Gene copy number for epidermal growth factor receptor (EGFR) and clinical response to antiEGFR treatment in colorectal cancer: a cohort study.

By M. Moroni, S. Veronese, S. Benvenuti, G. Marrapese, A. Sartore-Bianchi, F. Di Nicolantonio, M. Gambacorta, S. Siena, A. Bardelli. The Lancet Oncology, 2005

977 citations recorded by the source corpus.

Subfields: Cancer Research, Epidemiology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/3f52d4115bfbe3714361ad5f1fa8462542e385de

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In Cancer Research

1. J. Talmadge
2. A. Bardelli
3. Carlos L. Arteaga
4. I. J. Fidler
5. R. Weinberg
6. J. Massagué
7. Scott Valastyan

In Pulmonary and Respiratory Medicine

1. Carlos L. Arteaga
2. J. Engelman

Citations in the corpus

• KRAS wild-type state predicts survival and is associated to early radiological response in metastatic colorectal cancer treated with cetuximab. (2008, background): “Lastly, there has been a report on two KRAS mutant patients with an OR on CTX [9, 10].”
• Oncogenic activation of the RAS/RAF signaling pathway impairs the response of metastatic colorectal cancers to anti-epidermal growth factor receptor antibody therapies. (2007, methodology): “In our previous report, the mutational status of the EGFR signaling effectors (K-RAS, BRAF, or PIK3CA) was not statistically associated with the response, although the K-RAS mutations seemed to be slightly more frequent in nonresponsive patients (2).”
• Amplification of the MET receptor drives resistance to anti-EGFR therapies in colorectal cancer (2013, neutral): “DiFi cells over-express EGFR as a result of high-level amplification of the EGFR gene locus (26, 27).”
• KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer. (2006, methodology): “This is in good agreement with the in vitro proliferation inhibition observed with a low dose of cetuximab in the DiFi tumor cell line that has the highest copy number of EGFR of the different tested cell lines (5).”
• Association of KRAS p.G13D mutation with outcome in patients with chemotherapy-refractory metastatic colorectal cancer treated with cetuximab. (2010, methodology): “KRAS mutation analysis was performed by direct sequencing as described previously.(6-8) All patients in the Leuven and Italian datasetsprovidedwritten informedconsenttotheoriginalclinicaltrialandtomolecular analyses.”
• ERBB receptors: From oncogene discovery to basic science to mechanism-based cancer therapeutics (2014, background): “Although some reports suggest that EGFR amplification correlates with response to cetuximab (Moroni et al., 2005), this alteration is not currently used as a predictive biomarker.”