>
网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
KRAS基因在胰腺癌发生发展中的作用
作者:荚敏  黄培林 
单位:东南大学医学院, 江苏 南京 210009
关键词:胰腺癌 KRAS基因 炎症 文献综述 
分类号:R735.9
出版年·卷·期(页码):2014·33·第四期(513-516)
摘要:

胰腺癌是危害人类健康的恶性肿瘤之一。KRAS基因作为胰腺癌中常见的基因改变类型,其与胰腺癌间的关系一直是国内外学者研究的重要方向。近年来研究发现,KRAS不仅在胰腺癌的发生中发挥着重要作用,在胰腺癌的进展中也同样必不可少。KRAS将可能成为将来治疗胰腺癌的一个重要靶点。作者对KRAS基因在胰腺癌发生发展中的作用作一综述。

参考文献:

[1] FERLAY J,SHIN H R,BRAY F,et al.Estinates of worldwide burden of cancer in 2008:GLOBOCAN 2008[J].Int J Cancer,2010,127(12):2893-2917.
[2] 陈万青,张思维,郑荣寿,等.中国肿瘤登记地区 2007年肿瘤发病和死亡分析[J].中国肿瘤,2011,20(3):162-169.
[3] ALMOGUERA C,SHIBATA D,FORRESTER K,et al.Most human carcinomas of the exocrine pancreas contain mutant c-KRAS genes[J].Cell,1988,53(4):549-554.
[4] MALUMBRES M,BARBACID M.RAS oncogenes:the first 30 years[J].Nat Rev Cancer,2003,3(6):459-465.
[5] SPAARGAREN M,BISCHOFF J R,McCormick F.Signal transduction by Ras-like GTPases:a potential target for anticancer drugs[J].Gene Expr,1995,4(6):345-356.
[6] SCHEFFZEK K,AHMADIAN M R,KABSCH W,et al.The Ras-RasGAP complex:structural basis for GTPase activation and its loss in oncogenic Ras mutants[J].Science,1997,277(5324):333-338.
[7] JIMENO A,MESSERSMITH W A,HIRSCH F R,et al.KRAS mutations and sensitivity to epidermal growth factor receptor inhibitors in colorectal cancer:practical application of patient selection[J].J Clin Oncol,2009,27(7):1130-1136.
[8] MA E S,WONG C L,LAW F B,et al.Detection of KRAS mutations in colorectal cancer by high-resolution melting analysis[J].J Clin Pathol,2009,62(10):886-891.
[9] BIANKIN A V,WADDELL N,KASSAHN K S,et al.Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes[J].Nature,2012,491(7424):399-405.[ZK)]
[10] JONES S,ZHANG X,PARSONS D W,et al.Core signaling pathways in human pancreatic cancers revealed by global genomic analyses[J].Science,2008,321(5897):1801-1806.
[11] CAMPBELL P M,SINGH A,WILLIAMS F J,et al.Genetic and pharmacologic dissection of Ras effector utilization in oncogenesis[J].Methods Enzymol,2006,407:195-217.
[12] PARSONS B L,MENG F.KRAS mutation in the screening,prognosis and treatment of cancer[J].Biomark Med,2009,3(6):757-769.
[13] HUANG H,DANILUK J,LIU Y,et al.Oncogenic KRAS requires activation for enhanced activity[J].Oncogene,2014,33(4):532-536.
[14] NAVAS C,HERNANDEZ-PORRAS I,SCHUHMACHER A J,et al.EGF receptor signaling is essential for KRAS oncogene-driven pancreatic ductal adenocarcinoma[J].Cancer Cell,2012,22(3):318-330.
[15] DENICOLA G M,TUVESON D A.RAS in cellular transformation and senescence[J].Eur J Cancer,2009,45(1):211-216.
[16] BARDEESY N,AGUIRRE A J,CHU G C,et al.Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse[J].Proc Natl Acad Sci U S A,2006,103(15):5947-5952.
[17] LEE K E,BAR-SAGI D.Oncogenic KRAS suppresses inflammationassociated senescence of pancreatic ductal cells[J].Cancer Cell,2010,18(5):448-458.
[18] GUERRA C,SCHUHMACHER A J,CANAMERO M,et al.Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by KRAS oncogenes in adult mice[J].Cancer Cell,2007,11(3):291-302.
[19] KANDA M,MATTHAEI H,WU J,et al.Presence of somatic mutations in most early-stage pancreatic intraepithelial neoplasia[J].Gastroenterology,2012,142(4):730-733.
[20] COLLINS M A,BEDNAR F,ZHANG Y,et al.Oncogenic KRAS is required for both the initiation and maintenance of pancreatic cancer in mice[J].J Clin Invest,2012,122(2):639-653.
[21] YING H,KIMMELMAN A C,LYSSIOTIS C A,et al.Oncogenic KRAS maintains pancreatic tumors through regulation of anabolic glucose metabolism[J].Cell,2012,149(3):656-670.
[22] MORRIS J P 4TH,CANO D A,SEKINE S,et al.Beta-catenin blocks KRAS-dependent reprogramming of acini into pancreatic cancer precursor lesions in mice[J].J Clin Invest,2010,120(2):508-520.
[23] YACHIDA S,JONES S,BOZIC I,et al.Distant metastasis occurs late during the genetic evolution of pancreatic cancer[J].Nature,2010,467(7319):1114-1147.
[24] JI B,TSOU L,WANG H,et al.Ras activity levels control the development of pancreatic diseases[J].Gastroenterology,2009,137(3):1072-1082.
[25] COLLINS M A,BRISSET J C,ZHANG Y,et al.Metastatic pancreatic cancer is dependent on oncogenic KRAS in mice[J].PLoS One,2012,7(12):e49707.
[26] CLARK C E,HINGORANI S R,MICK R,et al.Dynamics of the immune reaction to pancreatic cancer from inception to invasion[J].Cancer Res,2007,67(19):9518-9527.
[27] CHARO C,HWANG R F,ARUMUGAM T,et al.PGE2 activation of the EP4 receptor regulates stellate cell activity in the pancreatic stromal microenvironment[J].Pancreas,2013,42:467-474.
[28] LESINA M,KURKOWSKI M U,LUDES K,et al.Stat3/Socs3 activation by IL-6 trans-signaling promotes progression of pancreatic intraepithelial neoplasia and development of pancreatic cancer[J].Cancer Cell,2011,19(4):456-469.
[29] PYLAYEVA-GUPTA Y,LEE K E,HAJDU C H,et al.Oncogenic KRAS-induced GM-CSF production promotes the development of pancreatic neoplasia[J].Cancer Cell,2012,21(6):836-847.
[30] HIDALGO M,MAITRA A.The hedgehog pathway and pancreatic cancer[J].N Engl J Med,2009,361:2094-2096.
[31] SEMENZA GL.HIF-1:upstream and downstream of cancer metabolism[J].Curr Opin Genet Dev,2010,20(1):51-60.
[32] NEESSE A,MICHL P,FRESE K K,et al.Stromal biology and therapy in pancreatic cancer[J].Gut,2011,60(6):861-868.

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 412856 位访问者


copyright ©《东南大学学报(医学版)》编辑部
联系电话:025-83272481 83272483
电子邮件:
bjb@pub.seu.edu.cn

苏ICP备09058364