[1] Navas C, HernándezPorras I, Schuhmacher AJ, et al. EGF receptor signaling is essential for kras oncogenedriven pancreatic ductal adenocarcinoma[J]. Cancer Cell, 2012, 22(3):318330.
[2] Sebio A, Paré L, Páez D, et al. The LCS6 polymorphism in the binding site of let7 microRNA to the KRAS 3′untranslated region: its role in the efficacy of antiEGFRbased therapy in metastatic colorectal cancer patients[J]. Pharmacogenet Genomics, 2013, 23(3):142147.
[3] Troiani T, Zappavigna S, Martinelli E, et al. Optimizing treatment of metastatic colorectal cancer patients with antiEGFR antibodies: overcoming the mechanisms of cancer cell resistance[J]. Expert Opin Biol Ther, 2013, 13(2):241255.
[4] Linardou H, Dahabreh IJ, Kanaloupiti D, et al. Assessment of somatic kRAS mutations as a mechanism associated with resistance to EGFRtargeted agents: a systematic review and metaanalysis of studies in advanced nonsmallcell lung cancer and metastatic colorectal cancer[J]. Lancet Oncol, 2008, 9(10):962972.
[5] Bach LA, Fu P, Yang Z. Insulinlike growth factorbinding protein6 and cancer[J]. Clin Sci (Lond), 2013, 124(4):215229.
[6] Ramos FJ, Macarulla T, Capdevila J, et al. Understanding the predictive role of Kras for epidermal growth factor receptortargeted therapies in colorectal cancer[J]. Clin Colorectal Cancer, 2008, 7 Suppl 2:S5257.
[7] Karapetis CS, KhambataFord S, Jonker DJ, et al. Kras mutations and benefit from cetuximab in advanced colorectal cancer[J]. N Engl J Med, 2008, 359(17):17571765.
[8] De Roock W, Piessevaux H, De Schutter J, et al. KRAS wildtype state predicts survival and is associated to early radiological response in metastatic colorectal cancer treated with cetuximab[J]. Ann Oncol, 2008, 19(3):508515.
[9] Dempke WC, Heinemann V. Ras mutational status is a biomarker for resistance to EGFR inhibitors in colorectal carcinoma[J]. Anticancer Res, 2010, 30(11):46734677.
[10] Phipps AI, Buchanan DD, Makar KW, et al. KRASmutation status in relation to colorectal cancer survival: the joint impact of correlated tumour markers[J]. Br J Cancer, 2013, 108(8):17571764.
[11] Chen X, Guo X, Zhang H, et al. Role of miR143 targeting KRAS in colorectal tumorigenesis[J]. Oncogene, 2009, 28(10):13851392.
[12] Borralho PM, Kren BT, Castro RE, et al. MicroRNA143 reduces viability and increases sensitivity to 5fluorouracil in HCT116 human colorectal cancer cells[J]. FEBS J, 2009, 276(22):66896700.
[13] Bengala C, Bettelli S, Bertolini F, et al. Prognostic role of EGFR gene copy number and KRAS mutation in patients with locally advanced rectal cancer treated with preoperative chemoradiotherapy[J]. Br J Cancer, 2010, 103(7):10191024.
[14] Van Cutsem E, Khne CH, Lng I, et al. Cetuximab plus irinotecan, fluorouracil, and leucovorin as firstline treatment for metastatic colorectal cancer: updated analysis of overall survival according to tumor KRAS and BRAF mutation status[J]. J Clin Oncol, 2011, 29(15):20112019.
[15] Bokemeyer C, Bondarenko I, Hartmann JT, et al. Efficacy according to biomarker status of cetuximab plus FOLFOX4 as firstline treatment for metastatic colorectal cancer: the OPUS study[J]. Ann Oncol, 2011, 22(7):15351546.
[16] Commisso C, Davidson SM, SoydanerAzeloglu RG, et al. Macropinocytosis of protein is an amino acid supply route in Rastransformed cells[J]. Nature, 2013, 497(7451):633637.
[17] Chang MH, Lee IK, Si Y, et al. Clinical impact of Kras mutation in colorectal cancer patients treated with adjuvant FOLFOX[J]. Cancer Chemother Pharmacol, 2011, 68(2):317323. |