References
- 1. Azoury SC, Lange JR. Epidemiology, risk factors, prevention, and early detection of melanoma. Surg Clin North Am. 2014; 94(5): 945–62.
- 2. Boyers LN, Karimkhani C, Naghavi M et al. Global mortality from conditions with skin manifestations. J Am Acad Dermatol. 2014; 71(6): 1137–1143.
- 3. Berwick M, Wiggins C. The current epidemiology of cutaneous malignant melanoma. Front Biosci. 2006; 11: 1244–54.
- 4. Thrift AP, Whiteman DC. Can we really predict risk of cancer? Cancer Epidemiol. 2013; 37(4): 349–52.
- 5. DeVita VT. RS, Hellman S. Cancer: Principle and Practice of Oncology. 7th ed: Lippncott Williams & Wilkins; 2004.
- 6. Iles MM, Bishop DT, Taylor JC, GenoMEL Consortium. The effect on melanoma risk of genes previously associated with telomere length. J Natl Cancer Inst 2014; 106(10). pii: dju267.
- 7. Tucker MA, Goldstein AM. Melanoma etiology: where are we? Oncogene 2003; 22(20): 3042–52.
- 8. Chang C, Murzaku EC, Penn L et al. More skin, more sun, more tan, more melanoma. Am J Public Health. 2014; 104(11): e92–9.
- 9. Svobodova A, Zdarilova A, Maliskova J et al. Attenuation of UVA-induced damage to human keratinocytes by silymarin. J Dermatol Sci. 2007; 46(1): 21–30.
- 10. Lee JH, Choi JW, Kim YS. Frequencies of BRAF and NRAS mutations are different in histological types and sites of origin of cutaneous melanoma: a meta-analysis. Br J Dermatol. 2011; 164(4): 776–84.
- 11. Liu J, Fukunaga-Kalabis M, Li L et al. Developmental pathways activated in melanocytes and melanoma. Arch Biochem Biophys. 2014; 563C: 13–21.
- 12. Carlino MS, Todd JR, Gowrishankar K et al. Differential activity of MEK and ERK inhibitors in BRAF inhibitor resistant melanoma. Mol Oncol. 2014; 8(3): 544–54.
- 13. Tomei S, Bedognetti D, De Giorgi V et al. The immune-related role of BRAF in melanoma. Mol Oncol 2015; 9(1): 93–104.
- 14. Conrad WH, Swift RD, Biechele TL et al. Regulating the response to targeted MEK inhibition in melanoma: enhancing apoptosis in NRAS- and BRAF-mutant melanoma cells with Wnt/β-catenin activation. Cell Cycle. 2012; 11(20): 3724–30.
- 15. Rojas AM, Fuentes G, Rausell A et al. The Ras protein superfamily: evolutionary tree and role of conserved amino acids. J Cell Biol. 2012; 196(2): 189–201.
- 16. Baines AT, Xu D, Der CJ. Inhibition of Ras for cancer treatment: the search continues. Future Med Chem. 2011; 3(14): 1787–808.
- 17. Gysin S, Salt M, Young A et al. Therapeutic strategies for targeting ras proteins. Genes Cancer 2011; 2(3): 359–72.
- 18. Martin-Liberal J, Larkin J. New RAF kinase inhibitors in cancer therapy. Expert Opin Pharmacother. 2014; 15(9): 1235–45.
- 19. Mandalà M, Voit C. Targeting BRAF in melanoma: biological and clinical challenges. Crit Rev Oncol Hematol. 2013; 87(3): 239–55.
- 20. Yajima I, Kumasaka MY, Thang ND et al. RAS/RAF/MEK/ERK and PI3K/PTEN/AKT Signali ng in Malignant Melanoma Progression and Therapy. Dermatol Res Pract. 2012; 2012: 354191.
- 21. Nogueira C, Kim KH, Sung H et al. Cooperative interactions of PTEN deficiency and RAS activation in melanoma metastasis. Oncogene. 2010; 29(47): 6222–32.
