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Literature DB >> 22318779

New insight puts CRAF in sight as a therapeutic target.

Abstract

By selectively depleting components of the RAF-MEK-ERK pathway in transgenic mice, it is now shown in 2 studies that CRAF is critical for signaling to MEK downstream of oncogenic Kras and that BRAF is not required.

Entities: Chemical Disease Gene Species

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Year: 2011 PMID： 22318779 PMCID： PMC3272431 DOI： 10.1158/2159-8290.CD-11-0118

Source DB: PubMed Journal: Cancer Discov ISSN： 2159-8274 Impact factor: 39.397

11 in total

1. c-Raf, but not B-Raf, is essential for development of K-Ras oncogene-driven non-small cell lung carcinoma.

Authors: Rafael B Blasco; Sarah Francoz; David Santamaría; Marta Cañamero; Pierre Dubus; Jean Charron; Manuela Baccarini; Mariano Barbacid
Journal: Cancer Cell Date: 2011-04-21 Impact factor: 31.743

2. In melanoma, RAS mutations are accompanied by switching signaling from BRAF to CRAF and disrupted cyclic AMP signaling.

Authors: Nicolas Dumaz; Robert Hayward; Jan Martin; Lesley Ogilvie; Douglas Hedley; John A Curtin; Boris C Bastian; Caroline Springer; Richard Marais
Journal: Cancer Res Date: 2006-10-01 Impact factor: 12.701

3. A Raf-induced allosteric transition of KSR stimulates phosphorylation of MEK.

Authors: Damian F Brennan; Arvin C Dar; Nicholas T Hertz; William C H Chao; Alma L Burlingame; Kevan M Shokat; David Barford
Journal: Nature Date: 2011-03-27 Impact factor: 49.962

4. Inhibition of mutated, activated BRAF in metastatic melanoma.

Authors: Keith T Flaherty; Igor Puzanov; Kevin B Kim; Antoni Ribas; Grant A McArthur; Jeffrey A Sosman; Peter J O'Dwyer; Richard J Lee; Joseph F Grippo; Keith Nolop; Paul B Chapman
Journal: N Engl J Med Date: 2010-08-26 Impact factor: 91.245

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

Authors: Georgia Hatzivassiliou; Kyung Song; Ivana Yen; Barbara J Brandhuber; Daniel J Anderson; Ryan Alvarado; Mary J C Ludlam; David Stokoe; Susan L Gloor; Guy Vigers; Tony Morales; Ignacio Aliagas; Bonnie Liu; Steve Sideris; Klaus P Hoeflich; Bijay S Jaiswal; Somasekar Seshagiri; Hartmut Koeppen; Marcia Belvin; Lori S Friedman; Shiva Malek
Journal: Nature Date: 2010-02-03 Impact factor: 49.962

6. Kinase-dead BRAF and oncogenic RAS cooperate to drive tumor progression through CRAF.

Authors: Sonja J Heidorn; Carla Milagre; Steven Whittaker; Arnaud Nourry; Ion Niculescu-Duvas; Nathalie Dhomen; Jahan Hussain; Jorge S Reis-Filho; Caroline J Springer; Catrin Pritchard; Richard Marais
Journal: Cell Date: 2010-01-22 Impact factor: 41.582

New insight puts CRAF in sight as a therapeutic target.

1. c-Raf, but not B-Raf, is essential for development of K-Ras oncogene-driven non-small cell lung carcinoma.

2. In melanoma, RAS mutations are accompanied by switching signaling from BRAF to CRAF and disrupted cyclic AMP signaling.

3. A Raf-induced allosteric transition of KSR stimulates phosphorylation of MEK.

4. Inhibition of mutated, activated BRAF in metastatic melanoma.

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

6. Kinase-dead BRAF and oncogenic RAS cooperate to drive tumor progression through CRAF.

Review 7. From basic research to clinical development of MEK1/2 inhibitors for cancer therapy.

8. Raf-1 addiction in Ras-induced skin carcinogenesis.

Review 9. Targeting RAS signalling pathways in cancer therapy.

10. RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF.

1. Synthesis and biological evaluation of sorafenib- and regorafenib-like sEH inhibitors.