نتایج جستجو برای: vemurafenib

تعداد نتایج: 1054  

2016
Rimda Wanchoo Kenar D. Jhaveri Gilbert Deray Vincent Launay-Vacher

Advanced melanoma has been traditionally unresponsive to standard chemotherapy agents and used to have a dismal prognosis. Genetically targeted small-molecule inhibitors of the oncogenic BRAF V600 mutation or a downstream signaling partner (MEK mitogen-activated protein kinase) are effective treatment options for the 40-50% of melanomas that harbor mutations in BRAF. Selective BRAF and MEK inhi...

2015
Mohammad Fallahi-Sichani Nathan J Moerke Mario Niepel Tinghu Zhang Nathanael S Gray Peter K Sorger

Drugs that inhibit RAF/MEK signaling, such as vemurafenib, elicit profound but often temporary anti-tumor responses in patients with BRAF(V) (600E) melanoma. Adaptive responses to RAF/MEK inhibition occur on a timescale of hours to days, involve homeostatic responses that reactivate MAP kinase signaling and compensatory mitogenic pathways, and attenuate the anti-tumor effects of RAF/MEK inhibit...

Journal: :Cancer research 2013
Meghna Das Thakur Darrin D Stuart

The RAS-RAF-MEK-ERK pathway is a key driver of proliferation and survival signals in tumor cells and has been the focus of intense drug development efforts over the past 20 years. The recent regulatory approval of RAF inhibitors and a MAP-ERK kinase (MEK) inhibitor for metastatic melanoma provides clinical validation of tumor dependency on this pathway. Unfortunately, the therapeutic benefit of...

2016
Luca Paoluzzi Douglas Hanniford Elena Sokolova Iman Osman Farbod Darvishian Jinhua Wang James E. Bradner Eva Hernando

Despite major advances in the treatment of metastatic melanoma, treatment failure is still inevitable in most cases. Manipulation of key epigenetic regulators, including inhibition of Bromodomain and extra-terminal domain (BET) family members impairs cell proliferation in vitro and tumor growth in vivo in different cancers, including melanoma. Here, we investigated the effect of combining the B...

2015
Zhenyu Ji Yiyin Erin Chen Raj Kumar Michael Taylor Ching-Ni Jenny Njauw Benchun Miao Dennie T. Frederick Jennifer A. Wargo Keith T. Flaherty Göran Jönsson Hensin Tsao

Response to targeted therapies varies significantly despite shared oncogenic mutations. Nowhere is this more apparent than in BRAF (V600E)-mutated melanomas where initial drug response can be striking and yet relapse is commonplace. Resistance to BRAF inhibitors have been attributed to the activation of various receptor tyrosine kinases (RTKs), although the underlying mechanisms have been large...

Journal: :The British journal of dermatology 2015
K Matter-Walstra R Braun C Kolb Z Ademi R Dummer B C Pestalozzi M Schwenkglenks

BACKGROUND The treatment of patients with metastatic melanomas that harbour BRAF V600E or V600K mutations with trametinib plus dabrafenib appears to be superior to treatment with vemurafenib alone. This treatment regimen is likely to become available in Switzerland in the near future. OBJECTIVES To determine the cost-effectiveness of trametinib plus dabrafenib. METHODS A Markov cohort simul...

2015
Meg R. Gerstenblith Tatyana A. Petukhova Henry B. Koon

CASE REPORT A66-year-oldwhitemanwith stage IIICmelanoma diagnosed in 2009 was treated with high-dose interferon alfa-2b for 1 year. He subsequently had subcutaneous and brainmetastases and underwent 2 cycles of high-dose interleukin-2 and whole-brain irradiation. Given disease progression, vemurafenib was initiated at 960 mg twice daily after testing confirmed the BRAF V600E mutation. After 4 m...

Journal: :The Journal of clinical investigation 2014
Niuscha Yaktapour Frank Meiss Justin Mastroianni Thorsten Zenz Hana Andrlova Nimitha R Mathew Rainer Claus Barbara Hutter Stefan Fröhling Benedikt Brors Dietmar Pfeifer Milena Pantic Ingrid Bartsch Timo S Spehl Philipp T Meyer Justus Duyster Katja Zirlik Tilman Brummer Robert Zeiser

Patients with BRAFV600E/K-driven melanoma respond to the BRAF inhibitor vemurafenib due to subsequent deactivation of the proliferative RAS/RAF/MEK/ERK pathway. In BRAF WT cells and those with mutations that activate or result in high levels of the BRAF activator RAS, BRAF inhibition can lead to ERK activation, resulting in tumorigenic transformation. We describe a patient with malignant melano...

Journal: :Molecular cancer therapeutics 2014
Yusuke Narita Kiyoshi Okamoto Megumi Ikemori Kawada Kazuma Takase Yukinori Minoshima Kotaro Kodama Masao Iwata Norimasa Miyamoto Kohei Sawada

Many clinical cases of acquired resistance to the BRAF inhibitor vemurafenib have recently been reported. One of the causes of this acquired resistance is the BRAF downstream kinase point mutation MEK1-C121S. This mutation confers resistance to not only vemurafenib, but also to the allosteric MEK inhibitor selumetinib (AZD6244). Here, we investigated the pharmacologic activities and effectivene...

2012
Ryan B. Corcoran Hiromichi Ebi Alexa B. Turke Erin M. Coffee Michiya Nishino Alexandria P. Cogdill Ronald D. Brown Patricia Della Pelle Dora Dias-Santagata Kenneth E. Hung Keith T. Flaherty Adriano Piris Jennifer A. Wargo Jeffrey Settleman Mari Mino-Kenudson Jeffrey A. Engelman

BRAF mutations occur in 10% to 15% of colorectal cancers and confer adverse outcome in the metastatic setting. Although RAF inhibitors such as vemurafenib (PLX4032) have proven effective in the treatment of BRAF-mutant melanoma, they are surprisingly ineffective in BRAF-mutant colorectal cancers, and the reason for this disparity remains unclear. Compared with BRAF-mutant melanoma cells, BRAF-m...

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