The dominant role of G12C over other KRAS mutation types in the negative prediction of efficacy of epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer

Cancer Genetics

Volumn 206, Issue 1-2, 2013, Pages 26-31

  Fiala, Ondrej ^a   Pesek, Milos ^a   Finek, Jindrich ^a   Benesova, Lucie ^b   Belsanova, Barbora ^b   Minarik, Marek ^b  

^a CHARLES UNIVERSITY   (Czech Republic)

^b Genomac Research Institute   (Czech Republic)

Author keywords

EGFR tyrosine kinase inhibitors; KRAS mutation; Non small cell lung cancer; Predictive factor; Targeted treatment of NSCLC

Indexed keywords

EPIDERMAL GROWTH FACTOR RECEPTOR; EPIDERMAL GROWTH FACTOR RECEPTOR KINASE INHIBITOR; ERLOTINIB; GEFITINIB; K RAS PROTEIN;

ADULT; ADVANCED CANCER; AGED; AMINO ACID SUBSTITUTION; ARTICLE; CANCER SURVIVAL; CONTROLLED STUDY; DRUG EFFICACY; EPIDERMAL GROWTH FACTOR RECEPTOR GENE; FEMALE; GENE MUTATION; GENOTYPE; HUMAN; LUNG ADENOCARCINOMA; LUNG NON SMALL CELL CANCER; LUNG SQUAMOUS CELL CARCINOMA; MAJOR CLINICAL STUDY; MALE; MOLECULARLY TARGETED THERAPY; MUTATION RATE; ONCOGENE K RAS; OUTCOME ASSESSMENT; OVERALL SURVIVAL; PRIORITY JOURNAL; PROGRESSION FREE SURVIVAL; RECEPTOR GENE; SMOKING; WILD TYPE;

ADULT; AGED; AMINO ACID SUBSTITUTION; ANTINEOPLASTIC AGENTS; BIOMARKERS, PHARMACOLOGICAL; CARCINOMA, NON-SMALL-CELL LUNG; CASE-CONTROL STUDIES; COHORT STUDIES; CYSTEINE; DRUG RESISTANCE, NEOPLASM; FEMALE; GLYCINE; HUMANS; LUNG NEOPLASMS; MALE; MIDDLE AGED; MUTATION, MISSENSE; PROGNOSIS; PROTEIN KINASE INHIBITORS; PROTEIN-TYROSINE KINASES; PROTO-ONCOGENE PROTEINS; RAS PROTEINS; RECEPTOR, EPIDERMAL GROWTH FACTOR; TREATMENT OUTCOME; TUMOR MARKERS, BIOLOGICAL;

EID: 84873415195     PISSN: 22107762     EISSN: 22107770     Source Type: Journal    
DOI: 10.1016/j.cancergen.2012.12.003     Document Type: Article

References (42)

