Analysis of PTEN, BRAF, and EGFR status in determining benefit from cetuximab therapy in wild-type KRAS metastatic colon cancer.
By P. Laurent-Puig, A. Cayre, G. Manceau, E. Buc, J. Bachet, T. Lecomte, P. Rougier, A. Lièvre, B. Landi, V. Boige and 7 more. Journal of Clinical Oncology, 2009
704 citations recorded by the source corpus.
Subfields: Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/72d08ec19ef66240496020cbefa6e6d6f552b100
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Citations in the corpus
- Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “For example, increased EGFR expression, typically determined by immunohistochemistry, was shown to not correlate with response to EGFR inhibitors [381,382], whereas another studied showed a positive correlation [383].”
- ESMO consensus guidelines for the management of patients with metastatic colorectal cancer. (2016, background): “PIK3CA and PTEN alterations often co-occur with KRAS or BRAF mutations [107, 112], but there is insufficient evidence for their use as biomarkers of resistance to EGFR-antibody therapy.”
- Predicting ligand-dependent tumors from multi-dimensional signaling features (2017, background): “Therefore, the approvals of EGFR inhibitors in non-small cell lung cancer (NSCLC) and CRC confirm the predicted dependence on EGFR signaling.(53,54) In contrast, the low dependence of NSCLC on HGF signaling might explain the failure of Onartuzumab (MetMAb), a Met blocking antibody in a Phase 3 study”
- 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 molecularly annotated platform of patient-derived xenografts ("xenopatients") identifies HER2 as an effective therapeutic target in cetuximab-resistant colorectal cancer. (2011, background): “In KRAS wild-type tumors, it has been demonstrated that patients with an EGFR FISH-positive phenotype show greater response rates (71%) compared with patients with normal EGFR copy number (37%) (34).”