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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6848950 | PMC |
| http://dx.doi.org/10.1016/j.ccell.2017.02.007 | DOI Listing |
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Analysis of RAS and drug induced homo- and heterodimerization of RAF and KSR1 proteins in living cells using split Nanoluc luciferase.
Cell Commun Signal
June 2023
Institute of Molecular Medicine and Cell Research (IMMZ), Zentrum für Biochemie und Molekulare Zellforschung (ZBMZ), Faculty of Medicine, University of Freiburg, Stefan-Meier-Str. 17, Freiburg, 79104, Germany.
The dimerization of RAF kinases represents a key event in their activation cycle and in RAS/ERK pathway activation. Genetic, biochemical and structural approaches provided key insights into this process defining RAF signaling output and the clinical efficacy of RAF inhibitors (RAFi). However, methods reporting the dynamics of RAF dimerization in living cells and in real time are still in their infancy.
View Article and Find Full Text PDFThe paradox-breaking panRAF plus SRC family kinase inhibitor, CCT3833, is effective in mutant KRAS-driven cancers.
Ann Oncol
February 2021
Drug Discovery Unit, Cancer Research UK Manchester Institute, the University of Manchester, Alderley Park, Manchester, UK; Gene and Oncogene Targeting Team, CR-UK Cancer Therapeutics Unit, the Institute of Cancer Research, London, UK. Electronic address:
Background: KRAS is mutated in ∼90% of pancreatic ductal adenocarcinomas, ∼35% of colorectal cancers and ∼20% of non-small-cell lung cancers. There has been recent progress in targeting KRAS specifically, but therapeutic options for other mutant forms of KRAS are limited, largely because the complexity of downstream signaling and feedback mechanisms mean that targeting individual pathway components is ineffective.
Design: The protein kinases RAF and SRC are validated therapeutic targets in KRAS-mutant pancreatic ductal adenocarcinomas, colorectal cancers and non-small-cell lung cancers and we show that both must be inhibited to block growth of these cancers.
Identifying the ErbB/MAPK Signaling Cascade as a Therapeutic Target in Canine Bladder Cancer.
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Flint Animal Cancer Center, Department of Clinical Sciences (K.E.C., B.G.H., D.L.G., D.L.D.), and Cell and Molecular Biology Graduate Program (K.E.C., D.L.G., D.L.D.), Colorado State University, Fort Collins, Colorado; and University of Colorado Cancer Center, Aurora, Colorado (D.L.G., D.L.D.) dawn.
Transitional cell carcinoma (TCC) of the bladder comprises 2% of diagnosed canine cancers. TCC tumors are generally inoperable and unresponsive to traditional chemotherapy, indicating a need for more effective therapies. BRAF, a kinase in the mitogen-activated protein kinase (MAPK) pathway, is mutated in 70% of canine TCCs.
View Article and Find Full Text PDFResponse and Resistance to Paradox-Breaking BRAF Inhibitor in Melanomas and .
Mol Cancer Ther
January 2018
Department of Cancer Biology, Thomas Jefferson University, Philadelphia, Pennsylvania.
FDA-approved BRAF inhibitors produce high response rates and improve overall survival in patients with BRAF V600E/K-mutant melanoma, but are linked to pathologies associated with paradoxical ERK1/2 activation in wild-type BRAF cells. To overcome this limitation, a next-generation paradox-breaking RAF inhibitor (PLX8394) has been designed. Here, we show that by using a quantitative reporter assay, PLX8394 rapidly suppressed ERK1/2 reporter activity and growth of mutant BRAF melanoma xenografts.
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