Results 101 to 110 of about 198,722 (342)

Melanoma Persister Cells Are Tolerant to BRAF/MEK Inhibitors via ACOX1-Mediated Fatty Acid Oxidation.

open access: yesCell Reports, 2020
Emerging evidence indicates that non-mutational drug tolerance mechanisms underlie the survival of residual cancer "persister" cells. Here, we find that BRAF(V600E) mutant melanoma persister cells tolerant to BRAF/MEK inhibitors switch their metabolism ...
Shensi Shen   +9 more
semanticscholar   +1 more source

Strawberry Notch 1 Acts as a Transcriptional Regulator Driving Oncogenic Programs in Liver Carcinogenesis

open access: yesAdvanced Science, EarlyView.
This study reports that SBNO1 protein is upregulated in several cancer entities. SBNO1 protein interacts with the basal transcription factor TFIID via TAF4, enabling its recruitment to transcription start sites and the modulation of target gene expression.
Sarah Fritzsche   +21 more
wiley   +1 more source

Concomitant BRAF Mutation in Hairy Cell Leukemia and Papillary Thyroid Cancer: Case Report

open access: yesCase Reports in Oncology, 2019
Hairy cell leukemia (HCL) is rare type of leukemia. This neoplasm is well-known to present with pancytopenia and splenomegaly. HCL is associated with BRAF mutation in 100% of cases.
Shehab F. Mohamed   +5 more
doaj   +1 more source

FOXD3 Regulates VISTA Expression in Melanoma. [PDF]

open access: yes, 2020
Immune checkpoint inhibitors have improved patient survival in melanoma, but the innate resistance of many patients necessitates the investigation of alternative immune targets.
Aplin, Andrew E.   +13 more
core   +1 more source

BRAF V600E Inhibitor (Vemurafenib) for BRAF V600E Mutated Low Grade Gliomas [PDF]

open access: yesFrontiers in Oncology, 2018
Low-grade gliomas (LGG) are the most common central nervous system tumors in children. Prognosis depends on complete surgical resection. For patients not amenable of gross total resection (GTR) new approaches are needed. The BRAF mutation V600E is critical for the pathogenesis of pediatric gliomas and specific inhibitors of the mutated protein, such as
Francesca Del Bufalo   +11 more
openaire   +3 more sources

Real‐Time Visualization of Isoform‐Specific RAF‐KRAS Interactions in Living Cells Using FRET‐BRET Hybrid Biosensors

open access: yesAdvanced Science, EarlyView.
Hybrid FRET–BRET biosensors were developed to monitor RAF–KRAS interactions in living cells. These sensors enable real‐time visualization of interaction dynamics, quantitative spectral analysis, and validation of mutation‐selective inhibitors, providing a versatile platform for probing KRAS regulation and therapeutic responses. ABSTRACT The RAS–RAF–MEK–
Jeong‐Min Go   +12 more
wiley   +1 more source

A phase II study of combined therapy with a BRAF inhibitor (vemurafenib) and interleukin-2 (aldesleukin) in patients with metastatic melanoma

open access: yesOncoImmunology, 2018
Background: Approximately 50% of melanomas harbor BRAF mutations. Treatment with BRAF +/− MEK inhibition is associated with favorable changes in the tumor microenvironment thus providing the rationale for combining targeted agents with immunotherapy ...
Meghan J. Mooradian   +14 more
doaj   +1 more source

Combination Immunotherapy as a Promising Strategy to Overcome Immunotherapy Resistance: From Emergence to Next‐Generation Approaches

open access: yesAdvanced Science, EarlyView.
This review examines emerging combination immunotherapy strategies tailored to distinct tumor microenvironments and highlights next‐generation biomarkers that guide response prediction and treatment personalization. It integrates lessons from unsuccessful trials, addresses toxicity challenges, and outlines approaches for early biomarker discovery and ...
Asmita Pandey   +6 more
wiley   +1 more source

Outcomes of BRAF V600E Pediatric Gliomas Treated With Targeted BRAF Inhibition

open access: yesJCO Precision Oncology, 2020
PURPOSE Children with pediatric gliomas harboring a BRAF V600E mutation have poor outcomes with current chemoradiotherapy strategies. Our aim was to study the role of targeted BRAF inhibition in these tumors. PATIENTS AND METHODS We collected clinical, imaging, molecular, and outcome information from patients with BRAF V600E–mutated glioma treated with
Nobre L.   +72 more
openaire   +7 more sources

NIBAN2/FLII/RREB1 Axis Drives Glioma Stem Cell Malignancy via TLR3 Pathway Activation

open access: yesAdvanced Science, EarlyView.
NIBAN2, highly expressed in glioma stem‐like cells (GSCs), assembles with FLII and transcription factor RREB1 to form a nuclear complex. This complex transcriptionally activates stemness‐associated genes (e.g., CD44, NANOG) and metabolic enzymes (e.g., LDHA), thereby sustaining both transcriptional and metabolic stemness programs.
Liang liang Shi   +14 more
wiley   +1 more source

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