Reply to E. Hawkes et al

[1]  D. Cunningham,et al.  Relationship between colorectal cancer biomarkers and response to epidermal growth factor receptor monoclonal antibodies. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[2]  A. Bardelli,et al.  Molecular mechanisms of resistance to cetuximab and panitumumab in colorectal cancer. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[3]  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.

[4]  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.

[5]  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.

[6]  J. Meyerhardt,et al.  Prognostic and predictive value of common mutations for treatment response and survival in patients with metastatic colorectal cancer , 2009, British Journal of Cancer.

[7]  D. Lambrechts,et al.  PIK3CA Mutations Are Not a Major Determinant of Resistance to the Epidermal Growth Factor Receptor Inhibitor Cetuximab in Metastatic Colorectal Cancer , 2009, Clinical Cancer Research.

[8]  Francesca Molinari,et al.  PIK3CA mutations in colorectal cancer are associated with clinical resistance to EGFR-targeted monoclonal antibodies. , 2009, Cancer research.

[9]  L. Mazzucchelli,et al.  Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[10]  Li Zhao,et al.  Helical domain and kinase domain mutations in p110α of phosphatidylinositol 3-kinase induce gain of function by different mechanisms , 2008, Proceedings of the National Academy of Sciences.