Results 1 to 10 of about 78,382 (206)

BRAF inhibitor or BRAF/MEK inhibitor treatment for patients with metastatic BRAF V600E mutated differentiated thyroid cancer [PDF]

open access: yesArchives of Endocrinology and Metabolism
Objective: The aim of this study is to demonstrate the real-life efficacy of BRAF and MEK inhibitors in patients with advanced thyroid cancer. Subjects and methods: This retrospective study evaluated the clinical efficacy of either a BRAF inhibitor ...
Inbar Finkel   +9 more
doaj   +3 more sources

Surrogate to predict overall survival in patients with BRAF V600E-mutant colorectal cancer treated with BRAF inhibitor combinations [PDF]

open access: yesESMO Gastrointestinal Oncology
Background: The BRAF V600E mutation, found in up to 12% of patients with metastatic colorectal cancer, is associated with aggressive disease and poor response to standard chemotherapy.
J. Ros   +11 more
doaj   +2 more sources

JUN dependency in distinct early and late BRAF inhibition adaptation states of melanoma. [PDF]

open access: yes, 2016
A prominent mechanism of acquired resistance to BRAF inhibitors in BRAF (V600) -mutant melanoma is associated with the upregulation of receptor tyrosine kinases.
Atefi, Mohammad   +16 more
core   +7 more sources

Rapid and dramatic responses to dabrafenib and trametinib in BRAF V600E‐mutated lung adenocarcinoma

open access: yesRespirology Case Reports, 2021
V‐raf murine sarcoma viral oncogene homologue B1 (BRAF) is a proto‐oncogene that regulates cell proliferation and survival. BRAF V600E‐mutated lung cancer has aggressive characteristics and is resistant to chemotherapies.
Takayo Ota   +2 more
doaj   +1 more source

CRISPR Screens Identify Essential Cell Growth Mediators in BRAF Inhibitor-resistant Melanoma

open access: yesGenomics, Proteomics & Bioinformatics, 2020
BRAF is a serine/threonine kinase that harbors activating mutations in ∼7% of human malignancies and ∼60% of melanomas. Despite initial clinical responses to BRAF inhibitors, patients frequently develop drug resistance.
Ziyi Li   +16 more
doaj   +1 more source

Targeting human apurinic/apyrimidinic endonuclease 1 (APE1) in phosphatase and tensin homolog (PTEN) deficient melanoma cells for personalized therapy [PDF]

open access: yes, 2014
Phosphatase and tensin homolog (PTEN) loss is associated with genomic instability. APE1 is a key player in DNA base excision repair (BER) and an emerging drug target in cancer.
Allinson   +49 more
core   +7 more sources

BRAF mutation and its inhibitors in sarcoma treatment

open access: yesCancer Medicine, 2020
The mitogen‐activated protein kinase (MAPK) signaling pathway plays a significant role in mediating cellular physiological activities, such as proliferation, differentiation, apoptosis, and senescence.
Haotian Liu   +4 more
doaj   +1 more source

Dabrafenib; preclinical characterization, increased efficacy when combined with trametinib, while BRAF/MEK tool combination reduced skin lesions. [PDF]

open access: yesPLoS ONE, 2013
Mitogen-Activated Protein Kinase (MAPK) pathway activation has been implicated in many types of human cancer. BRAF mutations that constitutively activate MAPK signalling and bypass the need for upstream stimuli occur with high prevalence in melanoma ...
Alastair J King   +14 more
doaj   +1 more source

PERK mediates resistance to BRAF inhibition in melanoma with impaired PTEN

open access: yesnpj Precision Oncology, 2021
Targeting mutant BRAF in patients with melanomas harboring this oncogene has been highly successful as a first-line treatment, but other mutations may affect its efficacy and alter the route of acquired resistance resulting in recurrence and poor ...
Yifei Qin   +5 more
doaj   +1 more source

BRAF Splice Variant Resistance to RAF Inhibitor Requires Enhanced MEK Association

open access: yesCell Reports, 2018
Summary: Expression of aberrantly spliced BRAF V600E isoforms (BRAF V600E ΔEx) mediates resistance in 13%–30% of melanoma patients progressing on RAF inhibitors. BRAF V600E ΔEx confers resistance, in part, through enhanced dimerization.
Michael J. Vido   +3 more
doaj   +1 more source

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