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Gene Review

CMM  -  cutaneous malignant melanoma/dysplastic nevus

Homo sapiens

Synonyms: CMM1, DNS, FAMMM, MLM
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Disease relevance of CMM

  • The individual tested had developed 2 CMMs but had no dysplastic nevi and lacked a family history of dysplastic nevi or CMM [1].
  • Uveal malignant melanoma (UMM) also occurs in a familial setting, or sometimes in association with familial or sporadic CMM [2].
  • There was, however, a statistically significant difference in age-adjusted median numbers of nevi (P =.004), and CMM case subjects from CDKN2A families without pancreatic cancer had greater numbers of nevi [3].
  • Expression of RASEF, a known gene in this region, was examined in tumor tissue from 10 sporadic CMM lesions and was found to be decreased in 70% of these tumors compared with RASEF expression in a human reference RNA pool from 10 different cell types and in 10 breast tumors [4].
  • We report the occurrence of five common MC1R variants in an Australian population-based sample of 460 individuals with familial and sporadic CMM and 399 control individuals-and their relationship to such other risk factors as skin, hair, and eye color; freckling; and nevus count [5].

Psychiatry related information on CMM

  • 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 [6].
  • There is, thus, a need for large prospective studies on the development of CMM and naevi, ideally in different contexts as concerns host factors, sun exposure, and other life-style habits within and across different populations [7].
  • CMM was also directly predictive of PTSD symptoms, but not depression symptoms in adulthood [8].
  • CONCLUSIONS: Findings support both direct and mediational effects of social resources on adult depression and PTSD symptoms in women with histories of CMM, suggesting that resources are key factors in psychological adjustment of CMM victims [8].

High impact information on CMM


Chemical compound and disease context of CMM


Biological context of CMM


Anatomical context of CMM


Associations of CMM with chemical compounds

  • Most of them were identified in sporadic CMM (six in codon 148 Ala/Thr, 12 in codon 84 Asp/Asp and six in 3'UTR) [26].
  • These findings provide additional evidence that tumor progression in CMM is associated with changes in integrin phenotypes which include the alpha 3/beta 1 heterodimer [27].
  • The most important, and consistent morphological difference was the greater thickness of tumours from the Oxford Region, which is thought to be consistent with the theory that CMM is diagnosed at an earlier stage in high incidence areas because of greater medical and public awareness of the condition [14].
  • We found a significant inverse association between vitamin A intake and CMM risk [28].
  • The probability of CMM significantly increased with the degree of relative clustering of CN (p less than 0.05) and of DN (p less than 0.01) [15].

Regulatory relationships of CMM


Other interactions of CMM

  • CDKN2A mutation in a non-FAMMM kindred with cancers at multiple sites results in a functionally abnormal protein [1].
  • Carriers of the p16-Leiden deletion in Dutch families with FAMMM show an increased risk of melanoma when they also carry MC1R variant alleles [30].
  • We have investigated whether the VEGF -2578, -1154, +405 and +936 SNPs and associated haplotypes confer susceptibility to and/or influence prognosis in cutaneous malignant melanoma (CMM) skin cancer [21].
  • These data suggest that among persons with hair colors traditionally associated with increased risk for melanoma, absence of both GSTM1 and GSTT1 may act to further elevate CMM risk [31].
  • Exclusion of the familial melanoma locus (MLM) from the PND/D1S47 and MYCL1 regions of chromosome arm 1p in 7 Australian pedigrees [20].

