Expression of epiregulin and amphiregulin and K-ras mutation status predict disease control in metastatic colorectal cancer patients treated with cetuximab.
By S. Khambata-Ford, C. Garrett, N. Meropol, M. Basik, C. Harbison, Shujian Wu, T. Wong, Xin Huang, C. Takimoto, A. Godwin and 8 more. Journal of Clinical Oncology, 2007
1,219 citations recorded by the source corpus.
Subfields: Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/9eeaa4caced0dbc03a2a119fd8afeb26a4c721be
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Oncology
- Carlos L. Arteaga
- J. Engelman
- Fortunato Ciardiello
- Y. Yarden
- C. Sawyers
- R. Avraham
- R. Roskoski
- M. Lacouture
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Feedback regulation of EGFR signalling: decision making by early and delayed loops (2011, background): “In line with antibody-mediated blocking of autocrine loops, patients with tumours that overexpress the EGFR ligands epiregulin and amphiregulin are more likely to benefit from antibody treatmen”
- KRAS wild-type state predicts survival and is associated to early radiological response in metastatic colorectal cancer treated with cetuximab. (2008, background): “If this model holds true, KRAS mutations may be negative predictors of response even in the presence of supra-normal upstream activation such as seen with EGFR amplifications or increased ligand expression [11].”
- EPIC: phase III trial of cetuximab plus irinotecan after fluoropyrimidine and oxaliplatin failure in patients with metastatic colorectal cancer. (2008, background): “Recent reports indicate that the presence of mutations on the KRAS gene is a strong predictor of nonresponsiveness to cetuximab,(27-29) and that overexpression of the EGFR ligands amphiregulin and epiregulin may be a robust marker of response.(28) While trials are ongoing to validate these biomarker”
- ERBB receptors: From oncogene discovery to basic science to mechanism-based cancer therapeutics (2014, background): “Importantly, cetuximab provides clinical benefit primarily in colorectal cancers that do not harbor KRAS mutations (Cunningham et al., 2004) and in those with high expression of the EGFR ligands amphiregulin and epiregulin (Khambata-Ford et al., 2007).”
- The cancer biomarker problem (2008, background): “Conversely, distinct mutations in KRAS predict that patients with lung cancer will fail to respond to these inhibitors and that patients with colon cancer will fail to respond to therapy with EGFR-specific antibod”
- Colorectal carcinoma: Pathologic aspects. (2012, background): “As a critical downstream molecule in the epidermal growth factor receptor (EGFR) signaling pathway, mutant KRAS renders tumors resistant to EGFR-targeted therapies (2,119-121).”
- 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, methodology): “The review of the evidence on which this PCO is based consists primarily of the rigorous systematic review of the literature conducted by the Blue Cross and Blue Shield Association (BCBSA) Technology Evaluation Center (TEC).(1-10) Details of the BCBSA TEC assessment can be found in the full TEC repo”
- Japanese Society for Cancer of the Colon and Rectum (JSCCR) guidelines 2016 for the treatment of colorectal cancer (2012, background): “• The usefulness of anti-EGFR antibody drugs has been reported in metastatic colorectal cancer without KRAS gene mutations [38–41, 47, 53, 55, 85–90].”