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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Melanoma

 
 
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Disease relevance of Melanoma

 

Psychiatry related information on Melanoma

  • Thus, melanoma cells, like other epidermal cells, exhibit the capacity to release the immunomodulating cytokine IL-1 and, therefore, probably have the potency to influence host defense mechanisms directed against malignant melanoma [7].
  • PURPOSE: A study was performed to assess the usefulness of a radiolabeled monoclonal antibody (MoAb; technetium 99m NR-ML-05 Fab) as a detecting agent, as well as to evaluate its role in the overall decision-making process in the management of cutaneous malignant melanoma [8].
  • The relationship between dietary habits and subsequent risk of cutaneous malignant melanoma (CMM) was studied in 25,708 men and 25,049 women aged 16-56 years attending a Norwegian health screening in 1977-1983 [9].
  • On whole body images, the anti-Fab HMWA appears to be more tumor selective than Fab preparations that target the p97 antigen for melanoma, and there is less uptake in liver [10].
  • Variables associated with self-detected melanomas were female sex, young age, absence of atypical nevi, knowledge of the ABCD rule, habit of performing skin self-examination [11].
 

High impact information on Melanoma

  • Differentiation antigens coded by genes such as tyrosinase are also recognized on human melanoma by autologous CTL [12].
  • A gene family named MAGE codes for antigens recognized by autologous CTL on a melanoma tumor [12].
  • Melanomas also commonly show impairment of the p16(INK4A)-CDK4-Rb and ARF-HDM2-p53 tumor suppressor pathways [13].
  • TERT amplification also occurs in melanoma [13].
  • These findings indicate that melanocyte-specific factors present before neoplastic transformation can have a pivotal role in governing melanoma progression [14].
 

Chemical compound and disease context of Melanoma

 

Biological context of Melanoma

 

Anatomical context of Melanoma

 

Gene context of Melanoma

  • Mutations associated with familial melanoma impair p16INK4 function [32].
  • Clinically, primary human melanoma expression microarrays revealed tight nearest neighbor linkage for MITF and BCL2 [36].
  • This linkage helps explain the vital roles of both Mitf and Bcl2 in the melanocyte lineage and the well-known treatment resistance of melanoma [36].
  • Activating mutations in one RAF gene, BRAF, have been found in a high proportion of melanomas and in a small fraction of other cancers [37].
  • Screening of primary tumours and linkage analysis of familial melanoma pedigrees have identified many potential mutations in p16, but the functional significance of these sequence variants has remained unclear [38].
  • Treatment of GRM1-expressing human melanoma cells with a GRM1 antagonist (LY367385 or BAY36-7620) or a glutamate release inhibitor (riluzole) leads to a suppression of cell proliferation as well as a decrease in levels of extracellular glutamate [39].
  • Mechanistic studies showed that inhibition of (V600E)B-Raf significantly reduced the constitutive secretion of IL-8 from melanoma cells as well as the capacity of endogenous IL-8 production from the melanoma-PMN microenvironment [40].
  • In a novel mouse model for melanoma, stabilized beta-catenin bypasses the requirement for p16(Ink4a) mutations and, together with an activated N-Ras oncogene, leads to melanoma with high penetrance and short latency [41].
  • A monoclonal antibody reactive with the N-terminal tail of EDNBR was found to internalize rapidly into melanoma cells [42].
  • Results show that KIT mutations are more common in vulvar melanomas than other types of mucosal melanomas and that both the RAF/MEK/ERK and PI3K/AKT pathways are activated in mucosal melanoma specimens [43].
  • Our study reveals a novel mechanism that TAMs enhance angiogenesis and melanoma growth via ADM and provides potential targets for melanoma therapies [44].
 

Analytical, diagnostic and therapeutic context of Melanoma

References

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  14. The melanocyte differentiation program predisposes to metastasis after neoplastic transformation. Gupta, P.B., Kuperwasser, C., Brunet, J.P., Ramaswamy, S., Kuo, W.L., Gray, J.W., Naber, S.P., Weinberg, R.A. Nat. Genet. (2005) [Pubmed]
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  20. Role of p53 up-regulated modulator of apoptosis and phosphorylated Akt in melanoma cell growth, apoptosis, and patient survival. Karst, A.M., Dai, D.L., Cheng, J.Q., Li, G. Cancer Res. (2006) [Pubmed]
  21. UV causation of melanoma in Xiphophorus is dominated by melanin photosensitized oxidant production. Wood, S.R., Berwick, M., Ley, R.D., Walter, R.B., Setlow, R.B., Timmins, G.S. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  22. Tunicamycin sensitizes human melanoma cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by up-regulation of TRAIL-R2 via the unfolded protein response. Jiang, C.C., Chen, L.H., Gillespie, S., Kiejda, K.A., Mhaidat, N., Wang, Y.F., Thorne, R., Zhang, X.D., Hersey, P. Cancer Res. (2007) [Pubmed]
  23. Therapeutic window for melanoma treatment provided by selective effects of the proteasome on Bcl-2 proteins. Wolter, K.G., Verhaegen, M., Fernández, Y., Nikolovska-Coleska, Z., Riblett, M., de la Vega, C.M., Wang, S., Soengas, M.S. Cell Death Differ. (2007) [Pubmed]
  24. Melanoma activation of 3-o-(3,4,5-trimethoxybenzoyl)-(-)-epicatechin to a potent irreversible inhibitor of dihydrofolate reductase. Sánchez-del-Campo, L., Tárraga, A., Montenegro, M.F., Cabezas-Herrera, J., Rodríguez-López, J.N. Mol. Pharm. (2009) [Pubmed]
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  26. Phase II Study of Nilotinib in Melanoma Harboring KIT Alterations Following Progression to Prior KIT Inhibition. Carvajal, R.D., Lawrence, D.P., Weber, J.S., Gajewski, T.F., Gonzalez, R., Lutzky, J., O'Day, S.J., Hamid, O., Wolchok, J.D., Chapman, P.B., Sullivan, R.J., Teitcher, J.B., Ramaiya, N., Giobbie-Hurder, A., Antonescu, C.R., Heinrich, M.C., Bastian, B.C., Corless, C.L., Fletcher, J.A., Hodi, F.S. Clin. Cancer Res. (2015) [Pubmed]
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  35. A p16INK4a-insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma. Wölfel, T., Hauer, M., Schneider, J., Serrano, M., Wölfel, C., Klehmann-Hieb, E., De Plaen, E., Hankeln, T., Meyer zum Büschenfelde, K.H., Beach, D. Science (1995) [Pubmed]
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