Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer.

By F. Di Nicolantonio, M. Martini, F. Molinari, A. Sartore-Bianchi, S. Arena, P. Saletti, S. De Dosso, L. Mazzucchelli, M. Frattini, S. Siena and 1 more. Journal of Clinical Oncology, 2008

1,660 citations recorded by the source corpus.

Subfields: Oncology, Pathology and Forensic Medicine, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/9b53c6f002fa0b56c2352beb67024de1890e2c9a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Oncology

1. Hans Clevers
2. J. Engelman
3. Alexander van Oudenaarden
4. Fortunato Ciardiello
5. Michael R. Stratton
6. K. Flaherty
7. Gad Getz
8. J. Wargo

In Pathology and Forensic Medicine

1. A. Bardelli
2. Hans Clevers
3. J. Engelman

In Pulmonary and Respiratory Medicine

1. J. Engelman
2. Hans Clevers
3. M. V. Vander Heiden

Citations in the corpus

• Prospective derivation of a Living Organoid Biobank of colorectal cancer patients (2015, background): “Accession Numbers GSE64392 GSE65253”
• EGFR-mediated re-activation of MAPK signaling contributes to insensitivity of BRAF mutant colorectal cancers to RAF inhibition with vemurafenib (2012, background): “Furthermore, some investigators (6) have suggested that the presence of BRAF mutation predicts a lack of response to monoclonal antibodies against the epidermal growth factor receptor (EGFR), such as cetuximab.”
• A molecularly annotated platform of patient-derived xenografts ("xenopatients") identifies HER2 as an effective therapeutic target in cetuximab-resistant colorectal cancer. (2011, background): “7% frequency already described in metastatic colorectal cancer (13, 24).”
• Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR (2012, neutral): “shRNA inserts were retrieved from 8mg genomic DNA by PCR amplification (PCR1 and PCR2, see below for primer information) using the following conditions: (1) 98 uC, 30 s; (2) 98 uC, 10 s; (3) 60 uC, 20 s; (4) 72 uC, 1 min; (5) to step (2), 15 cycles; (6) 72 uC, 5 min; (7) 4 uC.”
• Impact of BRAF Mutation and Microsatellite Instability on the Pattern of Metastatic Spread and Prognosis in Metastatic Colorectal Cancer (2011, background): “They are present in approximately 10% of CRC, are a significant negative prognostic factor in advanced disease, and may predict resistance to EGFR inhibitors.(3,17) BRAF mutation testing is recommended for metastatic CRC in the latest National Comprehensive Cancer Network guidelines.”
• Amplification of the MET receptor drives resistance to anti-EGFR therapies in colorectal cancer (2013, neutral): “BRAF mutations, which are mutually exclusive with KRAS , have also been associated to lack of response to cetuximab and panitumumab (9).”