MEK1 mutations confer resistance to MEK and B-RAF inhibition
By Caroline M. Emery, K. Vijayendran, M. Zipser, Allison M. Sawyer, Lili Niu, Jessica J. Kim, C. Hatton, R. Chopra, P. Oberholzer, M. Karpova and 6 more. Proceedings of the National Academy of Sciences of the United States of America, 2009
656 citations recorded by the source corpus.
Subfields: Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/6e1c9c773e2fc66820b424e24d8152ac5e998ddc
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
Citations in the corpus
- Lessons from the cancer genome. (2013, neutral): “Multiple genetic mechanisms of resistance have been described (oncogenicNRASmutations, COT/MAP3K8 gains,BRAF amplification, activatingMEK1mutations, and NF1 loss), each of which produces sustained MAP kinase (ERK) activity in the presence of drug (Emery et al., 2009; Johannessen et al., 2010; Nazari”
- Discovery of a novel ERK inhibitor with activity in models of acquired resistance to BRAF and MEK inhibitors. (2013, background): “BRAF amplification, as well as expression of drug resistant BRAF splice-variants lacking N-terminal regulatory regions, have been described as clinical resistance mechanisms in PLX4032-relapsed melanoma patients while MEK1 was identified in a patient who relapsed on treatment with the MEK inhibitor ”
- Combined BRAF and MEK Inhibition in Melanoma with BRAF V600 Mutations (2012, neutral): “Constipation 0 6 (11) 1 (2) 9 (17) 0 12 (22)”
- BRAF inhibition is associated with enhanced melanoma antigen expression and a more favorable tumor microenvironment in patients with metastatic melanoma (2013, background): “There is a great deal of ongoing research to determine mechanisms of resistance and strategies to overcome resistance (7-9).”
- Selective BRAFV600E inhibition enhances T-cell recognition of melanoma without affecting lymphocyte function. (2010, background): “Functional redundancy and compensatory activity through alternate signaling pathways might explain the low response rates to MEK inhibitors and the emergence of resistance seen in patients treated with selective BRAF inhibitors (7, 8).”
- Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling. (2011, methodology): “cells and sequenced using an Illumina GAIIx instrument, as described previously.(59)”