Korn E L, Liu P Y, Lee S J, et al. Meta-analysis of phase II cooperative group trials in metastatic stage IV melanoma to determine progressionfree and overall survival benchmarks for future phase II trials[J]. Journal of clinical oncology: Official Journal of the American Society of Clinical Oncology, 2008, 26(4): 527-534.
[2]
Atkins M B, Lotze M T, Dutcher J P, et al. High-dose recombinant interleukin 2 therapy for patients with metastatic melanoma: Analysis of 270 patients treated between 1985 and 1993[J]. Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology, 1999, 17(7): 2105-2116.
[3]
Kaplan F M, Kugel C H, Dadpey N, et al. SHOC2 and CRAF mediate ERK1/2 reactivation in mutant NRAS- mediated resistance to RAF inhibitor[J]. The Journal of Biological Chemistry, 2012, 287(50): 41797-41807.
[4]
Carlino M S, Fung C, Shahheydari H, et al. Correlation between preexisting MEK1P124 mutations and clinical and in vitro response to BRAF inhibitors in metastatic melanoma[C]. ASCO Annual Meeting, Chicago, May 30-June 3, 2014.
[5]
Long G V, Stroyakovsky D L, Gogas H, et al. COMBI-d: A randomized, double- blinded, Phase III study comparing the combination of dabrafenib and trametinib to dabrafenib and trametinib placebo as first- line therapy in patients (pts) with unresectable or metastatic BRAFV600E/K mutation-positive cutaneous melanoma[C]. ASCO Annual Meeting, Chicago, May 30-June 3, 2014.
[6]
Hersey P, Wroblewski D, Mijatov B, et al. Effect of the BH3 mimetic ABT-737 on human melanoma cells to apoptosis induced by selective BRAF inhibitors[J]. Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology, 2012, 30(Sl): a8553.
[7]
Lebbe C, Howkit A, Sadoux A, et al. BRAFV600 mutation levels and response to vemurafenib in metastatic melanoma[C]. ASCO Annual Meeting, Chicago, May 30-June 3, 2014.
[8]
Kirkwood J M, Georgina V L, Trefzer U, et al. A phase II study assessing overall intracranial response rate (OIRR) to dabrafenib (GSK2118436) in patients (pts) with BRAFV600E/k mutation- positive melanoma with brain metastases[J]. Official Journal of the American Society of Clinical Oncology, 2012, 30(Sl): a8501.
[9]
Van Elsas A, Hurwitz A A, Allison J P. Combination immunotherapy of B16 melanoma using anti-cytotoxic T lymphocyte-associated antigen 4 (CTLA- 4) and granulocyte/macrophage colony- stimulating factor (GM-CSF)-producing vaccines induces rejection of subcutaneous and metastatic tumors accompanied by autoimmune depigmentation[J]. Journal of Experimental Medicine, 1999, 190(3): 355-366.
[10]
Hodi F S, Mihm M C, Soiffer R J, et al. Biologic activity of cytotoxic T lymphocyte- associated antigen 4 antibody blockade in previously vaccinated metastatic melanoma and ovarian carcinoma patients[J]. Proceedings of the National Academy of Sciences USA, 2003, 100(8): 4712-4717.
[11]
O'Day S J, Maio M, Chiarion-Sileni V, et al. Efficacy and safety of ipilimumab monotherapy in patients with pretreated advanced melanoma: A multicenter single-arm phase II study[J]. Annals of Oncology, 2010, 21(8): 1712-1717.
[12]
Weber J S, O'Day S, Urba W, et al. Phase I/II study of ipilimumab for patients with metastatic melanoma[J]. Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology, 2008, 26(36): 5950-5956.
[13]
Ribas A, Pavlov D, Marshall M A, et al. Phase III randomized clinical trial comparing tremelimumab with standard-of-care chemotherapy in patients with advanced melanoma[J]. Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology, 2013, 31(5): 616-622.
[14]
Lian B, Si L, Cui C, et al. Phase II randomized trial comparing highdose IFN-α2b with temozolomide plus cisplatin as systemic adjuvant therapy for resected mucosal melanoma[J]. Clinical Cancer Research, 2013, 19(16): 4488-4498.
[15]
Bodenham D C. A study of 650 observed malignant melanomas in the South- West region[J]. Annals of the Royal College of Surgeons of England, 1968, 43(4): 218-239.
[16]
Yang A, Chapman P. The history and future of chemotherapy for melanoma[J]. Hamatology/Oncology Clinics of N America, 2009, 23(3): 583-597.
[17]
Kirkwood J M, Manola J, Ibrahim J, et al. A pooled analysis of eastern cooperative oncology group and intergroup trials of adjuvant high-dose interferon for melanoma[J]. Clinical Cancer Research, 2004, 10(5): 1670-1677.
[18]
Dong J, Phelps R G, Qiao R, et al. BRAF oncogenic mutations correlate with progression rather than initiation of human melanoma[J]. Cancer Research, 2003, 63(14): 3883-3885.
[19]
Chapman P B, Hauschild A, Robert C, et al. Improved survival with vemurafenib in melanoma with BRAF V600E mutation[J]. New England Journal of Medicine, 2011, 364(26): 2507-2516.
[20]
Si L, Kong Y, Xu X, et al. Prevalence of BRAFV600E mutation in Chinese melanoma patients: Large scale analysis of BRAF and NRAS mutations in a 432-case cohort[J]. European Journal of Cancer, 2012, 48(1): 94- 100.