Analytical, diagnostic and therapeutic context of CMM


  1. CDKN2A mutation in a non-FAMMM kindred with cancers at multiple sites results in a functionally abnormal protein. Sun, S., Pollock, P.M., Liu, L., Karimi, S., Jothy, S., Milner, B.J., Renwick, A., Lassam, N.J., Hayward, N.K., Hogg, D., Narod, S.A., Foulkes, W.D. Int. J. Cancer (1997) [Pubmed]
  2. Individuals with presumably hereditary uveal melanoma do not harbour germline mutations in the coding regions of either the P16INK4A, P14ARF or cdk4 genes. Soufir, N., Bressac-de Paillerets, B., Desjardins, L., Lévy, C., Bombled, J., Gorin, I., Schlienger, P., Stoppa-Lyonnet, D. Br. J. Cancer (2000) [Pubmed]
  3. Genotype-phenotype relationships in U.S. melanoma-prone families with CDKN2A and CDK4 mutations. Goldstein, A.M., Struewing, J.P., Chidambaram, A., Fraser, M.C., Tucker, M.A. J. Natl. Cancer Inst. (2000) [Pubmed]
  4. Mapping of a novel ocular and cutaneous malignant melanoma susceptibility locus to chromosome 9q21.32. Jönsson, G., Bendahl, P.O., Sandberg, T., Kurbasic, A., Staaf, J., Sunde, L., Crüger, D.G., Ingvar, C., Olsson, H., Borg, A. J. Natl. Cancer Inst. (2005) [Pubmed]
  5. Melanocortin-1 receptor polymorphisms and risk of melanoma: is the association explained solely by pigmentation phenotype? Palmer, J.S., Duffy, D.L., Box, N.F., Aitken, J.F., O'Gorman, L.E., Green, A.C., Hayward, N.K., Martin, N.G., Sturm, R.A. Am. J. Hum. Genet. (2000) [Pubmed]
  6. Diet and risk of cutaneous malignant melanoma: a prospective study of 50,757 Norwegian men and women. Veierød, M.B., Thelle, D.S., Laake, P. Int. J. Cancer (1997) [Pubmed]
  7. Cutaneous malignant melanoma: epidemiological considerations. Franceschi, S., Cristofolini, M. Seminars in surgical oncology. (1992) [Pubmed]
  8. Child multi-type maltreatment and associated depression and PTSD symptoms: The role of social support and stress. Vranceanu, A.M., Hobfoll, S.E., Johnson, R.J. Child abuse & neglect (2007) [Pubmed]
  9. Homozygotes for CDKN2 (p16) germline mutation in Dutch familial melanoma kindreds. Gruis, N.A., van der Velden, P.A., Sandkuijl, L.A., Prins, D.E., Weaver-Feldhaus, J., Kamb, A., Bergman, W., Frants, R.R. Nat. Genet. (1995) [Pubmed]
  10. Mapping the gene for hereditary cutaneous malignant melanoma-dysplastic nevus to chromosome 1p. Bale, S.J., Dracopoli, N.C., Tucker, M.A., Clark, W.H., Fraser, M.C., Stanger, B.Z., Green, P., Donis-Keller, H., Housman, D.E., Greene, M.H. N. Engl. J. Med. (1989) [Pubmed]
  11. Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers. Nobori, T., Miura, K., Wu, D.J., Lois, A., Takabayashi, K., Carson, D.A. Nature (1994) [Pubmed]
  12. Repair of UV light-induced DNA damage and risk of cutaneous malignant melanoma. Wei, Q., Lee, J.E., Gershenwald, J.E., Ross, M.I., Mansfield, P.F., Strom, S.S., Wang, L.E., Guo, Z., Qiao, Y., Amos, C.I., Spitz, M.R., Duvic, M. J. Natl. Cancer Inst. (2003) [Pubmed]
  13. Immunohistochemical analysis of the N-ras p21 and the p53 proteins in naevi, primary tumours and metastases of human cutaneous malignant melanoma: increased immunopositivity in hereditary melanoma. Platz, A., Ringborg, U., Grafström, E., Höög, A., Lagerlöf, B. Melanoma Res. (1995) [Pubmed]
  14. A histological comparison of cutaneous malignant melanoma between the Oxford Region and Western Australia. Heenan, P.J., Holman, C.D. Histopathology (1982) [Pubmed]
  15. Regional distribution of common and dysplastic naevi in relation to melanoma site and sun exposure. A case-control study. Stierner, U., Augustsson, A., Rosdahl, I., Suurküla, M. Melanoma Res. (1992) [Pubmed]
  16. Structure of the capsular polysaccharide from Alteromonas sp. CMM 155. Zubkov, V.A., Nazarenko, E.L., Gorshkova, R.P., Ivanova, E.P., Shashkov, A.S., Knirel, Y.A., Paramonov, N.A., Ovodov, Y.S. Carbohydr. Res. (1995) [Pubmed]
  17. Collagenase-3 (MMP-13) expression in cutaneous malignant melanoma. Corte, M.D., Gonzalez, L.O., Corte, M.G., Quintela, I., Pidal, I., Bongera, M., Vizoso, F. Int. J. Biol. Markers (2005) [Pubmed]