1. Lynch T.J., Bell D.W., Sordella R., et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med 2004, 350:2129-2139.
2. Paez J.G., Jänne P.A., Lee J.C., et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science 2004, 304:1497-1500.
3. Zhang Z., Stiegler A.L., Boggon T.J., et al. EGFR-mutated lung cancer: a paradigm of molecular oncology. Oncotarget 2010, 1:497-514.
4. Sequist L.V., Bell D.W., Lynch T.J., et al. Molecular predictors of response to epidermal growth factor receptor antagonists in non-small-cell lung cancer. J Clin Oncol 2007, 25:587-595.
5. Gandara D.R., Lara P.N., Mack P., et al. Individualizing therapy for non-small-cell lung cancer: a paradigm shift from empiric to integrated decision-making. Clin Lung Cancer 2009, 10:148-150.
6. West H., Lilenbaum R., Harpole D., et al. Molecular analysis-based treatment strategies for the management of non-small cell lung cancer. J Thorac Oncol 2009, 4:S1029-S1039.
7. Molina J.R., Adjei A.A. The Ras/Raf/MAPK pathway. J Thorac Oncol 2006, 1:7-9.
8. Malumbres M., Barbacid M. RAS oncogenes: the first 30 years. Nat Rev Cancer 2003, 3:459-465.
9. Siddiqui A.D., Piperdi B. KRAS mutation in colon cancer: a marker of resistence to EGFR-I therapy. Ann Surg Oncol 2010, 4:1168-1176.
10. Santos E., Martin-Zanca D., Reddy E., et al. Malignant activation of a K-RAS oncogene in lung carcinoma but not in normal tissue of the same patient. Science 1984, 223:661-664.
11. Suda K., Tomizava K., Mitsudomi T. Biological and clinical significance of KRAS mutations in lung cancer: an oncogenic driver that contrasts with EGFR mutation. Cancer Metastasis Rev 2010, 29:49-60.
12. Rodenhuis S., van de Wetering M.L., Mooi W.J., et al. Mutational activation of the K-RAS oncogene: a possible pathogenetic factor in adenocarcinoma af the lung. N Engl J Med 1987, 317:929-935.
13. Lopez-Chavez A., Carter C.A., Giaccone G. The role of KRAS mutations in resistance to EGFR inhibition in the treatment of cancer. Curr Opin Investig Drugs 2009, 10:1305-1314.
14. Ding L., Getz G., Wheeler D.A., et al. Somatic mutations affect key pathways in lung adenocarcinoma. Nature 2008, 455:1069-1075.
15. Slebos R.J., Hruban R.H., Dalesio O. Relationship between K-RAS oncogene activation and smoking in adenocarcinoma of the human lung. J Natl Cancer Inst 1991, 83:1024-1027.
16. Ahrendt S.A., Decker P.A., Alawi E.A., et al. Cigarette smoking is strongly associated with mutation of the K-RAS gene in patients with primary adenocarcinoma of the lung. Cancer 2001, 92:1525-1530.
17. Marchetti A., Milella M., Felicioni L., et al. Clinical implications of KRAS mutations in lung cancer patients treated with tyrosine kinase inhibitors: an important role for mutations in minor clones. Neoplasia 2009, 11:1084-1092.
18. Eberhard D.A., Johnson B.E., Amler L.C., et al. Mutations in the epidermal growth factor receptor and in KRAS are predictive and prognostic indicators in patients with non-small-cell lung cancer treated with chemotherapy alone and in combination with erlotinib. J Clin Oncol 2005, 23:5900-5909.
19. Bonanno L., Schiavon M., Nardo G., et al. Prognostic and predictive implications of EGFR mutations, EGFR copy number and KRAS mutations in advanced stage lung adenocarcinoma. Anticancer Res 2010, 30:5121-5128.
20. Liu H.P., Isaac Wu H.D., Chang J.W., et al. Prognostic implications of epidermal growth factor receptor and KRAS gene mutations and epidermal growth factor receptor gene copy numbers in patients with surgically resectable non-small cell lung cancer in Taiwan. J Thorac Oncol 2010, 5:1175-1184.
21. Zhu C.Q., da Cunha Santos G., Ding K., et al. Role of KRAS and EGFR as biomarkers of response to erlotinib in National Cancer Institute of Canada Clinical Trials Group Study BR.21. J Clin Oncol 2008, 26:4268-4275.
22. Hirsch F.R., Varella-Garcia M., Bunn P.A., et al. Molecular predictors of outcome with gefitinib in a phase III placebo-controlled study in advanced non-small-cell lung cancer. J Clin Oncol 2006, 24:5034-5042.