[21]
Hauschild A, Grob J J, Demidov L V, et al. Dabrafenib in BRAFmutated metastatic melanoma: A multicentre, open- label, phase 3 randomised controlled trial[J]. Lancet, 2012, 380(9839): 358-365.
[22]
Sosman J A, Kim K B, Schuchter L, et al. Survival in BRAF V600- mutant advanced melanoma treated with vemurafenib[J]. New England Journal of Medicine, 2012, 366(8): 707-714.
[23]
Kong Y, Si L, Zhu Y, et al. Large scale analysis of KIT aberrations in Chinese patients with melanoma[J]. Clinical Cancer Research, 2011, 17(7): 1684-1691.
[24]
Guo J, Si L, Kong Y, et al. A phase II, open label, single-arm trial of imatinib mesylate in patients with metastatic melanoma harboring c- Kit mutation or amplification[J]. Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology, 2011, 29(21): 2904-2909.
[25]
Carvajal R D, Antonescu C R, Wolchok J D, et al. KIT as a therapeutic target in metastatic melanoma[J]. The Journal of the American Medical Association, 2011, 305(22): 2327-2334.
[26]
Hodi F S, Friedlander P, Corless C L, et al. Major response to imatinib mesylate in KIT-mutated melanoma[J]. Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology, 2008, 26: 2046-2051.
[27]
Si L, Xu X, Kong Y, et al. Major response to everolimus in melanoma with acquired imatinib- resistance[J]. Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology, 2012, 30(4): e37-40.
[28]
Flaherty K T, Robert C, Hersey P, et al. Improved survival with MEK inhibition in BRAF- mutated melanoma[J]. New England Journal of Medicine, 2012, 367(2): 107-114.
[29]
Ascierto P A, Schadendorf D, Berking C, et al. MEK162 for patients with advanced melanoma harbouring NRAS or Val600 BRAF mutations: A non- randomised, open- label phase 2 study[J]. Lancet Oncology, 2013, 14(3): 249-256.
[30]
Sosman J A, Kittaneh M, Martijn P J K, et al. A phase 1b/2 study of LEE011 in combination with binimetinib (MEK162) in patients with NRAS-mutant melanoma: Early encouraging clinical activity[C]. ASCO Annual Meeting, Chicago, May 30-June 3, 2014.
[31]
Alegre M L, Shiels H, Thompson C B, et al. Expression and function of CTLA-4 in Th1 and Th2 cells[J]. Journal of Immunology, 1998, 161 (7): 3347-3356.
[32]
Hurwitz A A, Foster B A, Kwon E D, et al. Combination immunotherapy of primary prostate cancer in a transgenic mouse model using CTLA- 4 blockade[J]. Cancer Research, 2000, 60(9): 2444-2448.
[33]
Kwon E D, Foster B A, Hurwitz A A, et al. Elimination of residual metastatic prostate cancer after surgery and adjunctive cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) blockade immunotherapy[J]. Proceedings of the National Academy of Sciences USA, 1999, 96 (26): 15074-15079.
[34]
Phan G Q, Yang J C, Sherry R M, et al. Cancer regression and autoimmunity induced by cytotoxic T lymphocyte-associated antigen 4 blockade in patients with metastatic melanoma[J]. Proceedings of the National Academy of Sciences USA, 2003, 100(14): 8372-8377.
[35]
Attia P, Phan G Q, Maker A V, et al. Autoimmunity correlates with tumor regression in patients with metastatic melanoma treated with anti-cytotoxic T-lymphocyte antigen-4[J]. Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology, 2005, 23(25): 6043-6053.
[36]
Maker A V, Phan G Q, Attia P, et al. Tumor regression and autoimmunity in patients treated with cytotoxic T lymphocyteassociated antigen 4 blockade and interleukin 2: A phase I/II study[J]. Annals of Surgical Oncology, 2005, 12(12): 1005-1016.
[37]
Hodi F S, O'Day S J, McDermott D F, et al. Improved survival with ipilimumab in patients with metastatic melanoma[J]. New England Journal of Medicine, 2010, 363(8): 711-723.
[38]
Kahler K C, Hauschild A. Treatment and side effect management of CTLA- 4 antibody therapy in metastatic melanoma[J]. Journal Der Ddutschen Dermatologischen Gesellschaft, 2011, 9(4): 277-286.
[39]
Kirkwood J M, Lorigan P, Hersey P, et al. Phase II trial of tremelimumab (CP- 675,206) in patients with advanced refractory or relapsed melanoma[J]. Clinical Cancer Research, 2010, 16(3): 1042-1048.
[40]
Ribas A, Hodi F S, Kefford R, et al. Efficacy and safety of the anti- PD-1 monoclonal antibody MK-3475 in 411 patients (pts) with melanoma (MEL)[C]. ASCO Annual Meeting, Chicago, May 30-June 3, 2014.
[41]
Sznol M, Kluger H M, Margaret K, et al. Survival, response duration, and activity by BRAF mutation (MT) status of nivolumab (NIVO, anti- PD- 1, BMS- 936558, ONO- 4538) and ipilimumab (IPI) concurrent therapy in advanced melanoma (MEL) [C]. ASCO Annual Meeting, Chicago, May 30-June 3, 2014.
