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Cancer and Metastasis Reviews

Erschienen in:

12.03.2016

Genetic progression of malignant melanoma

verfasst von: J. Tímár, L. Vizkeleti, V. Doma, T. Barbai, E. Rásó

Erschienen in: Cancer and Metastasis Reviews | Ausgabe 1/2016

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Abstract

Malignant melanoma of the skin is the most aggressive human cancer given that a primary tumor a few millimeters in diameter frequently has full metastatic competence. In view of that, revealing the genetic background of this potential may also help to better understand tumor dissemination in general. Genomic analyses have established the molecular classification of melanoma based on the most frequent driver oncogenic mutations (BRAF, NRAS, KIT) and have also revealed a long list of rare events, including mutations and amplifications as well as genetic microheterogeneity. At the moment, it is unclear whether any of these rare events have role in the metastasis initiation process since the major drivers do not have such a role. During lymphatic and hematogenous dissemination, the clonal selection process is evidently reflected by differences in oncogenic drivers in the metastases versus the primary tumor. Clonal selection is also evident during lymphatic progression, though the genetic background of this immunoselection is less clear. Genomic analyses of metastases identified further genetic alterations, some of which may correspond to metastasis maintenance genes. The natural genetic progression of melanoma can be modified by targeted (BRAF or MEK inhibitor) or immunotherapies. Some of the rare events in primary tumors may result in primary resistance, while further new genetic lesions develop during the acquired resistance to both targeted and immunotherapies. Only a few genetic lesions of the primary tumor are constant during natural or therapy-modulated progression. EGFR4 and NMDAR2 mutations, MITF and MET amplifications and PTEN loss can be considered as metastasis drivers. Furthermore, BRAF and MITF amplifications as well as PTEN loss are also responsible for resistance to targeted therapies, whereas NRAS mutation is the only founder genetic lesion showing any association with sensitivity to immunotherapies. Unfortunately, there are hardly any data on the possible organ-specific metastatic drivers in melanoma. These observations suggest that clinical management of melanoma patients must rely on the genetic analysis of the metastatic lesions to be able to monitor progression-associated changes and to personalize therapies.

Balch, C. M., Soong, S.-J., & Thompson, J. F. (2004). The natural history of melanoma and factors predicting outcome. In J. F. Thompson, D. L. Morton, & B. B. R. Kroon (Eds.), Textbook of melanoma (pp. 181–199). London: Taylor & Francis Group.

Whiteman, D. C., Pavan, W. J., & Bastian, B. C. (2011). The melanomas: a synthesis of epidemiological, clinical, histopathological, genetic, and biological aspects, supporting distinct subtypes, causal pathways, and cells of origin. Pigment Cell & Melanoma Research, 24(5), 879–897.CrossRef

The Cancer Genome Atlas Network. (2015). Genomic classification of cutaneous melanoma. Cell, 161(7), 1681–1696.CrossRef

Wiesner, T., Murali, R., Fried, I., Cerroni, L., Busam, K., Kutzner, H., & Bastian, B. C. (2012). A distinct subset of atypical Spitz tumors is characterized by BRAF mutation and loss of BAP1 expression. American Journal of Surgical Pathology, 36(6), 818–30.CrossRefPubMedPubMedCentral

Ismail, I. H., Davidson, R., Gagné, J. P., Xu, Z. Z., Poirier, G. G., & Hendzel, M. J. (2014). Germline mutations in BAP1 impair its function in DNA double-strand break repair. Cancer Research, 74(16), 4282–94.CrossRefPubMed

Scheuermann, J. C., Alonso, A. G. D., Oktaba, K., Ly-Hartig, N., McGinty, R. K., Fraterman, S., et al. (2010). Histone H2A deubiquitinase activity of the Polycomb repressive complex PR-DUB. Nature, 465(7295), 243–247.CrossRefPubMedPubMedCentral

Ventii, K. H., Devi, N. S., Friedrich, K. L., Chernova, T. A., Tighiouart, M., Van Meir, E. G., et al. (2008). BRCA1-associated protein-1 is a tumor suppressor that requires deubiquitinating activity and nuclear localization. Cancer Research, 68(17), 6953–6962.CrossRefPubMedPubMedCentral

Hodis, E., Watson, I. R., Kryukov, G. V., Arold, S. T., Imielinski, M., Theurillat, J. P., et al. (2012). A landscape of driver mutations in melanoma. Cell, 150(2), 251–263.CrossRefPubMedPubMedCentral

Berger, M. F., Hodis, E., Heffernan, T. P., Deribe, Y. L., Lawrence, M. S., Protopopov, A., et al. (2012). Melanoma genome sequencing reveals frequent PREX2 mutations. Nature, 485(7399), 502–506.PubMedPubMedCentral

10.

