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KRAS mutations and sensitivity to anti-EGFR monoclonal antibodies in metastatic colorectal carcinoma: an open issue

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Pages 565-577 | Published online: 16 Apr 2009

Bibliography

  • Grothey A, Sargent D, Goldberg RM, Schmoll HJ. Survival of patients with advanced colorectal cancer improves with the availability of fluorouracil-leucovorin, irinotecan, and oxaliplatin in the course of treatment. J Clin Oncol 2004;22:1209-14
  • Cunningham D, Humblet Y, Siena S, et al. Cetuximab monotherapy and cetuximab plus irinotecan in irinotecan-refractory metastatic colorectal cancer. N Engl J Med 2004;351:337-45
  • Jonker DJ, O'Callaghan CJ, Karapetis CS, et al. Cetuximab for the treatment of colorectal cancer. N Engl J Med 2007;357:2040-8
  • Van Cutsem E, Peeters M, Siena S, et al. Open-label Phase III trial of panitumumab plus best supportive care compared with best supportive care alone in patients with chemotherapy-refractory metastatic colorectal cancer. J Clin Oncol 2007;25:1658-64
  • Chung KY, Shia J, Kemeny NE, et al. Cetuximab shows activity in colorectal cancer patients with tumors that do not express the epidermal growth factor receptor by immunohistochemistry. J Clin Oncol 2005;23:1803-10
  • Spano JP, Milano G, Vignot S, et al. Potential predictive markers of response to EGFR-targeted therapies in colorectal cancer. Crit Rev Oncol Hematol 2008;66:21-30
  • Malumbres M, Barbacid M, Barbacid M. RAS oncogenes: the first 30 years. Nat Rev Cancer 2003;3:459-65
  • Frattini M, Balestra D, Suardi S, et al. Different genetic features associated with colon and rectal carcinogenesis. Clin Cancer Res 2004;10:4015-21
  • Ogino S, Meyerhardt JA, Kawasaki T, et al. CpG island methylation, response to combination chemotherapy, and patient survival in advanced microsatellite stable colorectal carcinoma. Virchows Arch 2007;450:529-37
  • Barault L, Charon-Barra C, Jooste V, et al. Hypermethylator phenotype in sporadic colon cancer: study on a population-based series of 582 cases. Cancer Res 2008;68:8541-6
  • Ogino S, Nosho K, Kirkner GJ, et al. CpG island methylator phenotype, microsatellite instability, BRAF mutation and clinical outcome in colon cancer. Gut 2009;58:90-6
  • Paradiso A, Mangia A, Azzariti A, Tommasi S. Phosphatidylinositol 3-kinase in breast cancer: where from here? Clin Cancer Res 2007;13:5988-90
  • McClellan M, Kievit P, Auersperg N, Rodland K. Regulation of proliferation and apoptosis by epidermal growth factor and protein kinase C in human ovarian surface epithelial cells. Exp Cell Res 1999;246:471-9
  • Haura EB, Turkson J, Jove R. Mechanisms of disease: insights into the emerging role of signal transducers and activators of transcription in cancer. Nat Clin Pract Oncol 2005;2:315-24
  • Roberts PJ, Der CJ. Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer. Oncogene 2007;26:3291-310
  • Benvenuti S, Sartore-Bianchi A, Di Nicolantonio F, et al. Oncogenic activation of the RAS/RAF signaling pathway impairs the response of metastatic colorectal cancers to anti-epidermal growth factor receptor antibody therapies. Cancer Res 2007;67:2643-8
  • Di Nicolantonio F, Martini M, Molinari F, et al. Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer. J Clin Oncol 2008;26:5705-12
  • De Reynies A, Boige V, Milano G, et al. KRAS mutation signature in colorectal tumors significantly overlaps with the cetuximab response signature. J Clin Oncol 2008;26:2228-30
  • Khambata-Ford S, Garrett CR, Metropol NJ, et al. Expression of epiregulin and amphiregulin and K-ras mutation status predict disease control in metastatic colorectal cancer patients treated with cetuximab. J Clin Oncol 2007;25:3230-7
  • Mc Sherry EA, Mc Goldrick A, Kay EW, et al. Formalin-fixed paraffin-embedded clinical tissues show spurious copy number changes in array-CGH profiles. Clin Genet 2007;72:441-7
  • Cler L, Bu D, Lewis C, Euhus DA. Comparison of five methods for extracting DNA from paucicellular clinical samples. Mol Cell Probes 2006;20:191-6
  • Available from: http://esp-pathology.org
