American society of clinical oncology provisional clinical opinion: Testing for KRAS gene mutations in patients with metastatic colorectal carcinoma to predict response to anti-epidermal growth factor receptor monoclonal antibody therapy

Journal of Clinical Oncology

Volumn 27, Issue 12, 2009, Pages 2091-2096

  Allegra, Carmen J ^a,c   Jessup, J Milburn ^b   Somerfield, Mark R ^c   Hamilton, Stanley R ^d   Hammond, Elizabeth H ^e   Hayes, Daniel F ^f   McAllister, Pamela K ^g   Morton, Roscoe F ^h   Schilsky, Richard L ⁱ  

^a UNIVERSITY OF FLORIDA COLLEGE OF MEDICINE   (United States)

^b NATIONAL INSTITUTES OF HEALTH   (United States)

^c AMERICAN SOCIETY OF CLINICAL ONCOLOGY   (United States)

^d C3: Colorectal Cancer Coalition   (United States)

^e UNIVERSITY OF TEXAS   (United States)

^f UNIVERSITY OF UTAH SCHOOL OF MEDICINE   (United States)

^g UNIVERSITY OF MICHIGAN   (United States)

^h Medical Oncology and Hematology Associates   (United States)

ⁱ UNIVERSITY OF CHICAGO   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CAPECITABINE; CETUXIMAB; EPIDERMAL GROWTH FACTOR RECEPTOR ANTIBODY; FLUOROURACIL; FOLINIC ACID; IRINOTECAN; MONOCLONAL ANTIBODY; OXALIPLATIN; PANITUMUMAB;

CANCER CHEMOTHERAPY; CANCER COMBINATION CHEMOTHERAPY; CLINICAL PRACTICE; CLINICAL TRIAL; CODON; COLORECTAL CARCINOMA; GENE MUTATION; HEALTH CARE PERSONNEL; HUMAN; MEDICAL RESEARCH; METASTASIS; ONCOGENE K RAS; ONCOLOGY; OUTCOME ASSESSMENT; PATIENT CARE; PREDICTION; PRIORITY JOURNAL; RETROSPECTIVE STUDY; REVIEW; TREATMENT RESPONSE;

ADENOCARCINOMA; ANTIBODIES, MONOCLONAL; CLINICAL TRIALS, PHASE II AS TOPIC; CLINICAL TRIALS, PHASE III AS TOPIC; COLONIC NEOPLASMS; HUMANS; MUTATION; PATIENT SELECTION; PROTO-ONCOGENE PROTEINS; RANDOMIZED CONTROLLED TRIALS AS TOPIC; RAS PROTEINS; RECEPTOR, EPIDERMAL GROWTH FACTOR;

EID: 65349189958     PISSN: 0732183X     EISSN: None     Source Type: Journal    
DOI: 10.1200/JCO.2009.21.9170     Document Type: Review

References (19)

1. Amado RG, Wolf M, Peeters M, et al: Wildtype KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer. J Clin Oncol 26:1626-1634, 2008
2. 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 67:2643-2648, 2007
3. Bokemeyer C, Bondarenko I, Hartmann JT, et al: KRAS status and efficacy of first-line treatment of patients with metastatic colorectal (metastatic CRC) with FOLFOX with or without cetuximab: The OPUS experience. J Clin Oncol 26:178s, 2008 (suppl; abstr 4000)
4. 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 19:508-515, 2008
5. 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 96:1166-1169, 2007
6. Karapetis CS, Khambata-Ford S, Jonker DJ, et al: K-ras mutations and benefit from cetuximab in advanced colorectal cancer. N Engl J Med 359:1757- 1765, 2008
7. 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 25:3230-3237, 2007
8. Lièvre 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 26:374-379, 2008
9. 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). J Clin Oncol 26:180s, 2008 (suppl; abstr LBA4011)
10. Van Cutsem E, Lang I, D'haens G, et al: KRAS status and efficacy in the first-line treatment of patients with metastatic colorectal cancer (metastatic CRC) treated with FOLFIRI with or without cetuximab: The CRYSTAL experience. J Clin Oncol 26:5s, 2008 (suppl; abstr 2)
11. BlueCross BlueShield Association: Technology Evaluation Center: KRAS Mutations and Epidermal Growth Factor Receptor Inhibitor Therapy in Metastatic Colorectal Cancer TEC Assessments (vol 23, tab 6). Chicago, IL, BlueCross BlueShield Association, 2008
12. Cappuzzo F, Varella-Garcia M, Finocchiaro G, et al: Primary resistance to cetuximab therapy in EGFR FISH-positive colorectal cancer patients. Br J Cancer 99:83-89, 2008
13. 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 26:5705-5712, 2008
14. Jhawer M, Goel S, Wilson AJ, et al: PIK3CA mutation/PTEN expression status predicts response of colon cancer cells to the epidermal growth factor receptor inhibitor cetuximab. Cancer Res 68:1953- 1961, 2008
15. Perrone F, Lampis A, Orsenigo M, et al: PI3KCA/PTEN deregulation contributes to impaired responses to cetuximab in metastatic colorectal cancer patients. Ann Oncol 20:84-90, 2009
16. Frattini M, Saletti P, Romagnani E, et al: PTEN loss of expression predicts cetuximab efficacy in metastatic colorectal cancer patients. Br J Cancer 97:1139-1145, 2007
17. Moroni M, Sartore-Bianchi A, Veronese S, et al: EGFR FISH in colorectal cancer: What is the current reality? Lancet Oncol 9:402-403, 2008
18. Razis E, Briasoulis E, Vrettou E, et al: Potential value of PTEN in predicting cetuximab response in colorectal cancer: An exploratory study. BMC Cancer 8:234, 2008
19. Jimeno A, Messersmith WA, Hirsch FR, et al: KRAS mutations and sensitivity to epidermal growth factor receptor inhibitors in colorectal cancer: Practical application of patient selection. J Clin Oncol 27:1130-1136, 2009