Abstract
Despite worldwide prevention programs, the incidence for cutaneous melanoma is continuously increasing. Mucosal melanoma (MM) represents a rare but highly aggressive phenotype of common melanoma with predilection in the sinonasal system. Far away from ultraviolet sun exposure, the molecular mechanisms underlying tumorigenesis and the highly aggressive clinical behavior are poorly understood. In many solid malignomas of the head and neck region, p53 tumor suppressor functions as oncogene due to p53 protein stabilizing mutation. Interestingly, the vast majority of MM demonstrates constitutively expressed p53 protein, with protein stabilizing mutations being rare. Abrogated activation of p53 target genes results in derogation of the apoptotic signal cascade and contributes to the strong resistance against chemotherapeutic agents activating p53 dependent apoptosis. The current review illustrates the role of p53 and its pathway in MM.
Highlights
Mucosal melanoma is a rare but highly aggressive phenotype of melanomas representing 1–5%of the overall cohort [1,2,3]
P53 stabilization stabilization is regulated through posttranslational modifications (PTMs) and inhibition of proteasomal degradation, is regulated through posttranslational modifications (PTMs) and inhibition of proteasomal resulting in apoptosis
In previous experiments we showed, that p53 target genes BBC3, Bcl2 associated X
Summary
Mucosal melanoma is a rare but highly aggressive phenotype of melanomas representing 1–5%. Melanocytes which function as ultraviolet (UV)-light protector in the skin are peculiarly found in the mucosa. Melanocytes can be found from 20 weeks of gestation [7]. Their function is not fully understood, but it seems that these melanocytes have antimicrobial and immunological functions, such as antigen presentation and cytokine production [8]. Control (UICC) staging system takes the poor prognosis into account and relinquishes T1/2 status. Lymph node positivity and distant metastasis that usually result in advanced UICC disease stages occur infrequently. Molecular mechanisms in MM that contribute to the highly aggressive phenotype remain unclear [11]
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