نتایج جستجو برای: vemurafenib

تعداد نتایج: 1054  

Journal: :American journal of cancer research 2015
Nicholas Beazley-Long Kevin Gaston Steven J Harper Antonio Orlando David O Bates

Targeting activating mutations in the proto-oncogene B-Raf, in melanoma, has led to increases in progression free survival. Treatment with vemurafenib, which inhibits the most common activating-mutated form of B-Raf (B-Raf(V600E)), eventually results in resistance to therapy. VEGF-A is the principal driver of angiogenesis in primary and metastatic lesions. The bioactivity of VEGF-A is dependent...

2015
Piotr Rutkowski Katarzyna Kozak Jacek Mackiewicz Krzysztof Krzemieniecki Sergiusz Nawrocki Ewa Wasilewska-Teśluk Łukasz Kwinta Piotr Wysocki Hanna Koseła-Paterczyk Tomasz Świtaj

AIM OF THE STUDY The BRAF inhibitor vemurafenib has improved progression-free survival and overall survival in patients with BRAFV600-mutation-positive metastatic melanoma. Here we present the results of an open-label safety study with vemurafenib in patients with metastatic melanoma enrolled in Polish oncological centres. MATERIAL AND METHODS Patients with untreated or previously treated Sta...

2014
Matthew Peacock Reto Brem Peter Macpherson Peter Karran

Cutaneous photosensitization is a common side effect of drug treatment and can be associated with an increased skin cancer risk. The immunosuppressant azathioprine, the fluoroquinolone antibiotics and vemurafenib-a BRAF inhibitor used to treat metastatic melanoma-are all recognized clinical photosensitizers. We have compared the effects of UVA radiation on cultured human cells treated with 6-th...

2012
Richard C. Koya Stephen Mok Nicholas Otte Kevin J. Blacketor Begonya Comin-Anduix Paul C. Tumeh Aspram Minasyan Nicholas A. Graham Thomas G. Graeber Thinle Chodon Antoni Ribas

Combining immunotherapy with targeted therapy blocking oncogenic BRAF may result in improved treatments for advanced melanoma. In this study, we developed a BRAF-driven murine model of melanoma, SM1, which is syngeneic to fully immunocompetent mice. SM1 cells exposed to the BRAF inhibitor vemurafenib (PLX4032) showed partial in vitro and in vivo sensitivity resulting from the inhibition of MAPK...

2015
Kristel Kemper Oscar Krijgsman Paulien Cornelissen-Steijger Aida Shahrabi Fleur Weeber Ji-Ying Song Thomas Kuilman Daniel J Vis Lodewyk F Wessels Emile E Voest Ton NM Schumacher Christian U Blank David J Adams John B Haanen Daniel S Peeper

The development of targeted inhibitors, like vemurafenib, has greatly improved the clinical outcome of BRAF(V600E) metastatic melanoma. However, resistance to such compounds represents a formidable problem. Using whole-exome sequencing and functional analyses, we have investigated the nature and pleiotropy of vemurafenib resistance in a melanoma patient carrying multiple drug-resistant metastas...

2013
Heike Niessner Andrea Forschner Bernhard Klumpp Jürgen B. Honegger Maria Witte Antje Bornemann Reinhard Dummer Annemarie Adam Jürgen Bauer Ghazaleh Tabatabai Keith Flaherty Tobias Sinnberg Daniela Beck Ulrike Leiter Cornelia Mauch Alexander Roesch Benjamin Weide Thomas Eigentler Dirk Schadendorf Claus Garbe Dagmar Kulms Leticia Quintanilla-Martinez Friedegund Meier

Brain metastases are the most common cause of death in patients with metastatic melanoma, and the RAF-MEK-ERK and PI3K-AKT signaling pathways are key players in melanoma progression and drug resistance. The BRAF inhibitor vemurafenib significantly improved overall survival. However, brain metastases still limit the effectiveness of this therapy. In a series of patients, we observed that treatme...

2015
Audrey Delmas Julia Cherier Magdalena Pohorecka Claire Medale-Giamarchi Nicolas Meyer Anne Casanova Olivier Sordet Laurence Lamant Ariel Savina Anne Pradines Gilles Favre

The response of BRAF-mutant melanoma patients to BRAF inhibitors is dramatically impaired by secondary resistances and rapid relapse. So far, the molecular mechanisms driving these resistances are not completely understood. Here, we show that, in BRAF-mutant melanoma cells, inhibition of BRAF or its target MEK induces RHOB expression by a mechanism that depends on the transcription factor c-Jun...

Journal: :Archives of hematology case reports and reviews 2022

Histiocytoses are clonal disorders diseases derived from the monocyte-macrophage lineage. The Erdheim–Chester Disease (ECD) and Langerhans Cell Histiocytosis (LCH) may occur in association with overlapping clinical, histopathological molecular features, harboring somatic MAP2K1 mutations more than 50% of patients. BRAF MEK inhibitors have shown to be efficacious ECD LCH, including responses pat...

Journal: :Nature Reviews Clinical Oncology 2018

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