RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth

By G. Hatzivassiliou, Kyung Song, Ivana Yen, B. Brandhuber, Daniel J. Anderson, Ryan Alvarado, M. J. C. Ludlam, D. Stokoe, S. Gloor, G. Vigers and 11 more. Nature, 2010

1,601 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/93848ac042b4b5801fbba1b97ebcfb5ef7b04970

How researchers see this paper

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In Molecular Biology

1. C. Der
2. T. Graeber
3. Li Xie
4. Philip E. Bourne
5. M. Bahar
6. D. Kim
7. Hyun Joon Kim
8. S. Lippman

In Oncology

1. Antoni Ribas
2. C. Der
3. K. Flaherty
4. J. Wargo
5. J. Engelman
6. J. Settleman
7. R. Weinberg

In Pathology and Forensic Medicine

1. M. Bahar
2. D. Kim
3. Hyun Joon Kim
4. C. Der
5. J. Engelman

Citations in the corpus

• EGFR-mediated re-activation of MAPK signaling contributes to insensitivity of BRAF mutant colorectal cancers to RAF inhibition with vemurafenib (2012, background): “Recent studies have elegantly shown that activated RAS can cause MAPK pathway activation through direct activation of CRAF, or by the transactivation of BRAF-CRAF heterodimers in the presence of vemurafenib (11-13), or possibly through a combination of both mechanisms.”
• Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies (2023, background): “…V600E – mutant BRAF that dimerizes with other RAF mutants or with wild-type BRAF or CRAF exhibit drug resistance due to the unintended paradoxical activation of ERK, 322,389,393 which may also be responsible for the elevated toxicity and disruption in RAF signaling observed in non-cancer cells.”
• A Comprehensive Review on MAPK: A Promising Therapeutic Target in Cancer (2019, background): “These two mutated genes are found in over 30% of all human tumors and in 40% of melanomas [92,93].”
• KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer (2018, background): “In RAS-mutant cells, the BRAF-selective inhibitors cause paradoxical activation of ERK signaling (Hatzivassiliou et al. 2010; Heidorn et al. 2010; Poulikakos et al. 2010).”
• Combined BRAF and MEK Inhibition in Melanoma with BRAF V600 Mutations (2012, neutral): “Nausea 0 11 (21) 3 (6) 25 (46) 1 (2) 24 (44)”
• RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E) (2011, background): “The sequences are JC-1, 59-GGACAGUGGACUUGAUUAGUU-39; JC-2, 59-AGGA CAGUGGACUUGAUUAUU-39; ex[4-8]-1, 59-ACUGAUAUUUCCUGGCUU AUU-39; ex[4-8]-2, 59-CUGUCAAACAUGUGGUUAUUU-39.”
• Personalized Oncology Through Integrative High-Throughput Sequencing: A Pilot Study (2011, neutral): “/0A $((13,2), G56 $(3 ))2 !4/0*++3CFH<I>! &? !"UG$1%&"'()31+(-! .”