BRAF mutation predicts sensitivity to MEK inhibition

By D. Solit, Levi A. Garraway, C. Pratilas, A. Sawai, Gad Getz, A. Basso, Q. Ye, Jose Lobo, Yuhong She, I. Osman and 4 more. Nature, 2006

1,346 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/f7025775912975c6b5ab44cd59f0b2fa6d0af93e

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

1. J. Baselga
2. Jianming Zhang
3. C. Der
4. P. Roberts
5. Walter Kolch
6. J. Sáez-Rodríguez
7. Michael P. Menden
8. Kevan M. Shokat

In Pathology and Forensic Medicine

1. C. Der
2. P. Roberts
3. A. Bardelli
4. R. Roskoski

Citations in the corpus

• Organoid cultures derived from patients with advanced prostate cancer (2014, neutral): “…Scardino,2 Vincent P. Laudone,2 Kristen R. Curtis,11 Dana E. Rathkopf,10,11 Michael J. Morris,10,11 Daniel C. Danila,10,11 Susan F. Slovin,10,11 Stephen B. Solomon,9 James A. Eastham,2 Ping Chi,1,10,11 Brett Carver,1,2 Mark A. Rubin,4,8 Howard I. Scher,10,11 Hans Clevers,5 Charles L.…”
• Oncogenic activation of the RAS/RAF signaling pathway impairs the response of metastatic colorectal cancers to anti-epidermal growth factor receptor antibody therapies. (2007, background): “signal-regulated kinase kinase inhibitors, such as PD0325901 and ARRY-142886, have shown good preclinical activity (20, 21) and have entered recently clinical trials.”
• Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. (2008, positive): “Thus, treatment of BRAFV600E-positive melanoma cells with a BRAF shRNA (Hoeflich et al., 2006) or an inhibitor of BRAF (Sharma et al., 2005) or MEK (Solit et al., 2006) blocks cellular proliferation.”
• MAP kinase signalling pathways in cancer (2007, background): “This may explain why tumour cells with B-Raf mutations apparently are exquisitely sensitive to MEK inhibition whereas tumour cells with Ras mutations are rather resistant (Solit et al., 2006).”
• Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer (2007, background): “, (2006) recently reported that B-Raf mutant tumors are exquisitely sensitive to MEK inhibition (Solit et al., 2006).”
• The Epidermal Growth Factor Receptor Pathway: A Model for Targeted Therapy (2006, background): “Th ese fi ndings are of considerable importance, as B-Raf mutant tumors are exquisitely sensitive to small-molecule MAPK/extracellular signal-regulated kinase kinase inhibitors (49).”
• Phase I pharmacokinetic and pharmacodynamic study of the oral, small-molecule mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244 (ARRY-142886) in patients with advanced cancers. (2008, background): “DNA Mutation Analysis Activating mutations in the RAS genes (KRAS and NRAS) and in the BRAF gene have been reported to identify tumors that may be sensitive to MEK inhibition.(6,15) Therefore, the presence of specific mutations in these genes was evaluated in tumor samples from this study.”
• MEK1 mutations confer resistance to MEK and B-RAF inhibition (2009, background): “Preclinical studies suggest that some NRAS-mutant melanomas may also exhibit sensitivity to RAF or MEK inhibition (4, 29), whereas KRAS mutations have conferred only marginal sensitivity (30).”
• Targeting the cancer kinome through polypharmacology (2010, positive): “Sorafenib has yet to show clinical benefit for tumours that contain frequent Ras mutations, such as lung and pancreatic cancer, and has also failed in clinical trials for the treatment of melanoma 82 , a disease that has a high rate of BRAF mutations 43,83 .”
• Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity (2008, result): “(2004)BAY43–9006exhibitsbroadspectrumoralantitumoractivityand targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis.”