title: BuCy RAFs drive cells into MEK addiction.
abstract: RAF research is booming since the discovery of mutant B-RAF in approximately 8% of human cancer. One reason for the excitement is the availability of RAF-targeted therapies. RAF inhibitors have been developed because RAF functions at a convergence point of signal transduction. Two recent papers by the groups of Rosen and Marais dramatically advance our understanding of RAF oncogenes in human tumors. The results confirm that the mitogenic cascade (RAF-MEK-ERK) is essential for RAF transformation, that RAF kinases work in concert, and that RAF-transformed cells are hooked on MEK, making them sensitive to growth inhibition by kinase inhibitors.
authors.affiliation: Institut für Medizinische Strahlenkunde und Zellforschung,Versbacher Strasse 5, 97078 Würzburg, Germany. rappur@mail.uni-wuerzburg.de
authors.forename: Ulf R
authors.initials: UR
authors.lastname: Rapp
authors.forename: Rudolf
authors.initials: R
authors.lastname: Götz
authors.forename: Stefan
authors.initials: S
authors.lastname: Albert
mesh_terms: D000818:Animals; D049109:Cell Proliferation / Q000187:drug effects; D004789:Enzyme Activation; D011905:Genes, ras; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000502:physiology*; D009154:Mutation; D015398:Signal Transduction / Q000502:physiology*; D048490:raf Kinases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology*
chemical_list: D048490:raf Kinases; D020928:Mitogen-Activated Protein Kinases