Abstract
KRAS mutational analysis is a genetic test used in clinical practice for determining the status of the KRAS gene (wild type or mutant) in tumors from patients with metastatic colorectal cancer (CRC). Persons whose tumors are wild type may respond to therapies cetuximab (Erbitux) or panitumumab (Vectibix).
Clinical Scenario
In patients with metastatic colorectal cancer (CRC), KRAS mutational analysis is used to determine the status of the KRAS gene (wild type or mutant) in tumor specimens. Persons whose tumors are wild type may respond to therapies cetuximab (Erbitux) or panitumumab (Vectibix). [1] Patients whose tumors harbor a mutation in codons 12, 13, or 61 of the KRAS gene do not benefit from cetuximab or panitumumab. Data are mixed whether the presence of a KRAS mutation in colorectal tumors is prognostic (i.e. whether it influences patient outcomes independent of treatment). KRAS mutational analysis is also used to refine prognosis and treatment decisions in patients with non-small cell lung cancer (NSCLC) and is under investigation as a prognostic and/or predictive factor in other malignancies.
Test Description
KRAS mutational analysis is commercially available as a laboratory-developed test on tumor tissue. PCR methods are used to detect the most common mutations in codons 12, 13, and 61 of the KRAS gene in formalin fixed paraffin-embedded or frozen tumor tissue. Results are reported as positive (presence of a mutation) or negative (no mutation detected). [2]
Public Health Importance
This test applies to persons with colorectal cancer. It is estimated that 142,570 men and women (72,090 men and 70,480 women) will be diagnosed with and 51,370 men and women will die of colorectal cancer in 2010. The age-adjusted incidence rate for colorectal cancer is 47.9 per 100,000 men and women per year. Median age at diagnosis is 70 years. The overall 5-year relative survival is 65.0%, but varies depending on stage distribution. [3]
Approximately 20% of colorectal cancer diagnoses are in the distant or metastatic stage (for whom cetuximab or panitumumab may be indicated). The median survival in patients with metastatic CRC is less than 2 years. [3]
Published Reviews, Recommendations and Guidelines
Systematic evidence reviews
BlueCross BlueShield Technology Evaluation Center (BCBS TEC) published a systematic review in January 2009 based on retrospective analyses of 5 RCT and 5 single-arm studies. [2]
Recommendations by independent group
Guidelines by professional groups
National Comprehensive Cancer Network (NCCN) and the American Society of Clinical Oncology (ASCO) have issued clinical guidelines recommending KRAS mutational analysis on the tumors of all patients with metastatic CRC prior to prescribing cetuximab or panitumumab. [4][5][6]
Evidence Overview
Analytic Validity :
KRAS gene mutation analysis is commercially available through several labs. However, the labs themselves have not provided information on analytic performance. [2]
A recent, industry sponsored study compared different KRAS testing assays from 5 labs (Agencourt, Gentris, Genzyme, HistoGeneX, and Invitek) against the Amgen DNA Sequencing Laboratory direct sequencing assay. KRAS was classified as either wild type or mutant. Techniques were in agreement if both assays identified wild type or a mutant. Agreement was assessed by ? statistics. Agreement for each assay were reported as: HistoGeneX (kappa=0.95), Genzyme (kappa=0.94), Agencourt (kappa=0.94), Gentris (kappa=0.75), and Invitek (kappa=0.13). [7]
Clinical Validity in Metastatic Colorectal Cancer :
Retrospective, subset analyses of tumor tissue samples from small clinical trials have demonstrated that tumor KRAS gene mutations are associated with lack of response to both of the EGFR-targeted monoclonal antibodies approved for use in colorectal cancer, cetuximab and panitumumab. [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34] The strength of this association has been substantiated in retrospective analyses of patients treated in six, large randomized studies. [35][36][37][38][39][40]
A review of 8 studies (306 of 817 patients with tumors mutant for the KRAS gene) conducted by Linardou et al found that KRAS mutations were significantly associated with an absence of response to anti-EGFR monoclonal-antibody-based treatments (sensitivity=0.47 [0.43-0.52]; specificity=0.93 [0.83-0.97]; +LR=6.82; -LR=0.57). [41]
A recent meta-analysis of 22 studies including persons with metastatic colorectal cancer treated with cetuximab found that progression free and overall survival in persons with wildtype KRAS tumors was better compared to persons with mutated KRAS tumors. [42]
The data are mixed whether KRAS mutation is indicative of worse prognosis independent of therapy. At present, KRAS mutational analysis is not recommended for risk assessment.