  • Van Krieken JHJM, Jung A, Kirchner T, et al. KRAS mutation testing for predicting response to anti-EGFR therapy for colorectal carcinoma: proposal for an European quality assurance program. Virchows Arch 2008;453:417-31
  • Clayton SJ, Scott FM, Walker J, et al. K-ras point mutation detection in lung cancer: comparison of two approaches to somatic mutation detection using ARMS allele-specific amplification. Clin Chem 2000;46:1929-38
  • Ogino S, Kawasaki T, Brahmandam M, et al. Sensitive sequencing method for KRAS mutation detection by pyrosequencing. J Mol Diagn 2005;7:413-21
  • Simi L, Pratesi N, Vignoli M, et al. High-resolution melting analysis for rapid detection of KRAS, BRAF, and PIK3CA gene mutations in colorectal cancer. Am J Clin Pathol 2008;130:247-53
  • Lievre A, Bachet JB, Le Corre D, et al. KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer. Cancer Res 2006;66:3992-5
  • Lievre A, Bachet JB, Boige V, et al. KRAS mutations as an independent prognostic factor in patients with advanced colorectal cancer treated with cetuximab. J Clin Oncol 2008;26:374-9
  • De Roock W, Piessevaux H, De Schutter J, et al. KRAS wild-type state predicts survival and is associated to early radiological response in metastatic colorectal cancer treated with cetuximab. Ann Oncol 2008;19:508-15
  • Di Fiore F, Blanchard F, Charbonnier F, et al. Clinical relevance of KRAS mutation detection in metastatic colorectal cancer treated by Cetuximab plus chemotherapy. Br J Cancer 2007;96:1166-9
  • Di Fiore F, Charbonnier F, Lefebure B, et al. Clinical interest of KRAS mutation detection in blood for anti-EGFR therapies in metastatic colorectal cancer. Br J Cancer 2008;99:551-2
  • Finocchiaro G, Cappuzzo F, Janne PA, et al. EGFR, HER2 and Kras as predictive factors for cetuximab sensitivity in colorectal cancer [abstract 4021]. Presented at 43rd Annual Meeting of the American Society of Clinical Oncology (ASCO); 1-5 June 2007; Chicago, USA
  • Freeman DJ, Juan T, Reiner M, et al. Association of K-ras mutational status and clinical outcomes in patients with metastatic colorectal cancer receiving panitumumab alone. Clin Colorectal Cancer 2008;7:184-90
  • Jonker DJ, O'Callaghan CJ, Karapetis CS, et al. Cetuximab for the treatment of colorectal cancer. N Engl J Med 2007;357:2040-8
  • Karapetis CS, Khambata-Ford S, Jonker DJ, et al. K-ras mutations and benefit from cetuximab in advanced colorectal cancer. N Engl J Med 2008;359:1757-65
  • Amado RG, Wolf M, Peeters M, et al. Wild-type KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer. J Clin Oncol 2008;26:1626-34
  • Van Cutsem E, Humblet Y, Gerdelblom H, et al. Cetuximab dose-escalation study in patients with metastatic colorectal cancer (mCRC) with no or slight skin reactions on cetuximab standard dose treatment (EVEREST): Pharmacokinetic and efficacy data of a randomized study [abstract 237]. Presented at 43th Annual Meeting of the American Society of Clinical Oncology (ASCO); 1-5 June 2007; Chicago, USA
  • Tejpar S, Peeters M, Humblet Y, et al. Relationship of efficacy with KRAS status (wild type versus mutant) in patients with irinotecan-refractory metastatic colorectal cancer (mCRC), treated with irinotecan (q2w) and escalating doses of cetuximab (q1w): the Everest experience. Preliminary data [abstract 4001]. Presented at 44th Annual Meeting of the American Society of Clinical Oncology (ASCO); 30 May – 3 June 2008; Chicago, USA
  • Tabernero J, Cervantes A, Ciardiello F, et al. Correlation of efficacy to KRAS status (wt v smut) in patients (pts) with metastatic colorectal cancer (mCRC) treated with weekly (q1w) and q2w schedules of cetuximab combined with FOLFIRI [abstract 435]. Presented at the 2008 Gastrointestinal Cancers Symposium of the American Society of Clinical Oncology (ASCO); 25–27 January 2008; Orlando, USA
  • Van Cutsem E, Nowacki M, Lang I, et al. Randomized Phase III study of irinotecan and 5-FU/FA with or without cetuximab in the first-line treatment of patients with metatstatic colorectal cancer: the CRYSTAL trial [abstract 4000]. Presented at 43rd Annual Meeting of the American Society of Clinical Oncology (ASCO); 1-5 June 2007; Chicago, USA