Krauthammer, M., Kong, Y., Bacchiocchi, A., Evans, P., Pornputtapong, N., Wu, C., et al. (2015). Exome sequencing identifies recurrent mutations in NF1 and RASopathy genes in sun-exposed melanomas. Nature Genetics, 47(9), 996–1002.CrossRefPubMed

11.

Manca, A., Lissia, A., Cossu, A., Rubino, C., Ascierto, P. A., Stanganelli, I., et al. (2013). Mutations in ERBB4 may have a minor role in melanoma pathogenesis. Jornal of Investigative Dermatology, 133(6), 1685–1687.CrossRef

12.

Guan, J., Gupta, R., & Filipp, F. V. (2015). Cancer systems biology of TCGA SKCM: efficient detection of genomic drivers in melanoma. Scientific Reports, 5, 7857.CrossRefPubMedPubMedCentral

13.

Lee, J. J., Sholl, L. M., Lindeman, N. I., Granter, S. R., Laga, A. C., Shivdasani, P., et al. (2015). Targeted next-generation sequencing reveals high frequency of mutations in epigenetic regulators across treatment-naive patient melanomas. Clinical Epigenetics, 7(1), 59.CrossRefPubMedPubMedCentral

14.

Timar, J., Barbai, T., Győrffy, B., & Rásó, E. (2013). Understanding melanoma progression by gene expression signatures. In U. Pfeffer (Ed.), Cancer genomics: Molecular classification, prognosis and response prediction (pp. 47–79). Dordrecht: Springer.CrossRef

15.

Wei, X., Walia, V., Lin, J. C., Teer, J. K., Prickett, T. D., Gartner, J., et al. (2011). Exome sequencing identifies GRIN2A as frequently mutated in melanoma. Nature Genetics, 43(5), 442–446.CrossRefPubMedPubMedCentral

16.

Viros, A., Fridlyand, J., Bauer, J., Lasithiotakis, K., Garbe, C., Pinkel, D., et al. (2008). Improving melanoma classification by integrating genetic and morphologic features. PLoS Medicine, 5(6), e120.CrossRefPubMedPubMedCentral

17.

Harbst, K., Staaf, J., Lauss, M., Karlsson, A., Masback, A., Johansson, I., et al. (2012). Molecular profiling reveals low- and high-grade forms of primary melanoma. Clinical Cancer Research, 18(15), 4026–4036.CrossRefPubMedPubMedCentral

18.

Hoek, K. S., Schlegel, N. C., Brafford, P., Sucker, A., Ugurel, S., Kumar, R., et al. (2006). Metastatic potential of melanomas defined by specific gene expression profiles with no BRAF signature. Pigment Cell Research, 19(4), 290–302.CrossRefPubMed

19.

Allison, K. H., & Sledge, G. W. (2014). Heterogeneity and cancer. [Review]. Oncology (Williston Park), 28(9), 772–778.

20.

Jamal-Hanjani, M., Quezada, S. A., Larkin, J., & Swanton, C. (2015). Translational implications of tumor heterogeneity. Clinical Cancer Research, 21(6), 1258–1266.CrossRefPubMedPubMedCentral

21.

Wang, E., Voiculescu, S., Le Poole, I. C., El-Gamil, M., Li, X., Sabatino, M., et al. (2006). Clonal persistence and evolution during a decade of recurrent melanoma. The Journal of Investigative Dermatology, 126(6), 1372–1377.CrossRefPubMed

22.

