Results 61 to 70 of about 56,924 (160)

FBP1 loss contributes to BET inhibitors resistance by undermining c-Myc expression in pancreatic ductal adenocarcinoma

open access: yesJournal of Experimental & Clinical Cancer Research, 2018
Background Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal tumor types worldwide. BET inhibitors display anti-tumor activity in pancreatic cancer, however the cells often develop resistance after a long-term treatment and the underlying
Bo Wang   +5 more
doaj   +1 more source

Clinical progress and pharmacology of small molecule bromodomain inhibitors [PDF]

open access: yes, 2016
Bromodomains have emerged as an exciting target class for drug discovery over the past decade. Research has primarily focused on the bromodomain and extra terminal (BET) family of bromodomains, which has led to the development of multiple small molecule ...
Humphreys, Philip G   +3 more
core   +1 more source

Combinational BET and mTOR inhibition unveils EGR1 as acute myeloid leukemia prognostic biomarker

open access: yesScientific Reports
This study investigated the anti-leukemic potential of BET inhibitors in combination with mTOR inhibitors, focusing on both BET-resistant and BET-sensitive AML cell lines.
Marcela Teatin Latancia   +17 more
doaj   +1 more source

Isoprenoids determine Th1/Th2 fate in pathogenic T cells, providing a mechanism of modulation of autoimmunity by atorvastatin. [PDF]

open access: yes, 2006
3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is a critical enzyme in the mevalonate pathway that regulates the biosynthesis of cholesterol as well as isoprenoids that mediate the membrane association of certain GTPases.
Dunn, Shannon E   +6 more
core   +1 more source

Comprehensive transcriptome profiling of BET inhibitor-treated HepG2 cells.

open access: yesPLoS ONE, 2022
Hepatocellular carcinoma (HCC) is the most common primary liver cancer and poor prognosis. Emerging evidence suggests that epigenetic alterations play a crucial role in HCC, suggesting epigenetic inhibition as a promising therapeutic approach.
Mina Baek   +7 more
doaj   +1 more source

HiJAKing innate lymphoid cells? [PDF]

open access: yes, 2017
The family of innate lymphoid cells (ILCs) consists of a heterogeneous group of cytokine-producing cells that have features in common with adaptive T helper (Th) cells.
Gadina, Massimo   +2 more
core   +1 more source

A novel dual epigenetic approach targeting BET proteins and HDACs in Group 3 (MYC-driven) Medulloblastoma

open access: yesJournal of Experimental & Clinical Cancer Research, 2022
Background Medulloblastoma (MB) patients with MYC oncogene amplification or overexpression exhibit extremely poor clinical outcomes and respond poorly to current therapies. Epigenetic deregulation is very common in MYC-driven MB.
Matthew J. Kling   +9 more
doaj   +1 more source

Central role of Yes-associated protein and WW-domain-containing transcriptional co-activator with PDZ-binding motif in pancreatic cancer development. [PDF]

open access: yes, 2019
Pancreatic ductal adenocarcinoma (PDAC) remains a deadly disease with no efficacious treatment options. PDAC incidence is projected to increase, which may be caused at least partially by the obesity epidemic.
Eibl, Guido, Rozengurt, Enrique
core  

Expression and purification of an NSD3-GB1 fusion protein as a way to study the structure of complex formation with Brd4 ET. [PDF]

open access: yes, 2020
The BRD4 protein belongs to the bromodomain and extraterminal domain (BET) family of eukaryotic transcription factors, and is linked to several types of cancer, inflammation, and obesity.
Tuokkola, Jennifer
core  

Exploring Protein-Protein Interactions as Drug Targets for Anti-cancer Therapy with In Silico Workflows [PDF]

open access: yes, 2017
We describe a computational protocol to aid the design of small molecule and peptide drugs that target protein-protein interactions, particularly for anti-cancer therapy. To achieve this goal, we explore multiple strategies, including finding binding hot
A Goncearenco   +44 more
core   +1 more source

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