Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity

By J. Tsai, John T. Lee, Weiru Wang, Jiazhong Zhang, Hanna Cho, Shumeye Mamo, R. Bremer, S. Gillette, Jun Kong, N. Haass and 28 more. Proceedings of the National Academy of Sciences of the United States of America, 2008

1,352 citations recorded by the source corpus.

Subfields: Molecular Biology, Organic Chemistry, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/329baec0f07adeca0b381240500002c5df7732fe

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. Jianming Zhang
2. J. Reis-Filho
3. A. Wang-Gillam
4. Ivet Bahar
5. D. DeNardo
6. Yu Zhu
7. William R. Sellers
8. B. West

In Organic Chemistry

1. Benjamin P. Roscoe

In Pathology and Forensic Medicine

1. J. Reis-Filho
2. R. Roskoski

Citations in the corpus

• Resistance to vemurafenib resulting from a novel mutation in the BRAFV600E kinase domain (2013, methodology): “Images of BRAF bound to PLX4720 were generated from Protein Data Bank (PDB) entry 3C4C (Tsai et al., 2008) using the Pymol software package (Delano Inc.”
• Leukocyte Complexity Predicts Breast Cancer Survival and Functionally Regulates Response to Chemotherapy (2011, methodology): “The 80-day-old MMTV-PyMT female littermates were randomized by initial tumor volume and fed either PLX3397 (20, 61, 62) formulated in mouse chow or control chow (provided by Plexxikon Inc).”
• RAF inhibitors transactivate RAF dimers and ERK signaling in cells with wild-type BRAF (2010, neutral): “Structuralstudies 6 predict that the T421M mutation should prevent drug binding and catC(T421M) was indeed resistant to inhibition by PLX4032/PLX4720 in vitro (Supplementary Fig.”
• Kinase-Dead BRAF and Oncogenic RAS Cooperate to Drive Tumor Progression through CRAF (2010, background): “…why PLX4720 only induces weak binding of BRAF to CRAF, but this may stem from its unique property of displacing the a-C helix of BRAF when it binds (Tsai et al., 2008) and suggests that this helix is important for BRAF binding to CRAF, something that will only be resolved when the BRAF:CRAF…”
• MEK1 mutations confer resistance to MEK and B-RAF inhibition (2009, methodology): “To determine whether MEK1 mutations confer crossresistance to RAF inhibition, we examined the effects of the selective B-RAF inhibitor PLX4720 (21) in the cultured melanoma lines described above.”