  • Van Cutsem E, Lang I, D'haens G, et al. KRAS status and efficacy in the first-line treatment of patients with metatstatic colorectal cancer (mCRC) treated with FOLFIRI with or without cetuximab: the CRYSTAL experience [abstract 2]. Presented at 44th Annual Meeting of the American Society of Clinical Oncology (ASCO); 30 May–3 June 2008; Chicago, USA
  • Bokemeyer C, Boudarenko I, Makhson A, et al. Cetuximab plus 5-FU/FA/oxaliplatin (FOLFOX-4) cerus FOLFOX-4 in the first-line treatment of metastatic colorectal cancer (mCRC): OPUS, a randomized Phase II study [abstract 4035]. Presented at 43th Annual Meeting of the American Society of Clinical Oncology (ASCO); 1-5 June 2007; Chicago, USA
  • Bokemeyer C, Bondarenko I, Hartmann JT, et al. KRAS status and efficacy of first-line treatment of patients with metastatic colorectal cancer (mCRC) with FOLFOX with or without cetuximab: the OPUS experience [abstract 4000]. Presented at 44th Annual Meeting of the American Society of Clinical Oncology (ASCO); 30 May – 3 June 2008; Chicago, USA
  • Bazan V, Agnese V, Corsale S, et al. Specific TP53 and/or Ki-ras mutations as independent predictors of clinical outcome in sporadic colorectal adenocarcinomas: results of a 5-year Gruppo Oncologico dell'Italia Meridionale (GOIM) prospective study. Ann Oncol 2005;16(Suppl 4):iv50-55
  • Punt CJ, Tol J, Rodenburg CJ, et al. Randomized Phase III study of capecitabine, oxaliplatin, and bevacizumab with or without cetuximab in advanced colorectal cancer (ACC), the CAIRO2 study of the Dutch Colorectal Cancer Group (DCCG) [abstract LBA4011]. Presented at 44th Annual Meeting of the American Society of Clinical Oncology (ASCO); 30 May – 3 June 2008; Chicago, USA
  • Sartore-Bianchi A, Moroni M, Veronese S, et al. Epidermal growth factor receptor gene copy number and clinical outcome of metastatic colorectal cancer treated with panitumumab. J Clin Oncol 2007;25:3238-45
  • Loupakis F, Vasile E, Santini D, et al. EGF-receptor targeting with monoclonal antibodies in colorectal carcinoma: rationale for a pharmacogenomic approach. Pharmacogenomics 2008;9:55-69
  • Edkins S, O'Meara S, Parker A, et al. Recurrent KRAS codon 146 mutations in human colorectal cancer. Cancer Biol Ther 2006;5:928-32
  • Morgillo F, Bareschino MA, Bianco R, et al. Primary and acquired resistance to anti-EGFR targeted drugs in cancer therapy. Differentiation 2007;75:788-99
  • Zauber P, Sabbath-Solitare M, Marotta SP, et al. Molecular changes in the ki-ras and APC genes in primary colorectal carcinoma and synchronous metastases compared with the findings in accompanying adenomas. Mol Pathol 2003;56:137-40
  • Artale S, Sartore-Bianchi A, Veronese SM, et al. Mutations of KRAS and BRAF in primry and matched metastatic sites of colorectal cancer. J Clin Oncol 2008;26:4217-9
  • Santini D, Loupakis F, Vincenzi B, et al. High concordance of KRAS status between primary colorectal tumours and related metastatic sites: implications for clinical practice. Oncologist 2008;13:1270-5
  • Houghton JA, Ebanks R, Harwood TG, et al. Inhibition of apoptosis after thymineless stress is conferred by oncogeic K-Ras in colon carcinoma cells. Clin Cancer Res 1998;4:2841-8
  • Etienne-Grimaldi MC, Formento JL, Francoual M, et al. K-Ras mutations and treatment outcome in colorectal cancer patients receiving exclusive fluoropyrimidine therapy. Clin Cancer Res 2008;14:4830-5
  • Andreyev HJ, Norman AR, Cunningham D, et al. Kirsten ras mutations in patients with colorectal cancer: the “RASCAL” study. Br J Cancer 2001;85:692-6
  • Samowitz WS, Curtin K, Schaffer D, et al. Relationship of Ki-ras mutations in colon cancers to tumor location, stage, and survival: a population-based study. Cancer Epidemiol Biomarkers Prev 2000;9:1193-7
  • Ince WL, Jubb AM, Holden SN, et al. Association of k-ras, b-raf, and p53 status with the treatment effect of bevacizumab. J Natl Cancer Inst 2005;97:981-9
  • Friday BB, Adjei AA. Advances in targeting the Ras/Raf/MEK/Erk mitogen-activated protein kinase cascade with MEK inhibitors for cancer therapy. Clin Cancer Res 2008;14:342-6
  • Jasinski P, Zwolak P, Terai K, Dudek AZ. Novel Ras pathway inhibitor induces apoptosis and growth inhibition of K-ras-mutated cancer cells in vitro and in vivo. Transl Res 2008;152:203-12

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