K-Ras mutation status as a predictive biomarker in metastatic colorectal cancer

Biomarkers in Medicine

Volumn 2, Issue 2, 2008, Pages 97-99

  Ramos, Francisco Javier ^a   Tabernero, Josep ^a  

^a HOSPITAL UNIVERSITARI VALL D HEBRON   (Spain)

Author keywords

[No Author keywords available]

Indexed keywords

AMINO ACID; AMPHIREGULIN; BEVACIZUMAB; BIOLOGICAL MARKER; CETUXIMAB; EPIDERMAL GROWTH FACTOR RECEPTOR; EPIREGULIN; FLUOROURACIL; FOLINIC ACID; IRINOTECAN; K RAS PROTEIN; OXALIPLATIN; PANITUMUMAB;

AMINO ACID SUBSTITUTION; CANCER SURVIVAL; CLINICAL TRIAL; COLORECTAL CANCER; COMBINATION CHEMOTHERAPY; CORRELATION ANALYSIS; DISEASE FREE SURVIVAL; DRUG EFFICACY; DRUG TARGETING; EDITORIAL; GENE EXPRESSION PROFILING; GENE FUNCTION; GENE IDENTIFICATION; GENE MUTATION; HUMAN; METASTASIS POTENTIAL; MONOTHERAPY; ONCOGENE K RAS; OVERALL SURVIVAL; PREDICTION; PROGNOSIS; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION; TREATMENT RESPONSE;

EID: 44449108636     PISSN: 17520363     EISSN: None     Source Type: Journal    
DOI: 10.2217/17520363.2.2.97     Document Type: Editorial

References (13)

1. Goldstein NS, Armin M: Epidermal growth factor receptor immunohistochemical reactivity in patientswith American Joint Committee on Cancer Stage IV colon adenocarcinoma: implications for a standardized scoring system. Cancer 92, 1331-1346 (2001).
2. Stites EC, Trampont PC, Ma Z et al.: Network analysis of oncogenic ras activation in cancer. Science 318, 463-467 (2007).
3. Malumbres M, Barbacid M: RAS oncogenes: the first 30 years. Nat. Rev. Cancer 3, 7-13 (2003).
4. Cunningham D, Humblet Y, Siena S et al.: Cetuximab monotherapy and cetuximab plus irinotecan in irinotecan-refractory metastatic colorectal cancer. N. Engl. J. Med. 351, 337-345 (2004).
5. Lièvre A, Bachet JB, Le Corre D et al.: KRAS mutations status is predictive of response to cetuximab therapy in colorectal cancer. Cancer Res. 66, 3992-3995 (2006).
6. Li-grevre 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).
7. 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).
8. 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).
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. 19(3), 508-515 (2007).
10. 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).
11. Finocchiaro G, Cappuzzo F, Jänne PA et al.: EGFR, HER2 and Kras as predictive factors for cetuximab sensitivity in colorectal cancer. Proc. Am. Soc. Clin. Oncol. 25, 18S (2007).
12. Amado RG, Wolf M, Freeman D et al.: Panitumumab (pmab) efficacy and patient-reported outcomes (PRO) in metastatic colorectal cancer (mCRC) patients (pts) with wild-type (WT) KRAS tumor status. Presented at: ASCO Gastrointestinal Cancer Symposium. Orlando, FL, USA. 25-27 January 2008 (Abstract 278).
13. Tabernero J, Cervantes A, Ciardiello F et al.: Correlation of efficacy to KRAS status (wt vs mut) in patients (pts) with metastatic colorectal cancer (mCRC), treated with weekly (q1w) and q2w schedules of cetuximab combined with FOLFIRI. Presented at: ASCO Gastrointestinal Cancer Symposium. Orlando, FL, USA. 25-27 January 2008 (Abstract 435).