The predictive value of KRAS, NRAS, BRAF, PIK3CA and PTEN for anti-EGFR treatment in metastatic colorectal cancer: A systematic review and meta-analysis
暂无分享,去创建一个
Mef Nilbert | S. Ladelund | M. Nilbert | C. Therkildsen | Christina Therkildsen | Troels K. Bergmann | Tine Henrichsen-Schnack | Steen Ladelund | T. Bergmann | Tine Henrichsen-Schnack
[1] L. Mazzucchelli,et al. Multi-Determinants Analysis of Molecular Alterations for Predicting Clinical Benefit to EGFR-Targeted Monoclonal Antibodies in Colorectal Cancer , 2009, PloS one.
[2] V. Heinemann,et al. The influence of KRAS and BRAF mutations on the efficacy of cetuximab‐based first‐line therapy of metastatic colorectal cancer: An analysis of the AIO KRK‐0104‐trial , 2012, International journal of cancer.
[3] J. Tabernero,et al. Panitumumab-FOLFOX4 treatment and RAS mutations in colorectal cancer. , 2013, The New England journal of medicine.
[4] S. Kato,et al. Clinical usefulness of KRAS, BRAF, and PIK3CA mutations as predictive markers of cetuximab efficacy in irinotecan- and oxaliplatin-refractory Japanese patients with metastatic colorectal cancer , 2013, International Journal of Clinical Oncology.
[5] F. Siannis,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. , 2008, The Lancet. Oncology.
[6] J. Hancock,et al. Ras proteins: different signals from different locations , 2003, Nature Reviews Molecular Cell Biology.
[7] N. Funel,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. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[8] Sabine Tejpar,et al. Effects of KRAS, BRAF, NRAS, and PIK3CA mutations on the efficacy of cetuximab plus chemotherapy in chemotherapy-refractory metastatic colorectal cancer: a retrospective consortium analysis. , 2010, The Lancet. Oncology.
[9] S. Andreola,et al. PI3KCA/PTEN deregulation contributes to impaired responses to cetuximab in metastatic colorectal cancer patients. , 2009, Annals of oncology : official journal of the European Society for Medical Oncology.
[10] Seung-Yong Jeong,et al. Analysis of KRAS, BRAF, PTEN, IGF1R, EGFR intron 1 CA status in both primary tumors and paired metastases in determining benefit from cetuximab therapy in colon cancer , 2011, Cancer Chemotherapy and Pharmacology.
[11] Armando Santoro,et al. Cetuximab monotherapy and cetuximab plus irinotecan in irinotecan-refractory metastatic colorectal cancer. , 2004, The New England journal of medicine.
[12] T. Cenci,et al. Is there a role for IGF1R and c-MET pathways in resistance to cetuximab in metastatic colorectal cancer? , 2011, Clinical colorectal cancer.
[13] Barry S Taylor,et al. Genomic and biological characterization of exon 4 KRAS mutations in human cancer. , 2010, Cancer research.
[14] S. Pauker,et al. Summary of recommendations: The Evaluation of Genomic , 2022 .
[15] S. Erdamar,et al. Analysis of PTEN, BRAF and PI3K status for determination of benefit from cetuximab therapy in metastatic colorectal cancer patients refractory to chemotherapy with wild-type KRAS , 2014, Tumor Biology.
[16] C. Bokemeyer,et al. Addition of cetuximab to chemotherapy as first-line treatment for KRAS wild-type metastatic colorectal cancer: pooled analysis of the CRYSTAL and OPUS randomised clinical trials. , 2012, European journal of cancer.
[17] T. Eberlein. Cetuximab Plus Irinotecan, Fluorouracil, and Leucovorin as First-Line Treatment for Metastatic Colorectal Cancer: Updated Analysis of Overall Survival According to Tumor KRAS and BRAF Mutation Status , 2012 .
[18] E. Van Cutsem,et al. Randomized phase III study of panitumumab with fluorouracil, leucovorin, and irinotecan (FOLFIRI) compared with FOLFIRI alone as second-line treatment in patients with metastatic colorectal cancer. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[19] H. Hurwitz,et al. A phase II study of capecitabine, oxaliplatin, bevacizumab and cetuximab in the treatment of metastatic colorectal cancer. , 2011, Anticancer research.
[20] Reiko Nishihara,et al. Aspirin use, tumor PIK3CA mutation, and colorectal-cancer survival. , 2012, The New England journal of medicine.
[21] Josep Tabernero,et al. Randomized, phase III trial of panitumumab with infusional fluorouracil, leucovorin, and oxaliplatin (FOLFOX4) versus FOLFOX4 alone as first-line treatment in patients with previously untreated metastatic colorectal cancer: the PRIME study. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[22] Zuyao Yang,et al. Promising biomarkers for predicting the outcomes of patients with KRAS wild‐type metastatic colorectal cancer treated with anti‐epidermal growth factor receptor monoclonal antibodies: A systematic review with meta‐analysis , 2013, International journal of cancer.
[23] J. Reid,et al. Analysis of PTEN, BRAF, and EGFR status in determining benefit from cetuximab therapy in wild-type KRAS metastatic colon cancer. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[24] M. Somerfield,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. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[25] J. Higgins,et al. Cochrane Handbook for Systematic Reviews of Interventions, Version 5.1.0. The Cochrane Collaboration , 2013 .
[26] J. Mariadason,et al. PTEN gene expression and mutations in the PIK3CA gene as predictors of clinical benefit to anti-epidermal growth factor receptor antibody therapy in patients with KRAS wild-type metastatic colorectal cancer. , 2012, Clinical colorectal cancer.
[27] L. Shen,et al. Wild-type KRAS and BRAF could predict response to Cetuximab in Chinese colorectal cancer patients , 2011, Chinese journal of cancer research = Chung-kuo yen cheng yen chiu.
[28] F. Cavalli,et al. PTEN loss of expression predicts cetuximab efficacy in metastatic colorectal cancer patients , 2007, British Journal of Cancer.
[29] M. Tzardi,et al. Impact of KRAS, BRAF, PIK3CA Mutations, PTEN, AREG, EREG Expression and Skin Rash in ≥2nd Line Cetuximab-Based Therapy of Colorectal Cancer Patients , 2011, PloS one.
[30] G. Tortora,et al. EGFR antagonists in cancer treatment. , 2008, The New England journal of medicine.
[31] P. Gascón,et al. Serum matrilysin correlates with poor survival independently of KRAS and BRAF status in refractory advanced colorectal cancer patients treated with irinotecan plus cetuximab , 2011, Tumor Biology.
[32] G. Fontanini,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 , 2009, British Journal of Cancer.
[33] A. Jemal,et al. Cancer statistics, 2013 , 2013, CA: a cancer journal for clinicians.
[34] I. Nagtegaal,et al. Markers for EGFR pathway activation as predictor of outcome in metastatic colorectal cancer patients treated with or without cetuximab. , 2010, European journal of cancer.
[35] Renzo Boldorini,et al. Increased Detection Sensitivity for KRAS Mutations Enhances the Prediction of Anti-EGFR Monoclonal Antibody Resistance in Metastatic Colorectal Cancer , 2011, Clinical Cancer Research.
[36] E. Van Cutsem,et al. Massively Parallel Tumor Multigene Sequencing to Evaluate Response to Panitumumab in a Randomized Phase III Study of Metastatic Colorectal Cancer , 2013, Clinical Cancer Research.
[37] E. Scarpi,et al. Predictive role of multiple gene alterations in response to cetuximab in metastatic colorectal cancer: A single center study , 2012, Journal of Translational Medicine.