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Sci. Signal., 29 January 2013
Vol. 6, Issue 260, p. pc3
Science Signaling Podcast: 29 January 2013
Friedegund Meier1 and
Annalisa M. VanHook2
1 Division of Dermatologic Oncology, Department of Dermatology, University of Tübingen, 72076 Tübingen, Germany. 2 Web Editor, Science Signaling, American Association for the Advancement of Science, 1200 New York Avenue, NW, Washington, DC 20005, USA.
This Podcast features an interview with Friedegund Meier, senior author of a Research Article that appears in the 29 January 2013 issue of Science Signaling. Beck et al. focuses on the role of endoplasmic reticulum (ER) stress in tumor cell killing by the drug vemurafenib. Vemurafenib is an effective therapy for melanomas that harbor a particular mutant form of the kinase BRAF, but melanomas often develop resistance to the drug, thus reducing its efficacy. The authors found that, in addition to inhibiting survival signaling mediated by the kinase ERK, vemurafenib also triggered apoptosis by inducing ER stress. Treating vemurafenib-resistant melanoma cells with an ER stress inducer in combination with vemurafenib improved cell killing, suggesting that this might be an effective combined therapy for treating melanoma.
Citation: F. Meier, A. M. VanHook, Science Signaling Podcast: 29 January 2013. Sci. Signal.6, pc3 (2013).
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In Science Signaling
Daniela Beck, Heike Niessner, Keiran S. M. Smalley, Keith Flaherty, Kim H. T. Paraiso, Christian Busch, Tobias Sinnberg, Sophie Vasseur, Juan Lucio Iovanna, Stefan Drießen, Björn Stork, Sebastian Wesselborg, Martin Schaller, Tilo Biedermann, Jürgen Bauer, Konstantinos Lasithiotakis, Benjamin Weide, Jürgen Eberle, Birgit Schittek, Dirk Schadendorf, Claus Garbe, Dagmar Kulms, and Friedegund Meier (29 January 2013) Sci. Signal.6 (260), ra7.
[DOI: 10.1126/scisignal.2003057] |Editor's Summary »|Abstract »|Full Text »|PDF »|Supplementary Materials »