نتایج جستجو برای: vemurafenib

تعداد نتایج: 1054  

2014
Omar Abdel-Wahab Virginia M. Klimek Alisa A. Gaskell Donavan Cheng Eunhee Kim Raajit Rampal Mark Bluth James J. Harding Margaret K. Callahan Taha Merghoub Michael F. Berger David B. Solit 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...

2015
Inna V. Fedorenko Keiran S.M. Smalley

Since the FDA approval of vemurafenib for the treatment of disseminated melanoma in 2011, followed by approval of dabrafenib in 2013 and dabrafenib/trametinib combination in 2014, melanoma has become the poster child for targeted kinase therapy. Despite encouraging initial clinical responses, most patients ultimately develop drug resistance and relapse, prompting an enormous research effort foc...

Journal: :P & T : a peer-reviewed journal for formulary management 2012
Walter Alexander

Mutations of the serine/threonine-protein kinase BRAF protein are found in 80% of melanomas. Vemurafenib (Zelboraf, Genentech/Daiichi Sankyo), a specific inhibitor of BRAF, was approved by the FDA for metastatic melanoma in August 2011. Dabrafenib (GlaxoSmithKline, GSK 2118436), tested in the BREAK-2 trial, demonstrated a 59% confirmed response rate with a median progression-free survival (PFS)...

Journal: :Annals of oncology : official journal of the European Society for Medical Oncology 2015
S Ugurel C Loquai K Kähler J Hassel C Berking L Zimmer I Haubitz I Satzger T Müller-Brenne N C Mikhaimer J C Becker K J Kilian D Schadendorf L Heinzerling M Kaatz J Utikal D Göppner C Pföhler A Pflugfelder R Mössner R Gutzmer

BACKGROUND Kinase inhibitors targeting the BRAF V600 mutation have become standard in the treatment of metastatic melanoma. Albeit in wide clinical use, the patterns associated with therapy outcome are not fully elucidated. The present study was aimed to identify predictive factors of therapy response and survival under the BRAF inhibitor vemurafenib. PATIENTS AND METHODS This multicenter ret...

Journal: :Cancer discovery 2013
Bissan Al-Lazikani Paul Workman

Large-scale, unbiased combinatorial drug screening has been used to identify effective genotype-selective therapeutic combinations that show promising activity in preclinical models of mutant BRAF andRAS melanoma that are resistant to the clinical BRAF inhibitor vemurafenib.

Journal: :Blood 2016
Michael R Grever

In this issue of Blood, Dietrich et al report that the low-dose BRAF inhibitor, vemurafenib, is highly effective in refractory hairy cell leukemia. Despite enormous progress that has been made with purine nucleoside analogs as the initial treatment of patients with hairy cell leukemia, the relapse rate and eventual development of refractory disease mandate the continued search for effective new...

Journal: :JAMA dermatology 2015
Giuliana Carlos Rachael Anforth Arthur Clements Alexander M Menzies Matteo S Carlino Shaun Chou Pablo Fernandez-Peñas

IMPORTANCE The cutaneous adverse effects of the BRAF inhibitors vemurafenib and dabrafenib mesylate in the treatment of metastatic melanoma have been well reported. The addition of a MEK inhibitor to a BRAF inhibitor improves the blockade of the mitogen-activated protein kinase pathway. The combination of dabrafenib with the MEK inhibitor trametinib dimethyl sulfoxide (CombiDT therapy) increase...

2016
Tobias Sinnberg Elena Makino Marcel A. Krueger Ana Velic Boris Macek Ulrich Rothbauer Nicola Groll Oliver Pötz Stefan Czemmel Heike Niessner Friedegund Meier Kristian Ikenberg Claus Garbe Birgit Schittek

Acquired resistance to second generation BRAF inhibitors (BRAFis), like vemurafenib is limiting the benefits of long term targeted therapy for patients with malignant melanomas that harbor BRAF V600 mutations. Since many resistance mechanisms have been described, most of them causing a hyperactivation of the MAPK- or PI3K/AKT signaling pathways, one potential strategy to overcome BRAFi resistan...

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