K-ras mutations and benefit from cetuximab in advanced colorectal cancer

New England Journal of Medicine

Volumn 359, Issue 17, 2008, Pages 1757-1765

  Karapetis, Christos S ^a,n   Khambata Ford, Shirin ^b   Jonker, Derek J ^c   O'Callaghan, Chris J ^d   Tu, Dongsheng ^d   Tebbutt, Niall C ^e   Simes, R John ^f   Chalchal, Haji ^g   Shapiro, Jeremy D ^h   Robitaille, Sonia ^d   Price, Timothy J ⁱ   Shepherd, Lois ^d   Au, Heather Jane ^j   Langer, Christiane ^k   Moore, Malcolm J ^l   Zalcberg, John R ^m  

^a FLINDERS UNIVERSITY   (Australia)

^b BRISTOL MYERS SQUIBB RESEARCH AND DEVELOPMENT   (United States)

^c OTTAWA HOSPITAL RESEARCH INSTITUTE   (Canada)

^d Queen's Cancer Research Institute   (Canada)

^e AUSTIN HEALTH   (Australia)

^f UNIVERSITY OF SYDNEY   (Australia)

^g Allan Blair Cancer Centre   (Canada)

^h ALFRED HOSPITAL   (Australia)

ⁱ UNIVERSITY OF ADELAIDE   (Australia)

^j CROSS CANCER INSTITUTE   (Canada)

^k BRISTOL MYERS SQUIBB   (United States)

^l PRINCESS MARGARET HOSPITAL   (Canada)

^m UNIVERSITY OF MELBOURNE   (Australia)

ⁿ FLINDERS MEDICAL CENTRE   (Australia)

more..

Author keywords

[No Author keywords available]

Indexed keywords

CETUXIMAB;

ADULT; ADVANCED CANCER; AGED; ARTICLE; CANCER SURVIVAL; CLINICAL TRIAL; COLORECTAL CANCER; CONTROLLED CLINICAL TRIAL; CONTROLLED STUDY; CORRELATION ANALYSIS; DISEASE COURSE; DRUG EFFICACY; EXON; FEMALE; GENE MUTATION; HUMAN; HUMAN TISSUE; LOADING DRUG DOSE; MAJOR CLINICAL STUDY; MALE; ONCOGENE K RAS; PATIENT CARE; PRIORITY JOURNAL; QUALITY OF LIFE; RANDOMIZED CONTROLLED TRIAL; TREATMENT RESPONSE;

EID: 54949085398     PISSN: 00284793     EISSN: 15334406     Source Type: Journal    
DOI: 10.1056/NEJMoa0804385     Document Type: Article

References (32)

1. Jonker DJ, O'Callaghan CJ, Karapetis CS, et al. Cetuximab for the treatment of colorectal cancer. N Engl J Med 2007;357:2040-8.
2. Baselga J. The EGFR as a target for anticancer therapy - focus on cetuximab. Eur J Cancer 2001;37:Suppl 4:S16-S22.
3. 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.
4. Fransén K, Klintenäs M, Osterström A, Dimberg J, Monstein HJ, Söderkvist P. Mutation analysis of the BRAF, ARAF and RAF-1 genes in human colorectal adenocarcinomas. Carcinogenesis 2004;25:527-33.
5. 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.
6. 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.
7. Frattini M, Saletti P, Romagnani E, et al. PTEN loss of expression predicts cetuximab efficacy in metastatic colorectal cancer patients. Br J Cancer 2007;97:1139-45.
8. Andreyev HJ, Ross PJ, Cunningham D, Clarke PA. Antisense treatment directed against mutated Ki-ras in human colorectal adenocarcinoma. Gut 2001;48:230-7.
9. 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.
10. Esteller M, Gonzalez S, Risques RA, et al. K-ras and p16 aberrations confer poor prognosis in human colorectal cancer. J Clin Oncol 2001;19:299-304.
11. 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-iv5.
12. Osoba D, Rodrigues G, Myles J, Zee B, Pater J. Interpreting the significance of changes in health-related quality-of-life scores. J Clin Oncol 1998;16:139-44.
13. Liàvre 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.
14. 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.
15. Andreyev HJ, Norman AR, Cunningham D, Oates JR, Clarke PA. Kirsten ras mutations in patients with colorectal cancer: the multicenter "RASCAL" study. J Natl Cancer Inst 1998;90:675-84.
16. Barault L, Veyrie N, Jooste V, et al. Mutations in the RAS-MAPK, PI(3)K (phosphatidylinositol-3-OH kinase) signaling network correlate with poor survival in a population-based series of colon cancers. Int J Cancer 2008;122:2255-9.
17. Bleeker WA, Hayes VM, Karrenbeld A, et al. Impact of KRAS and TP53 mutations on survival in patients with left- and rightsided Dukes' C colon cancer. Am J Gastroenterol 2000;95:2953-7.
18. Khambata-Ford S, Garrett CR, Meropol 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.
19. 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.
20. Saltz LB, Meropol NJ, Loehrer PJ Sr, Needle MN, Kopit J, Mayer RJ. Phase II trial of cetuximab in patients with refractory colorectal cancer that expresses the epidermal growth factor receptor. J Clin Oncol 2004;22:1201-8.
21. Zhang W, Gordon M, Press OA, et al. Cyclin D1 and epidermal growth factor polymorphisms associated with survival in patients with advanced colorectal cancer treated with cetuximab. Pharmacogenet Genomics 2006;16:475-83.
22. Wierzbicki RD, Jonker DJ, Moore MJ, et al. A phase II multicenter study of cetuximab monotherapy in patients with EGFR-undetectable refractory metastatic colorectal carcinoma (mCRC). J Clin Oncol 2008;26:Suppl:15S. abstract.
23. Hebbar M, Wacrenier A, Desauw C, et al. Lack of usefulness of epidermal growth factor receptor expression determination for cetuximab therapy in patients with colorectal cancer. Anticancer Drugs 2006;17:855-7.
24. 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.
25. Penault-Llorca F, Cayre A, Arnould L, et al. Is there an immunohistochemical technique definitively valid in epidermal growth factor receptor assessment? Oncol Rep 2006;16:1173-9.
26. Francoual M, Etienne-Grimaldi MC, Formento JL, et al. EGFR in colorectal cancer: more than a simple receptor. Ann Oncol 2006;17:962-7.
27. Lièvre 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.
28. Moroni M, Veronese S, Benvenuti S, et al. Gene copy number for epidermal growth factor receptor (EGFR) and clinical response to antiEGFR treatment in colorectal cancer: a cohort study. Lancet Oncol 2005;6:279-86.
29. Lenz HJ, Van Cutsem E, Khambata-Ford S, et al. Multicenter phase II and translational study of cetuximab in metastatic colorectal carcinoma refractory to irinotecan, oxaliplatin, and fluoropyrimidines. J Clin Oncol 2006;24:4914-21.
30. van Zandwijk N, Mathy A, Boerrigter L, et al. EGFR and KRAS mutations as criteria for treatment with tyrosine kinase inhibitors: retro- and prospective observations in non-small-cell lung cancer. Ann Oncol 2007;18:99-103.
31. Massarelli E, Varella-Garcia M, Tang X, et al. KRAS mutation is an important predictor of resistance to therapy with epidermal growth factor receptor tyrosine kinase inhibitors in non-small-cell lung cancer. Clin Cancer Res 2007;13:2890-6.
32. Pao W, Wang TY, Riely GJ, et al. KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib. PLoS Med 2005;2(1):e17.