Chiappetta, C., Proietti, I., Soccodato, V., Puggioni, C., Zaralli, R., Pacini, L., et al. (2015). BRAF and NRAS mutations are heterogeneous and not mutually exclusive in nodular melanoma. Applied Immunohistochemistry & Molecular Morphology, 23(3), 172–177.CrossRef

23.

Lamy, P. J., Castan, F., Lozano, N., Montelion, C., Audran, P., Bibeau, F., et al. (2015). Next-generation genotyping by digital PCR to detect and quantify the BRAF V600E mutation in melanoma biopsies. The Journal of Molecular Diagnostics, 17(4), 366–373.CrossRefPubMed

24.

Ding, L., Kim, M. J., Kanchi, K. L., Dees, N. D., Lu, C., Griffith, M., et al. (2014). Clonal architectures and driver mutations in metastatic melanomas. PLoS One, 9(11).

25.

Menzies, A. M., Lum, T., Wilmott, J. S., Hyman, J., Kefford, R. F., Thompson, J. F., et al. (2014). Intrapatient homogeneity of BRAFV600E expression in melanoma. The American Journal of Surgical Pathology, 38(3), 377–382.CrossRefPubMed

26.

Riveiro-Falkenbach, E., Villanueva, C. A., Garrido, M. C., Ruano, Y., Garcia-Martin, R. M., Godoy, E., et al. (2015). Intra- and inter-tumoral homogeneity of BRAF mutations in melanoma tumors. The Journal of Investigative Dermatology. doi:10.1038/jid.2015.229.PubMed

27.

Orgaz, J. L., & Sanz-Moreno, V. (2013). Emerging molecular targets in melanoma invasion and metastasis. Pigment Cell & Melanoma Research, 26(1), 39–57.CrossRef

28.

Barbai, T., Fejős, Z., Puskas, L. G., Tímár, J., & Rásó, E. (2015). The importance of the microenvironment: the role of CCL8 in metastasis formation of melanoma. Oncotarget, 6, 29111–29128.PubMedPubMedCentral

29.

Dome, B., Paku, S., Somlai, B., & Timar, J. (2002). Vascularization of cutaneous melanoma involves vessel co-option and has clinical significance. Journal of Pathology, 197(3), 355–362.CrossRefPubMed

30.

Christianson, D. R., Dobroff, A. S., Proneth, B., Zurita, A. J., Salameh, A., Dondossola, E., et al. (2015). Ligand-directed targeting of lymphatic vessels uncovers mechanistic insights in melanoma metastasis. Proceedings of the National Academy of Sciences of the United States of America, 112(8), 2521–2526.CrossRefPubMedPubMedCentral

31.

Leong, S. P., Mihm, M. C., Jr., Murphy, G. F., Hoon, D. S., Kashani-Sabet, M., Agarwala, S. S., et al. (2012). Progression of cutaneous melanoma: implications for treatment. Clinical & Experimental Metastasis, 29(7), 775–796.CrossRef

32.

Pasquali, S., & Spillane, A. (2014). Contemporary controversies and perspectives in the staging and treatment of patients with lymph node metastasis from melanoma, especially with regards positive sentinel lymph node biopsy. [Review]. Cancer Treatment Reviews, 40(8), 893–899.CrossRefPubMed

33.

Hendrix, M. J. C., Seftor, E. A., Hess, A. R., & Seftor, R. E. B. (2003). Vasculogenic mimicry and tumour-cell plasticity: lessons from melanoma. Nature Reviews Cancer, 3(6), 411–421.CrossRefPubMed

34.

Trikha, M., Timar, J., Zacharek, A., Nemeth, J. A., Cai, Y. L., Dome, B., et al. (2002). Role for beta 3 integrins in human melanoma growth and survival. International Journal of Cancer, 101(2), 156–167.CrossRefPubMed

35.

Timar, J., Raso, E., Dome, B., Ladanyi, A., Banfalvi, T., Gilde, K., et al. (2002). Expression and function of the AMF receptor by human melanoma in experimental and clinical systems. Clinical & Experimental Metastasis, 19(3), 225–232.CrossRef

36.

Moro, N., Mauch, C., & Zigrino, P. (2014). Metalloproteinases in melanoma. European Journal of Cell Biology, 93(1–2), 23–29.CrossRefPubMed

37.