- 22. Scatolini M, Grand MM, Grosso E et al. Altered molecular pathways in melanocytic lesions. Int J Cancer. 2010; 126(8): 1869–81.
- 23. Jakob JA, Bassett RL Jr, Ng CS et al. NRAS mutation status is an independent prognostic factor in metastatic melanoma. Cancer. 2012; 118(16): 4014–23.
- 24. Rozenberg GI, Monahan KB, Torrice C et al. Metastasis in an orthotopic murine model of melanoma is independent of RAS/RAF mutation Melanoma Res. 2010; 20(5): 361–71.
- 25. Gray-Schopfer V, Wellbrock C, Marais R. Melanoma biology and new targeted therapy. Nature. 2007; 445(7130): 851–7.
- 26. Haydn JM, Hufnagel A, Grimm J et al. The MAPK pathway as an apoptosis enhancer in melanoma. Oncotarget. 2014; 5(13): 5040–53.
- 27. Witkiewicz AK, Knudsen KE, Dicker AP et al. The meaning of p16(ink4a) expression in tumors: functional significance, clinical associations and future developments. Cell Cycle. 2011; 10(15): 2497–503.
- 28. Conde-Perez A, Larue L. Human relevance of NRAS/BRAF mouse melanoma models. Eur J Cell Biol. 2014; 93(1–2): 82–6.
- 29. Wilson W, Merlino G. Flipping the phenotypic switch on novel antimelanoma differentiation strategy. Pigment Cell Melanoma Res. 2013; 26(6):791–3.
- 30. Leachman SA, Carucci J, Kohlmann W et al. Selection criteria for genetic assessment of patients with familial melanoma. J Am Acad Dermatol. 2009; 61(4): 677. e1–14.
- 31. Oikonomou E, Koustas E, Goulielmaki M et al. BRAF vs RAS oncogenes: Are mutations of the same pathway equal? Differential signalling and therapeutic implications. Oncotarget. 2014; 5(23): 11752–77.
- 32. Kumar R, Angelini S, Snellman E, et al. BRAF mutations are common somatic events in melanocytic nevi. J Invest Dermatol. 2004;122(2): 342–8.
- 33. Bauer J, Curtin JA, Pinkel D et al. Congenital melanocytic nevi frequently harbor NRAS mutations but no BRAF mutations. J Invest Dermatol. 2007; 127(1): 179–82.
- 34. Albino AP, Fountain JW. Molecular genetics of human malignant melanoma. Cancer Treat Res. 1993; 65:201–55.
- 35. Demunter A, Stas M, Degreef H et al. Analysis of N- and K-ras mutations in the distinctive tumor progression phases of melanoma. J Invest Dermatol. 2001; 117(6): 1483–9.
- 36. Omholt K, Karsberg S, Platz A et al. Screening of N-ras Codon 61 Mutations in Paired Primary and Metastatic Cutaneous Melanomas: Mutations Occur Early and Persist throughout Tumor Progression. Clin Cancer Res. 2002; 8(11): 3468–74.
- 37. Bradish JR, Cheng L. Molecular pathology of malignant melanoma: changing the clinical practice paradigm toward a personalized approach. Hum Pathol. 2014; 45(7): 1315–26.
- 38. Abschuetz O, Osen W, Frank K et al. T-Cell Mediated Immune Responses Induced in ret Transgenic Mouse Model of Malignant Melanoma. Cancers (Basel). 2012; 4(2): 490–503.
- 39. Mar VJ, Wong SQ, Li J et al. BRAF/NRAS wild-type melanomas have a high mutation load correlating with histologic and molecular signatures of UV damage. Clin Cancer Res. 2013; 19(17): 4589–98.
- 40. Jiveskog S, Ragnarsson-Olding B, Platz A et al. N-ras mutations are common in melanomas from sun-exposed skin of humans but rare in mucosal membranes or unexposed skin. J Invest Dermatol. 1998; 111(5): 757–61.
- 41. Davies H, Bignell GR, Cox C et al. Mutations of the BRAF gene in human cancer. Nature. 2002; 417(6892): 949–54.