23. Douillard J.Y., Shepherd F.A., Hirsh V., et al. Molecular predictors of outcome with gefitinib and docetaxel in previously treated non-small-cell lung cancer: data from the randomized phase III INTEREST trial. J Clin Oncol 2010, 28:744-752.
24. Cappuzzo F., Ciuleanu T., Stelmakh L., et al. Erlotinib as maintenance treatment in advanced non-small-cell lung cancer: a multicentre, randomised, placebo-controlled phase 3 study. Lancet Oncol 2010, 11:521-529.
25. Brugger W., Triller N., Blasinska-Morawiec M. Biomarker analyses from the phase III placebo-controlled SATURN study of maintenance erlotinib following first-line chemotherapy for advanced NSCLC. J Clin Oncol 2009, 27:S15. Abstract 8020.
26. Pesek M., Benesova L., Belsanova B., et al. Dominance of EGFR and insignificant KRAS mutations in prediction of tyrosine-kinase therapy for NSCLC patients stratified by tumor subtype and smoking status. Anticancer Res 2009, 29:2767-2773.
27. Minarik M., Benesova L., Belsanova B., et al. Impact of EGFR and KRAS mutations on survival prognosis of NSCLC patients treated with tyrosin-kinase inhibitors: comparison of gefitinib and erlotinib. Stud Pheumol Phthiseol 2009, 69:96-104.
28. Andreyev H.J.N., Norman A.R., Cunningham D., et al. Kirsten ras Mutations in Patients With Colorectal Cancer: the Multicenter " RASCAL" Study. J Natl Cancer Inst 1998, 90:675-684.
29. Winder T., Mündlein A., Rhomberg S., et al. Different types of K-RAS mutations are conversely associated with overall survival in patients with colorectal cancer. Oncol Rep 2009, 21:1283-1287.
30. Al Mulla F., MacKenzie E.M. Differences in in vitro invasive capacity induced by differences in Ki-Ras protein station. J Pathol 2001, 195:549-556.
31. Al Mulla F., Milner-White E.J., Going J.J., et al. Structural Differences between valine-12 and aspartate-12 Ras proteins may modify carcinoma aggression. J Pathol 1999, 187:433-438.
32. Janakiraman M., Vakiani E., Zeng Z., et al. Genomic and biological characterization of exon 4 KRAS mutations in human cancer. Cancer Res 2010, 70:5901-5911.
33. Garassino M.C., Marabese M., Rusconi P., et al. Different types of K-Ras mutations could affect drug sensitivity and tumour behavior in non-small-cell lung cancer. Ann Oncol 2011, 22:235-237.
34. Broggini M., Marabese M., Rusconi P., et al. Sorafenib activity in NSCLC cell lines seems related to a different type of K-RAS mutations. Ann Oncol 2011, 21(Supplement 8). viii131 (393P).
35. Ihle N.T., Byers L.A., Kim E.S., et al. Effect of KRAS oncogene substitutions on protein behavior: implications for signaling and clinical outcome. J Natl Cancer Inst 2012, 104:228-239.
36. Benesova L., Minarik M., Jancarikova D., et al. Multiplicity of EGFR and KRAS mutations in non-small cell lung cancer (NSCLC) patients treated with tyrosine kinase inhibitors. Anticancer Res 2010, 30:1667-1671.
37. Riely G.J., Pao W., Pham D., et al. Clinical course of patients with non-small cell lung cancer and epidermal growth factor receptor exon 19 and exon 21 mutations treated with gefitinib or erlotinib. Clin Cancer Res 2006, 12:839-844.
38. Won Y.W., Han J.Y., Lee G.K., et al. Comparison of clinical outcome of patients with non-small-cell lung cancer harbouring epidermal growth factor receptor exon 19 or exon 21 mutations. J Clin Pathol 2011, 64:947-952.
39. Mao C., Qiu L.X., Liao R.Y., et al. KRAS mutations and resistance to EGFR-TKIs treatment in patients with non-small cell lung cancer: a meta-analysis of 22 studies. Lung Cancer 2010, 69:272-278.
40. Neumann J., Zeindl-Eberhart E., Kirchner T., et al. Frequency and type of KRAS mutations in routine diagnostic analysis of metastatic colorectal cancer. Pathol Res Pract 2009, 205:858-862.
41. Haugen A., Mollerup S. Etiology of lung cancer. Textbook of Lung Cancer 2008, 1-9. Informa UK Ltd, London. 2nd ed. H. Hansen (Ed.).
42. Phillips D.H. Smoking-related DNA and protein adducts in human tissues. Carcinogenesis 2002, 23:1979-2004.