Menter, D. G., Tucker, S. C., Kopetz, S., Sood, A. K., Crissman, J. D., & Honn, K. V. (2014). Platelets and cancer: a casual or causal relationship: revisited. Cancer and Metastasis Reviews, 33(1), 231–269.CrossRefPubMedPubMedCentral

38.

Tellez, C., McCarty, M., Ruiz, M., & Bar-Eli, M. (2003). Loss of activator protein-2alpha results in overexpression of protease-activated receptor-1 and correlates with the malignant phenotype of human melanoma. The Journal of Biological Chemistry, 278(47), 46632–46642.CrossRefPubMed

39.

Raso, E., Dome, B., Somlai, B., Zacharek, A., Hagmann, W., Honn, K. V., et al. (2004). Molecular identification, localization and function of platelet-type 12-lipoxygenase in human melanoma progression, under experimental and clinical conditions. Melanoma Research, 14(4), 245–250.CrossRefPubMed

40.

Timar, J., Tovari, J., Raso, E., Meszaros, L., Bereczky, B., & Lapis, K. (2005). Platelet-mimicry of cancer cells: epiphenomenon with clinical significance. Oncology, 69(3), 185–201.CrossRefPubMed

41.

Morton, D. L., Thompson, J. F., Cochran, A. J., Mozzillo, N., Nieweg, O. E., Roses, D. F., et al. (2014). Final trial report of sentinel-node biopsy versus nodal observation in melanoma. The New England Journal of Medicine, 370(7), 599–609.CrossRefPubMedPubMedCentral

42.

Hendrix, M. J. C., Seftor, E. A., Hess, A. R., & Seftor, R. E. B. (2003). Molecular plasticity of human melanoma cells. Oncogene, 22(20), 3070–3075.CrossRefPubMed

43.

Zabierowski, S. E., & Herlyn, M. (2008). Melanoma stem cells: the dark seed of melanoma. [Review]. Journal of Clinical Oncology, 26(17), 2890–2894.CrossRefPubMed

44.

Murphy, G. F., Wilson, B. J., Girouard, S. D., Fraqnk, N. Y., & Frank, M. H. (2014). Stem cells and target approaches to melanoma cure. Molecular Aspects of Medicine, 39, 33–49.CrossRefPubMed

45.

Bramer, R. R., Watson, I. R., Wu, C.-J., Mobley, A. K., Kamiya, T., Shoshan, E., et al. (2013). Why is melanoma so metastatic? Pigment Cell & Melanoma Research, 27, 19–36.

46.

Shakhova, O. (2014). Neural crest stem cells in melanoma development. Current Opinion in Oncology, 26, 215–221.CrossRefPubMed

47.

Döme, B., Somlai, B., Ladányi, A., Fazekas, K., Zöller, M., & Tímár, J. (2001). Expression of CD44v3 splice variant is associated with the visceral metastatic phenotype of human melanoma. Virchows Archiv, 439, 628–635.CrossRefPubMed

48.

Raso-Barnett, L., Banky, B., Barbai, T., Becsagh, P., Timar, J., & Raso, E. (2013). Demonstration of a melanoma-specific CD44 alternative splicing pattern that remains qualitatively stable, but shows quantitative changes during tumour progression. Plos One, 8, e53883.CrossRefPubMedPubMedCentral

49.

Döme, B., Somlai, B., & Tímár, J. (2000). The loss of NM23 protein in malignant melanoma predicts lymphatic spread without affecting survival. Anticancer Research, 20, 3971–3974.PubMed

50.

Lee, J. H., Miele, M. E., Hicks, D. J., Phillips, K. K., Trent, J. M., Weissman, B. E., et al. (1996). KiSS-1, a novel human malignant melanoma metastasis-suppressor gene. Journal of the National Cancer Institute, 88(23), 1731–1737.CrossRefPubMed

51.

Kim, M., Gans, J. D., Nogueira, C., Wang, A., Paik, J. H., Feng, B., et al. (2006). Comparative oncogenomics identifies NEDD9 as a melanoma metastasis gene. Cell, 125(7), 1269–1281.CrossRefPubMed

52.