- 42. Cruz F 3rd, Rubin BP, Wilson D et al. Absence of BRAF and NRAS mutations in uveal melanoma. Cancer Res. 2003; 63(18): 5761–6.
- 43. Bastian BC, LeBoit PE, Hamm H et al. Chromosomal gains and losses in primary cutaneous melanomas detected by comparative genomic hybridization. Cancer Res. 1998; 58(10): 2170–5.
- 44. Curtin JA, Stark MS, Pinkel D et al. PI3-kinase subunits are infrequent somatic targets in melanoma. J Invest Dermatol. 2006; 126(7): 1660–3.
- 45. Omholt K, Krockel D, Ringborg U et al. Mutations of PIK3CA are rare in cutaneous melanoma. Melanoma Res. 2006; 16(2): 197–200.
- 46. Chudnovsky Y, Khavari PA, Adams AE. Melanoma genetics and the development of rational therapeutics. J Clin Invest. 2005; 115(4): 813–24.
- 47. Stahl JM, Sharma A, Cheung M et al. Deregulated Akt3 activity promotes development of malignant melanoma. Cancer Res. 2004; 64(19): 7002–10.
- 48. Held L, Eigentler TK, Metzler G et al. Proliferative activity, chromosomal aberrations, and tumor-specific mutations in the differential diagnosis between blue nevi and melanoma. Am J Pathol. 2013; 182(3): 640–5.
- 49. Wu H, Goel V, Haluska FG. PTEN signaling pathways in melanoma. Oncogene. 2003; 22(20): 3113–22.
- 50. Pollock PM, Walker GJ, Glendening JM et al. PTEN inactivation is rare in melanoma tumours but occurs frequently in melanoma cell lines. Melanoma Res. 2002; 12(6): 565–75.
- 51. Stahl JM, Cheung M, Sharma A et al. Loss of PTEN promotes tumor development in malignant melanoma. Cancer Res. 2003; 63(11): 2881–90.
- 52. Stewart AL, Mhashilkar AM, Yang XH et al. PI3 kinase blockade by Ad-PTEN inhibits invasion and induces apoptosis in RGP and metastatic melanoma cells. Mol Med. 2002; 8(8): 451–61.
- 53. Tsao H, Zhang X, Fowlkes K et al. Relative reciprocity of NRAS and PTEN/MMAC1 alterations in cutaneous melanoma cell lines. Cancer Res. 2000; 60(7): 1800–4.
- 54. Isabel ZY, Fitzpatrick JE. Expression of c-kit (CD117) in Spitz nevus and malignant melanoma. J Cutan Pathol. 2006; 33(1): 33–7.
- 55. Willmore-Payne C, Layfield LJ, Holden JA. c-KIT mutation analysis for diagnosis of gastrointestinal stromal tumors in fine needle aspiration specimens. Cancer. 2005; 105(3): 165–70.
- 56. Fukuda R, Hamamoto N, Uchida Y et al. Gastrointestinal stromal tumor with a novel mutation of KIT proto-oncogene. Intern Med. 2001; 40(4): 301–3.
- 57. Curtin JA, Busam K, Pinkel D et al. Somatic activation of KIT in distinct subtypes of melanoma. J Clin Oncol. 2006; 24(26): 4340–6.
- 58. Cachia AR, Indsto JO, McLaren KM et al. CDKN2A mutation and deletion status in thin and thick primary melanoma. Clin Cancer Res. 2000; 6(9): 3511–5.
- 59. Grafstrom E, Egyhazi S, Ringborg U et al. Biallelic deletions in INK4 in cutaneous melanoma are common and associated with decreased survival. Clin Cancer Res. 2005; 11(8): 2991–7.
- 60. Sherr CJ. Divorcing ARF and p53: an unsettled case. Nat Rev Cancer. 2006; 6(9): 663–73.
- 61. Dhomen N, Marais R. New insight into BRAF mutations in cancer. Curr Opin Genet Dev. 2007; 17(1): 31–9.