KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer.

By A. Lièvre, J. Bachet, D. Le Corre, V. Boige, B. Landi, J. Emile, J. Côté, G. Tomasic, C. Penna, Michel Ducreux and 3 more. Cancer Research, 2006

2,333 citations recorded by the source corpus.

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

View Paper: https://www.semanticscholar.org/paper/6feed2a3f8890aca7b76ca0769ce88c8ce55ef62

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. J. Baselga
2. Lewis C. Cantley
3. Ralph Weissleder
4. J. Engelman

In Pathology and Forensic Medicine

1. A. Bardelli
2. Kenichi Sugihara
3. J. Engelman

In Pulmonary and Respiratory Medicine

1. J. Engelman
2. J. Baselga
3. Kenichi Sugihara
4. Ralph Weissleder
5. D. Hanahan
6. Lee Josephson
7. Isaac Koh
8. Vasilis Ntziachristos

Citations in the corpus

• 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).”
• Effective Use of PI3K and MEK Inhibitors to Treat Mutant K-Ras G12D and PIK3CA H1047R Murine Lung Cancers (2008, background): “Although this study suggests that cancers with PIK3CA mutations may respond to PI3K inhibitors, human cancers with PIK3CA mutations often harbor other known oncogenic mutations such as mutations in KRAS (colon cancers) and HER2 (encoding human epidermal growth factor-2) amplification (breast”
• Phase I, dose-escalation study of BKM120, an oral pan-Class I PI3K inhibitor, in patients with advanced solid tumors. (2012, background): “Preclinical data suggest KRAS mutations may predict resistance to PI3K inhibition(36-38); however, the PR in a patient with breast cancer suggests that implications of breast cancer KRAS mutation may differ from colon cancer, in which it predicts resistance to inhibition of growth factor signaling.(”
• KRAS wild-type state predicts survival and is associated to early radiological response in metastatic colorectal cancer treated with cetuximab. (2008, background): “The KRAS mutation state of the tumor has been proposed as a promising marker of response to CTX in mCRC [4].”
• Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging (2011, background): “Recently the Ras/Raf/MEK/ERK and Ras/PI3K/PTEN/Akt/mTOR pathways have been shown to have roles in cancer stem cells, senescence, aging and sensitivity to targeted therapy [203-245].”
• A comprehensive survey of genomic alterations in gastric cancer reveals systematic patterns of molecular exclusivity and co-occurrence among distinct therapeutic targets (2012, neutral): “gastrointestinal cancers (eg, colorectal and pancreatic cancer).(40) 41 Confirming these earlier studies,(41) the KRASmutation rate in our own series was extremely lowdamong 139 gastric cancers genotyped for KRAS codon 12 and 13 mutations, only one tumour exhibited a KRAS mutation (G13D in 069LYK).”