Cirenajwis, H., Ekedahl, H., Lauss, M., Harbst, K., Carneiro, A., Enoksson, J., et al. (2015). Molecular stratification of metastatic melanoma using gene expression profiling: prediction of survival outcome and benefit from molecular targeted therapy. Oncotarget, 6(14), 12297–12309.CrossRefPubMedPubMedCentral

53.

Verfaillie, A., Imrichova, H., Atak, Z. K., Dewaele, M., Rambow, F., Hulselmans, G., et al. (2015). Decoding the regulatory landscape of melanoma reveals TEADS as regulators of the invasive cell state. Nature Communications, 6, 6683. doi:10.1038/Ncomms7683.CrossRefPubMedPubMedCentral

54.

Park, J. Y., Amankwah, E. K., Anic, G. M., Lin, H. Y., Walls, B., Park, H., et al. (2013). Gene variants in angiogenesis and lymphangiogenesis and cutaneous melanoma progression. Cancer Epidemiology, Biomarkers & Prevention, 22(5), 827–834.CrossRef

55.

Carlino, M. S., Haydu, L. E., Kakavand, H., Menzies, A. M., Hamilton, A. L., Yu, B., et al. (2014). Correlation of BRAF and NRAS mutation status with outcome, site of distant metastasis and response to chemotherapy in metastatic melanoma. British Journal of Cancer, 111(2), 292–299.CrossRefPubMedPubMedCentral

56.

Pracht, M., Mogha, A., Lespagnol, A., Fautrel, A., Mouchet, N., Le Gall, F., et al. (2015). Prognostic and predictive values of oncogenic BRAF, NRAS, c-KIT and MITF in cutaneous and mucous melanoma. Journal of the European Academy of Dermatology and Venereology, 29(8), 1530–1538.CrossRefPubMed

57.

Thomas, N. E., Edmiston, S. N., Alexander, A., Groben, P. A., Parrish, E., Kricker, A., et al. (2015). Association between and mutational status and melanoma-specific survival among patients with higher risk primary melanoma. JAMA Oncology, 1(3), 359–368.CrossRefPubMed

58.

Chiu, C. G., Nakamura, Y., Chong, K. K., Huang, S. K., Kawas, N. P., Triche, T., et al. (2014). Genome-wide characterization of circulating tumor cells identifies novel prognostic genomic alterations in systemic melanoma metastasis. Clinical Chemistry, 60(6), 873–885.CrossRefPubMed

59.

Colombino, M., Lissia, A., Capone, M., De Giorgi, V., Massi, D., Stanganelli, I., et al. (2013). Heterogeneous distribution of BRAF/NRAS mutations among Italian patients with advanced melanoma. Journal of Translational Medicine, 11, 202.CrossRefPubMedPubMedCentral

60.

Colombino, M., Capone, M., Lissia, A., Cossu, A., Rubino, C., De Giorgi, V., et al. (2012). BRAF/NRAS mutation frequencies among primary tumors and metastases in patients with melanoma. Journal of Clinical Oncology, 30(20), 2522–2529.CrossRefPubMed

61.

Shinozaki, M., Fujimoto, A., Morton, D. L., & Hoon, D. S. (2004). Incidence of BRAF oncogene mutation and clinical relevance for primary cutaneous melanomas. Clinical Cancer Research, 10(5), 1753–1757.CrossRefPubMed

62.

Saroufim, M., Habib, R. H., Gerges, R., Saab, J., Loya, A., Amr, S. S., et al. (2014). Comparing BRAF mutation status in matched primary and metastatic cutaneous melanomas: implications on optimized targeted therapy. Experimental and Molecular Pathology, 97(3), 315–320.CrossRefPubMed

63.

Bradish, J. R., Richey, J. D., Post, K. M., Meehan, K., Sen, J. D., Malek, A. J., et al. (2015). Discordancy in BRAF mutations among primary and metastatic melanoma lesions: clinical implications for targeted therapy. Modern Pathology, 28(4), 480–486.CrossRefPubMed

64.

Yancovitz, M., Litterman, A., Yoon, J., Ng, E., Shapiro, R. L., Berman, R. S., et al. (2012). Intra- and inter-tumor heterogeneity of BRAF(V600E))mutations in primary and metastatic melanoma. PLoS One, 7(1), e29336.CrossRefPubMedPubMedCentral

65.

