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BRAF突变的黑色素瘤耐药机制研究进展 被引量:10

Research progress of the mechanisms for drug resistance in melanoma with BRAF-mutation
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摘要 黑色素瘤是一种发生于黑色素细胞的恶性肿瘤,临床研究发现在晚期黑色素瘤患者中发生了BRAF(V600E)的突变。目前,临床上已批准的用于治疗BRAF突变黑色素瘤的靶向药物(如ipilimumab和vemurafenib)对黑色素瘤患者有很高的效率,与化疗相比能够明显延长无进展生存期和总生存期,但这些药物在体内所产生的效应是短暂的,大多数患者在不到1年内就会产生耐药。基于BRAF突变黑色素瘤耐药的现状,近几年对于其耐药机制的研究逐渐增多,该文对目前BRAF突变黑色素瘤耐药机制的研究进展及临床治疗策略进行综述,为临床的后续研究和治疗提供参考。 Melanoma is a malignant tumor originated from mela- nin ceils. Clinical researches indicate that BRAF (V600E) has been detected in about 50% of patients with advanced melano- ma. Currently, drugs (such as ipilimumab and vemurafenib ) that have been approved in clinical usage for treating BRAF-mu- tated melanoma show high responses and prolong the progress- free survival and overall survival significantly, as compared with chemotherapy. However, responses are often short-lived, andmost patients develop drug resistance within one year. Recently, an increasing number of studies on drug resistance have been conducted. This paper reviews the research progress of mecha- nisms for BRAF-mutated melanoma, it also includes discussion about the clinical therapy strategies, which may provide refer- ences for follow-up research and clinical treatment.
出处 《中国药理学通报》 CAS CSCD 北大核心 2013年第10期1349-1351,共3页 Chinese Pharmacological Bulletin
基金 国家自然科学基金资助项目(No 81173174 81202655) "十一五"科技支撑计划(No 2008BAI51B02) 教育部博士点基金资助项目(No 20113237110008)
关键词 黑色素瘤 BRAF突变 威罗菲尼 耐药 分子机制 治疗策略 melanoma BRAF-mutated vemurafenib drug re- sistance molecular mechanism therapy strategy
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  • 1初明,魏兰兰,胡志强.白黎芦醇的化学防癌作用及其分子机制的研究进展[J].中国新药与临床杂志,2005,24(3):235-238. 被引量:15
  • 2AGARWALA S S. Novel immunotherapies as potential ther- apeutic partners for traditional or targeted agents:cytotoxic T-lymphocyte antigen-4 blockade in advanced melanoma [J]. Melanoma Res,2010,20( 1 ) :1-10.
  • 3SLINGHIFF G LJR, FLAHERRY K, ROSENBERG S A, et al. Cutaneous melanoma [ M ]//Devita VT Jr, Lawrence T S, Rosenberg S A, Cancer: principles & practice of Oncology, 8thed, Lippincott Williams & wilkins, 2008: 1897-1951.
  • 4TARHINI A, LO E, MINER D R. Releasing the brake on the immune system: ipilimumab and other tumors [ J ]. Cancer Biother Radiopharm,2010,25 (6) :601-613.
  • 5WOLCHOK J O, NEYNS B, LINETI'E G, et al. Ipilimumab monotherapy in patients with pretreated advanced melanoma: a randomized, double-blind, multicentre, phase 2, dose-ranging study [ J ]. Lancet Oncol, 2010, 11 ( 2 ) : 155-164.
  • 6DI GLACOMO A M, DANIELLI R, CALABRO L, et al. Ipilimumab experience in heavily pretreated patients with melanoma in an expanded access program at university hospital of siena (Italy) [ J ]. Cancer Immunol Immunother,2011,60 ( 4 ) :467-477.
  • 7HOSI F S,O'DAY S J, MCDERMOTr D F,et al. Improved survival with ipilimumab in parients with metastatie melanoma [ J ]. N Engl J Med ,2010,363 ( 8 ) :711-723.
  • 8CULVER M E, GATESMAN M L, MANCL E E, et al. Ipili- mumab:a novel treatment for metastatic melanoma [ J ]. Ann Pharmacother ,2011,45(4) :510-519.
  • 9SAMAIK A A,YU B ,YU D ,et al. Extend close ipilimumab with a peptide vaccine:immume correlates associated with clinical benefit in patients with resected high-risk stage Ⅲc/Ⅳ melanoma [ J ]. Clin Cancer Res, 2011,17 ( 4 ) : 896-906.
  • 10KU G Y, YUAN J, PAGE D B, et al. Single-institution expe- rience with ipilimumab in advanced melanoma patients in the compassionate use setting:lymphocyte count after a dose correlates with survival [ J ]. Cancer, 2011,116 ( 7 ) : 1767 - 1775.

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  • 1黄祖杰,周淑清.草地重要有毒植物——狼毒[J].四川草原,1993(4):24-27. 被引量:36
  • 2Emmanuel Eustathios Lagoudianakis,Michael Genetzakis,Dimitrios Konstantinos Tsekouras,Artemisia Papadima,Georgia Kafiri,Konstantinos Toutouzas,Vaggelogiannis Katergiannakis,Andreas Manouras.Primary gastric melanoma: A case report[J].World Journal of Gastroenterology,2006,12(27):4425-4427. 被引量:8
  • 3ValastyanS,WeinbergRA.Tumormetastasis:molecularinsightsandevolvingparadigms[J].Cell,2011,147(2):275-92.
  • 4BuchheitCL,WeigelKJ,SchaferZT.Cancercellsurvivaldur-ingdetachmentfromtheECM:multiplebarrierstotumourprogres-sion[J].NatRevCancer,2014,14(9):632-41.
  • 5PathakA,KumarS.Independentregulationoftumorcellmigra-tionbymatrixstiffnessandconfinement[J].ProcNatlAcadSciUSA,2012,109(26):10334-9.
  • 6HynesRO.Theextracellularmatrix:notjustprettyfibrils[J].Science,2009,326(5957):1216-9.
  • 7KojimaM,HiguchiY,YokotaM,etal.Humansubperitonealfi-broblastandcancercellinteractioncreatesmicroenvironmentthatenhancestumorprogressionandmetastasis[J].PLoSOne,2014,9(2):e88018.
  • 8ShapiroFD,EyreDR.Collagenpolymorphisminextracellularmatrixofhumanosteosarcoma[J].JNatlCancerInst,1982,69(5):1009-16.
  • 9FangM,YuanJ,PengC,LiY.Collagenasadouble-edgedswordintumorprogression[J].TumourBiol,2014,35(4):2871-82.
  • 10MakaleM.Cellularmechanobiologyandcancermetastasis[J].BirthDefectsResCEmbryoToday,2007,81(4):329-43.

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