin is a substance present in the skin that produces pigment. Each person has a different amount of melanin in their skin. Sage E, Girard PM, Francesconi S (January 2012). "Unravelling UVA-induced mutagenesis". Photochemical & Photobiological Sciences. 11 (1): 74–80. doi: 10.1039/c1pp05219e. PMID 21901217. S2CID 45189513. About 200 genes are prognostic in melanoma, with both unfavorable genes where high expression is correlated to poor survival and favorable genes where high expression is associated with longer survival times. Examples of unfavorable genes are MCM6 and TIMELESS; an example of a favorable gene is WIPI1. [51] [52]