Heinzerling, L., Baiter, M., Kuhnapfel, S., Schuler, G., Keikavoussi, P., Agaimy, A., et al. (2013). Mutation landscape in melanoma patients clinical implications of heterogeneity of BRAF mutations. British Journal of Cancer, 109(11), 2833–2841.CrossRefPubMedPubMedCentral

66.

Boursault, L., Haddad, V., Vergier, B., Cappellen, D., Verdon, S., Bellocq, J. P., et al. (2013). Tumor homogeneity between primary and metastatic sites for BRAF status in metastatic melanoma determined by immunohistochemical and molecular testing. PLoS One, 8(8), e70826.CrossRefPubMedPubMedCentral

67.

Eriksson, H., Zebary, A., Vassilaki, I., Omholt, K., Ghaderi, M., & Hansson, J. (2015). BRAFV600E protein expression in primary cutaneous malignant melanomas and paired metastases. JAMA Dermatology, 151(4), 410–416.CrossRefPubMed

68.

Nardin, C., Puzenat, E., Pretet, J. L., Algros, M. P., Doussot, A., Puyraveau, M., et al. (2015). BRAF mutation screening in melanoma: is sentinel lymph node reliable? Melanoma Research, 25(4), 328–334.CrossRefPubMed

69.

Anaka, M., Hudson, C., Lo, P. H., Do, H., Caballero, O. L., Davis, I. D., et al. (2013). Intratumoral genetic heterogeneity in metastatic melanoma is accompanied by variation in malignant behaviors. BMC Medical Genomics, 6, 40. doi:10.1186/1755-8794-6-40.CrossRefPubMedPubMedCentral

70.

Gartner, J. J., Davis, S., Wei, X. M., Lin, J. C., Trivedi, N. S., Teer, J. K., et al. (2012). Comparative exome sequencing of metastatic lesions provides insights into the mutational progression of melanoma. BMC Genomics, 13, 505. doi:10.1186/1471-2164-13-505.CrossRefPubMedPubMedCentral

71.

Koh, S. S., Wei, J. P. J., Li, X. M., Huang, R. R., Doan, N. B., Scolyer, R. A., et al. (2012). Differential gene expression profiling of primary cutaneous melanoma and sentinel lymph node metastases. Modern Pathology, 25(6), 828–837.CrossRefPubMed

72.

Sabatino, M., Zhao, Y., Voiculescu, S., Monaco, A., Robbins, P., Karai, L., et al. (2008). Conservation of genetic alterations in recurrent melanoma supports the melanoma stem cell hypothesis. Cancer Research, 68(1), 122–131.CrossRefPubMed

73.

Carlino, M. S., Long, G. V., Kefford, R. F., & Rizos, H. (2015). Targeting oncogenic BRAF and aberrant MAPK activation in the treatment of cutaneous melanoma. [Review]. Critical Reviews in Oncology/Hematology. doi:10.1016/j.critrevonc.2015.08.021.PubMed

74.

Michielin, O., & Hoeller, C. (2015). Gaining momentum: new options and opportunities for the treatment of advanced melanoma. [Review]. Cancer Treatment Reviews, 41(8), 660–670.CrossRefPubMed

75.

Van Allen, E. M., Wagle, N., Sucker, A., Treacy, D. J., Johannessen, C. M., Goetz, E. M., et al. (2014). The genetic landscape of clinical resistance to RAF inhibition in metastatic melanoma. Cancer Discovery, 4(1), 94–109.CrossRefPubMedPubMedCentral

76.

Spagnolo, F., Ghiorzo, P., Orgiano, L., Pastorino, L., Picasso, V., Tornari, E., et al. (2015). BRAF-mutant melanoma: treatment approaches, resistance mechanisms, and diagnostic strategies. [Review]. Oncology Targets and Therapy, 8, 157–168.CrossRef

77.

Nazarian, R., Shi, H., Wang, Q., Kong, X., Koya, R. C., Lee, H., et al. (2010). Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation. Nature, 468(7326), 973–977.CrossRefPubMedPubMedCentral

78.