Clinical Utility :
NCCN and BCBS TEC conclude that tumor testing for KRAS mutation offers clinical utility, and testing is available outside of research settings in clinical practice. However, we did not identify studies reporting physician and patient acceptance or population-based health outcomes data from use in clinical practice.
Links
The lab-based tests are regulated under the Clinical Laboratory Improvement Amendments (CLIA), and FDA premarket approval is not required. [2]
Acknowledgments
Funding information
This project was funded in part by the National Cancer Institute, grant # P01CA130818.
Competing interests
The authors have declared that no competing interests exist.
References
- Normanno, N., et al., Implications for KRAS status and EGFR-targeted therapies in metastatic CRC. Nat Rev Clin Oncol, 2009. 6(9): p. 519-27.
- KRAS mutations and epidermal growth factor receptor inhibitor therapy in metastatic colorectal cancer. Technol Eval Cent Asses Program Exec Summ, 2009. 23(6): p. 1-3.
- National Cancer Institute. SEER Stat Fact Sheets: Colon and Rectum. 2010 [cited 2010 April 26];
Reference Link - NCCN Updates Guidelines for Colorectal Cancer ; NCCN announces new updates to the NCCN Guidelines for Colon and Rectal Cancers . The updates include recommendations to the pre-treatment work-up and use of anti- cancer agents in patients with metastatic colorectal cancer depending on the status of the tumor's KRAS gene. The changes are based on recent studies demonstrating that the tumor KRAS gene status is highly predictive of outcome with certain therapies, in Business Wire. 2008.
- National Comprehensive Cancer Network. Colon Cancer. NCCN Clinical Practice Guidelines in Oncology 2009 [cited 2009 October 21];
Reference Link - Allegra, C.J., et al., 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. J Clin Oncol, 2009. 27(12): p. 2091-6
- Oliner, K., et al., A comparability study of 5 commercial KRAS tests. Diagn Pathol. 5(1): p. 23
- Benvenuti, S., 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(6): p. 2643-8.
- Bibeau, F., et al., Impact of Fc{gamma}RIIa-Fc{gamma}RIIIa polymorphisms and KRAS mutations on the clinical outcome of patients with metastatic colorectal cancer treated with cetuximab plus irinotecan. J Clin Oncol, 2009. 27(7): p. 1122-9.
- Cappuzzo, F., et al., Primary resistance to cetuximab therapy in EGFR FISH-positive colorectal cancer patients. Br J Cancer, 2008. 99(1): p. 83-9.
- De Roock, W., 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(3): p. 508-15.
- Di Fiore, F., et al., Clinical relevance of KRAS mutation detection in metastatic colorectal cancer treated by Cetuximab plus chemotherapy. Br J Cancer, 2007. 96(8): p. 1166-9.
- Di Nicolantonio, F., et al., Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer. J Clin Oncol, 2008. 26(35): p. 5705-12.
- Frattini, M., et al., PTEN loss of expression predicts cetuximab efficacy in metastatic colorectal cancer patients. Br J Cancer, 2007. 97(8): p. 1139-45.
- Freeman, D.J., 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(3): p. 184-90.
- Garm Spindler, K.L., et al., The importance of KRAS mutations and EGF61A>G polymorphism to the effect of cetuximab and irinotecan in metastatic colorectal cancer. Ann Oncol, 2009. 20(5): p. 879-84.
- Goncalves, A., et al., A polymorphism of EGFR extracellular domain is associated with progression free-survival in metastatic colorectal cancer patients receiving cetuximab-based treatment. BMC Cancer, 2008. 8: p. 169.
- Khambata-Ford, S., 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(22): p. 3230-7.
- Laurent-Puig, P., et al., Analysis of PTEN, BRAF, and EGFR status in determining benefit from cetuximab therapy in wild-type KRAS metastatic colon cancer. J Clin Oncol, 2009. 27(35): p. 5924-30.
- Lievre, A., et al., KRAS mutations as an independent prognostic factor in patients with advanced colorectal cancer treated with cetuximab. J Clin Oncol, 2008. 26(3): p. 374-9.
- Lievre, A., et al., KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer. Cancer Res, 2006. 66(8): p. 3992-5.
- Loupakis, F., et al., PTEN expression and KRAS mutations on primary tumors and metastases in the prediction of benefit from cetuximab plus irinotecan for patients with metastatic colorectal cancer. J Clin Oncol, 2009. 27(16): p. 2622-9.