  18. CDKN2A point mutations D153spl(c.457G>T) and IVS2+1G>T result in aberrant splice products affecting both p16INK4a and p14ARF. Rutter, J.L., Goldstein, A.M., Dávila, M.R., Tucker, M.A., Struewing, J.P. Oncogene (2003) [Pubmed]
  19. Loss of expression of the p16INK4/CDKN2 gene in cutaneous malignant melanoma correlates with tumor cell proliferation and invasive stage. Talve, L., Sauroja, I., Collan, Y., Punnonen, K., Ekfors, T. Int. J. Cancer (1997) [Pubmed]
  20. Exclusion of the familial melanoma locus (MLM) from the PND/D1S47 and MYCL1 regions of chromosome arm 1p in 7 Australian pedigrees. Nancarrow, D.J., Palmer, J.M., Walters, M.K., Kerr, B.M., Hafner, G.J., Garske, L., McLeod, G.R., Hayward, N.K. Genomics (1992) [Pubmed]
  21. Influence of vascular endothelial growth factor single nucleotide polymorphisms on tumour development in cutaneous malignant melanoma. Howell, W.M., Bateman, A.C., Turner, S.J., Collins, A., Theaker, J.M. Genes Immun. (2002) [Pubmed]
  22. Benign nevus cell aggregates in the thymus: a case report. Parker, J.R., Ro, J.Y., Ordóñez, N.G. Mod. Pathol. (1999) [Pubmed]
  23. Impaired DNA repair capacity in skin fibroblasts from various hereditary cancer-prone syndromes. Abrahams, P.J., Houweling, A., Cornelissen-Steijger, P.D., Jaspers, N.G., Darroudi, F., Meijers, C.M., Mullenders, L.H., Filon, R., Arwert, F., Pinedo, H.M., Natarajan, A.P., Terleth, C., Van Zeeland, A.A., van der Eb, A.J. Mutat. Res. (1998) [Pubmed]
  24. Characterization of the neoplastic phenotype in the familial atypical multiple-mole melanoma-pancreatic carcinoma syndrome. Rulyak, S.J., Brentnall, T.A., Lynch, H.T., Austin, M.A. Cancer (2003) [Pubmed]
  25. Immunologic abnormalities in melanoma-prone families. Dean, J.H., Greene, M.H., Reimer, R.R., LeSane, F.V., McKeen, E.A., Mulvihill, J.J., Blattner, W.A., Herberman, R.B., Fraumeni, J.F. J. Natl. Cancer Inst. (1979) [Pubmed]
  26. Analysis of mutations in the p16/CDKN2A gene in sporadic and familial melanoma in the Polish population. Lamperska, K., Karezewska, A., Kwiatkowska, E., Mackiewicz, A. Acta Biochim. Pol. (2002) [Pubmed]
  27. Integrin expression in cutaneous malignant melanoma: association of the alpha 3/beta 1 heterodimer with tumor progression. Natali, P.G., Nicotra, M.R., Bartolazzi, A., Cavaliere, R., Bigotti, A. Int. J. Cancer (1993) [Pubmed]
  28. Risk of melanoma and vitamin A, coffee and alcohol: a case-control study from Italy. Naldi, L., Gallus, S., Tavani, A., Imberti, G.L., La Vecchia, C. Eur. J. Cancer Prev. (2004) [Pubmed]
  29. ICAM-1 polymorphisms and development of cutaneous malignant melanoma. Howell, W.M., Rose-Zerilli, M.J., Theaker, J.M., Bateman, A.C. International journal of immunogenetics. (2005) [Pubmed]
  30. Melanocortin-1 receptor variant R151C modifies melanoma risk in Dutch families with melanoma. van der Velden, P.A., Sandkuijl, L.A., Bergman, W., Pavel, S., van Mourik, L., Frants, R.R., Gruis, N.A. Am. J. Hum. Genet. (2001) [Pubmed]
  31. Interaction of glutathione S-transferase M1 and T1 genotypes and malignant melanoma. Kanetsky, P.A., Holmes, R., Walker, A., Najarian, D., Swoyer, J., Guerry, D., Halpern, A., Rebbeck, T.R. Cancer Epidemiol. Biomarkers Prev. (2001) [Pubmed]
  32. Etiologic factors associated with p53 immunostaining in cutaneousmalignant melanoma. Purdue, M.P., From, L., Kahn, H.J., Armstrong, B.K., Kricker, A., Gallagher, R.P., McLaughlin, J.R., Klar, N.S., Marrett, L.D. Int. J. Cancer (2005) [Pubmed]
  33. Malignant melanoma in renal-transplant recipients. Greene, M.H., Young, T.I., Clark, W.H. Lancet (1981) [Pubmed]
  34. Prospective evaluation of 2-[18F]-2-deoxy-D-glucose positron emission tomography in staging of regional lymph nodes in patients with cutaneous malignant melanoma. Macfarlane, D.J., Sondak, V., Johnson, T., Wahl, R.L. J. Clin. Oncol. (1998) [Pubmed]
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