Wheler, J., Yelensky, R., Falchook, G., Kim, K. B., Hwu, P., Tsimberidou, A. M., et al. (2015). Next generation sequencing of exceptional responders with BRAF-mutant melanoma: implications for sensitivity and resistance. BMC Cancer, 15, 61. doi:10.1186/s12885-015-1029-z.CrossRefPubMedPubMedCentral

79.

Hoogstraat, M., Gadellaa-van Hooijdonk, C. G., Ubink, I., Besselink, N. J., Pieterse, M., Veldhuis, W., et al. (2015). Detailed imaging and genetic analysis reveal a secondary BRAF(L505H) resistance mutation and extensive intrapatient heterogeneity in metastatic BRAF mutant melanoma patients treated with vemurafenib. Pigment Cell & Melanoma Research, 28(3), 318–323.CrossRef

80.

Wagle, N., Emery, C., Berger, M. F., Davis, M. J., Sawyer, A., Pochanard, P., et al. (2011). Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling. Journal of Clinical Oncology, 29(22), 3085–3096.CrossRefPubMedPubMedCentral

81.

Johannessen, C. M., Boehm, J. S., Kim, S. Y., Thomas, S. R., Wardwell, L., Johnson, L. A., et al. (2010). COT drives resistance to RAF inhibition through MAP kinase pathway reactivation. Nature, 468(7326), 968–972.CrossRefPubMedPubMedCentral

82.

Roesch, A. (2015). Tumor heterogeneity and plasticity as elusive drivers for resistance to MAPK pathway inhibition in melanoma. Oncotarget, 34, 2951–2957.

83.

Shi, H., Moriceau, G., Kong, X., Koya, R. C., Nazarian, R., Pupo, G. M., et al. (2012). Preexisting MEK1 exon 3 mutations in V600E/KBRAF melanomas do not confer resistance to BRAF inhibitors. Cancer Discovery, 2(5), 414–424.CrossRefPubMedPubMedCentral

84.

Jönsson, G., Busch, C., Knappskog, S., Geisler, J., Miletic, H., Ringner, M., et al. (2010). Gene expression profiling-based identification of molecular subtypes in stage IV melanomas with different clinical outcome. Clinical Cancer Research, 16(13), 3356–3367.CrossRefPubMed

85.

Krepler, C., Certa, U., Wacheck, V., Jansen, B., Wolff, K., & Pehamberger, H. (2004). Pegylated and conventional interferon-alpha induce comparable transcriptional responses and inhibition of tumor growth in a human melanoma SCID mouse xenotransplantation model. Journal of Investigative Dermatology, 123(4), 664–669.CrossRefPubMed

86.

Johnson, D. B., Lovly, C. M., Flavin, M., Panageas, K. S., Ayers, G. D., Zhao, Z., et al. (2015). Impact of NRAS mutations for patients with advanced melanoma treated with immune therapies. Cancer Immunology Research, 3(3), 288–295.CrossRefPubMedPubMedCentral

87.

Shin, D. S., & Ribas, A. (2015). The evolution of checkpoint blockade as a cancer therapy: what’s here, what’s next? Current Opinion in Immunology, 33, 23–35.CrossRefPubMed

88.

Snyder, A., Wolchok, J. D., & Chan, T. A. (2015). Genetic basis for clinical response to CTLA-4 blockade. [Comment Letter]. The New England Journal of Medicine, 372(8), 783.CrossRefPubMed

89.

Herbst, R. S., Soria, J. C., Kowanetz, M., Fine, G. D., Hamid, O., Gordon, M. S., et al. (2014). Predictive correlates of response to the anti-PD-L1 antibody MPDL3280A in cancer patients. Nature, 515(7528), 563–567.CrossRefPubMed

Titel: Genetic progression of malignant melanoma
verfasst von: J. Tímár
L. Vizkeleti
V. Doma
T. Barbai
E. Rásó
Publikationsdatum: 12.03.2016
Verlag: Springer US
Erschienen in: Cancer and Metastasis Reviews / Ausgabe 1/2016
Print ISSN: 0167-7659
Elektronische ISSN: 1573-7233
DOI: https://doi.org/10.1007/s10555-016-9613-5

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