- Loupakis, F., et al., KRAS codon 61, 146 and BRAF mutations predict resistance to cetuximab plus irinotecan in KRAS codon 12 and 13 wild-type metastatic colorectal cancer. Br J Cancer, 2009. 101(4): p. 715-21.
- Lurje, G., et al., Polymorphisms in cyclooxygenase-2 and epidermal growth factor receptor are associated with progression-free survival independent of K-ras in metastatic colorectal cancer patients treated with single-agent cetuximab. Clin Cancer Res, 2008. 14(23): p. 7884-95.
- Molinari, F., et al., Differing deregulation of EGFR and downstream proteins in primary colorectal cancer and related metastatic sites may be clinically relevant. Br J Cancer, 2009. 100(7): p. 1087-94.
- Moroni, M., 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(5): p. 279-86.
- Oden-Gangloff, A., et al., TP53 mutations predict disease control in metastatic colorectal cancer treated with cetuximab-based chemotherapy. Br J Cancer, 2009. 100(8): p. 1330-5.
- Perrone, F., et al., PI3KCA/PTEN deregulation contributes to impaired responses to cetuximab in metastatic colorectal cancer patients. Ann Oncol, 2009. 20(1): p. 84-90.
- Personeni, N., et al., Clinical usefulness of EGFR gene copy number as a predictive marker in colorectal cancer patients treated with cetuximab: a fluorescent in situ hybridization study. Clin Cancer Res, 2008. 14(18): p. 5869-76.
- Prenen, H., et al., PIK3CA mutations are not a major determinant of resistance to the epidermal growth factor receptor inhibitor cetuximab in metastatic colorectal cancer. Clin Cancer Res, 2009. 15(9): p. 3184-8.
- Sartore-Bianchi, A., et al., PIK3CA mutations in colorectal cancer are associated with clinical resistance to EGFR-targeted monoclonal antibodies. Cancer Res, 2009. 69(5): p. 1851-7.
- Sohn, B.S., et al., The role of KRAS mutations in predicting the efficacy of cetuximab-plus-irinotecan therapy in irinotecan-refractory Korean metastatic colorectal cancer patients. Oncology, 2009. 77(3-4): p. 224-30.
- Souglakos, J., et al., Prognostic and predictive value of common mutations for treatment response and survival in patients with metastatic colorectal cancer. Br J Cancer, 2009. 101(3): p. 465-72.
- Yen, L.C., et al., Activating KRAS mutations and overexpression of epidermal growth factor receptor as independent predictors in metastatic colorectal cancer patients treated with cetuximab. Ann Surg. 251(2): p. 254-60.
- Amado, R.G., et al., Wild-type KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer. J Clin Oncol, 2008. 26(10): p. 1626-34.
- Bokemeyer, C., et al., Fluorouracil, leucovorin, and oxaliplatin with and without cetuximab in the first-line treatment of metastatic colorectal cancer. J Clin Oncol, 2009. 27(5): p. 663-71.
- Hecht, J.R., et al., A randomized phase IIIB trial of chemotherapy, bevacizumab, and panitumumab compared with chemotherapy and bevacizumab alone for metastatic colorectal cancer. J Clin Oncol, 2009. 27(5): p. 672-80.
- Karapetis, C.S., et al., K-ras mutations and benefit from cetuximab in advanced colorectal cancer. N Engl J Med, 2008. 359(17): p. 1757-65.
- Tol, J., et al., Chemotherapy, bevacizumab, and cetuximab in metastatic colorectal cancer. N Engl J Med, 2009. 360(6): p. 563-72.
- Van Cutsem, E., et al., Cetuximab and chemotherapy as initial treatment for metastatic colorectal cancer. N Engl J Med, 2009. 360(14): p. 1408-17
- Linardou, H., et al., Assessment of somatic k-RAS mutations as a mechanism associated with resistance to EGFR-targeted agents: a systematic review and meta-analysis of studies in advanced non-small-cell lung cancer and metastatic colorectal cancer. Lancet Oncol, 2008. 9(10): p. 962-72
- Qiu, L.X. et al., Predictive and prognostic value of KRAS mutations in metastatic colorectal cancer patients treated with cetuximab: A meta-analysis of 22 studies. Eur J Cancer, 2010. (in press). doi:10.1016/j.ejca.2010.05.022
- Yen, L.C., et al., Activating KRAS mutations and overexpression of epidermal growth factor receptor as independent predictors in metastatic colorectal cancer patients treated with cetuximab. Ann Surg, 2010. 251(2): p. 254-60
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