نتایج جستجو برای: vemurafenib

تعداد نتایج: 1054  

Journal: :Acta dermato-venereologica 2014
Daniela Göppner Jan Müller Sabine Krüger Ingolf Franke Harald Gollnick Sven R Quist

There is growing evidence that not only malign keratinocytic but also melanocytic tumours can arise during treatment with vemurafenib. During an on-going early access trial, 13 patients harbouring a BRAF-V600E mutation received vemurafenib (Zelboraf®) 960 mg twice daily to test the safety, tolerability, efficacy and response rate for advanced melanoma. Clinically or dermatoscopically suspicious...

Journal: :The New England journal of medicine 2015
Caroline Robert Boguslawa Karaszewska Jacob Schachter Piotr Rutkowski Andrzej Mackiewicz Daniil Stroiakovski Michael Lichinitser Reinhard Dummer Florent Grange Laurent Mortier Vanna Chiarion-Sileni Kamil Drucis Ivana Krajsova Axel Hauschild Paul Lorigan Pascal Wolter Georgina V Long Keith Flaherty Paul Nathan Antoni Ribas Anne-Marie Martin Peng Sun Wendy Crist Jeff Legos Stephen D Rubin Shonda M Little Dirk Schadendorf

BACKGROUND The BRAF inhibitors vemurafenib and dabrafenib have shown efficacy as monotherapies in patients with previously untreated metastatic melanoma with BRAF V600E or V600K mutations. Combining dabrafenib and the MEK inhibitor trametinib, as compared with dabrafenib alone, enhanced antitumor activity in this population of patients. METHODS In this open-label, phase 3 trial, we randomly a...

Journal: :Molecular cancer therapeutics 2014
Tomoko Smyth Kim H T Paraiso Keisha Hearn Ana M Rodriguez-Lopez Joanne M Munck H Eirik Haarberg Vernon K Sondak Neil T Thompson Mohammad Azab John F Lyons Keiran S M Smalley Nicola G Wallis

Emergence of clinical resistance to BRAF inhibitors, alone or in combination with MEK inhibitors, limits clinical responses in melanoma. Inhibiting HSP90 offers an approach to simultaneously interfere with multiple resistance mechanisms. Using the HSP90 inhibitor AT13387, which is currently in clinical trials, we investigated the potential of HSP90 inhibition to overcome or delay the emergence ...

2014
Tomoko Smyth Kim H.T. Paraiso Keisha Hearn Ana M. Rodriguez-Lopez Joanne M. Munck H. Eirik Haarberg Vernon K. Sondak Neil T. Thompson Mohammad Azab John F. Lyons Nicola G. Wallis

Emergence of clinical resistance to BRAF inhibitors, alone or in combination with MEK inhibitors, limits clinical responses in melanoma. Inhibiting HSP90 offers an approach to simultaneously interfere with multiple resistance mechanisms. Using the HSP90 inhibitor AT13387, which is currently in clinical trials, we investigated the potential of HSP90 inhibition to overcome or delay the emergence ...

Journal: :ACS chemical biology 2015
Rebecca Horbert Boris Pinchuk Paul Davies Dario Alessi Christian Peifer

In this study, we report on novel photoactivatable caged prodrugs of vemurafenib. This kinase inhibitor was the first approved drug for the personalized treatment of BRAF-mutated melanoma and showed impressive results in clinical studies. However, the occurrence of severe side effects and drug resistance illustrates the urgent need for innovative therapeutic approaches. To conquer these limitat...

Journal: :Cancer research 2016
Akihiro Yoshida Eric K Lee J Alan Diehl

Dysregulation of the p16-cyclin D1-CDK4/6-Rb pathway occurs frequently in melanoma; however, the therapeutic efficacy of CDK4/6 inhibition remains to be critically evaluated. We demonstrate that CDK4/6 inhibition inhibits melanoma progression through induction of senescence. Palbociclib, a specific CDK4/6 inhibitor, rapidly induces cell cycle arrest within 24 hours and continued exposure for 8 ...

Journal: :Cancer discovery 2014
Omar Abdel-Wahab Virginia M Klimek Alisa A Gaskell Agnes Viale Donavan Cheng Eunhee Kim Raajit Rampal Mark Bluth James J Harding Margaret K Callahan Taha Merghoub Michael F Berger David B Solit Neal Rosen Ross L Levine Paul B Chapman

Vemurafenib, a RAF inhibitor, extends survival in patients with BRAF(V600)-mutant melanoma but activates extracellular signal-regulated kinase (ERK) signaling in RAS-mutant cells. In a patient with a BRAF(V600K)-mutant melanoma responding to vemurafenib, we observed accelerated progression of a previously unrecognized NRAS-mutant leukemia. We hypothesized that combining vemurafenib with a MAP-E...

2018
Jorine de Haan Johannes V. van Thienen Michael Casaer Rebekka A. Hannivoort Kristel Van Calsteren Minke van Tuyl Mathilde M. van Gerwen Anne Debeer Frédéric Amant Rebecca C. Painter

Targeted therapies have drastically changed the management of metastatic melanoma and have shown encouraging results on tumour progression but are also known for their high rates of adverse reactions. In general, targeted therapies are contraindicated during pregnancy due to concerns about teratogenesis. For the BRAF V600 inhibitor vemurafenib, the available literature about the effects on huma...

2015
Giselle de Barros Silva Adriana Pessoa Mendes Mariana Petaccia de Macedo Clóvis Antônio Lopes Pinto Ivana Lameiras Gibbons João Pedreira Duprat Neto

Vemurafenib is a selective inhibitor of V600E-mutant BRAF protein used to treat metastatic and unresectable melanoma. Clinical trials have shown increased overall survival and progression-free survival in patients treated with Vemurafenib. However, cutaneous adverse events are common during treatment. We report fi ve cases of metastatic melanoma with BRAF V600E positivity, treated with Vemurafe...

Journal: :Reactions Weekly 2021

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