Results 91 to 100 of about 438,950 (335)

IRE1 alpha may be causing abnormal loss of p53 at post transcriptional level in chronic myeloid leukemia [PDF]

open access: yesarXiv, 2017
Current treatment strategy for chronic myeloid leukemia (CML) mainly includes inhibition of tyrosine kinase activity, which has dramatically improved the prognosis of the disease but without cure. In addition some patients may become drug resistant. Thus there is still the need for other therapies to avoid resistance and if possible to cure the disease.
arxiv  

Second-generation tyrosine kinase inhibitors improve the survival of patients with chronic myeloid leukemia in whom imatinib therapy has failed

open access: yesHaematologica, 2011
Background It has not been clearly established whether second-generation tyrosine kinase inhibitors actually improve the survival of patients with chronic myeloid leukemia in chronic phase who are given nilotinib or dasatinib therapy after treatment ...
Amr R. Ibrahim   +9 more
doaj   +1 more source

Understanding and Overcoming Immunotherapy Resistance in Skin Cancer: Mechanisms and Strategies

open access: yesAging and Cancer, EarlyView.
This narrative review explores the mechanisms driving immunotherapy resistance in skin cancer, including tumor microenvironment factors, genetic mutations, and immune evasion strategies. It highlights potential strategies to overcome resistance, offering insights for improving therapeutic outcomes and guiding future research in personalized ...
Shreya Singh Beniwal   +8 more
wiley   +1 more source

Phase 1, First‐In‐Human, Single‐/Multiple‐Ascending Dose Study of Iluzanebart in Healthy Volunteers

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective To evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of iluzanebart, a fully human monoclonal antibody TREM2 (triggering receptor expressed on myeloid cells 2) agonist, after single‐ (SAD) and multiple‐ascending‐dose (MAD) administration.
Andreas Meier   +8 more
wiley   +1 more source

FLT3 and FLT3-ITD phosphorylate and inactivate the cyclin-dependent kinase inhibitor p27Kip1 in acute myeloid leukemia

open access: yesHaematologica, 2017
P27Kip1 (p27) can prevent cell proliferation by inactivating cyclin-dependent kinases. This function is impaired upon phosphorylation of p27 at tyrosine residue 88. We observed that FLT3 and FLT3-ITD can directly bind and selectively phosphorylate p27 on
Ines Peschel   +8 more
doaj   +1 more source

Integration of Genetic Algorithms and Deep Learning for the Generation and Bioactivity Prediction of Novel Tyrosine Kinase Inhibitors [PDF]

open access: yesarXiv
The intersection of artificial intelligence and bioinformatics has enabled significant advancements in drug discovery, particularly through the application of machine learning models. In this study, we present a combined approach using genetic algorithms and deep learning models to address two critical aspects of drug discovery: the generation of novel
arxiv  

Stochastic models of the binding kinetics of VEGF-A to VEGFR1 and VEGFR2 in endothelial cells [PDF]

open access: yesarXiv, 2016
Vascular endothelial growth factor receptors (VEGFRs) are receptor tyrosine kinases (RTKs) that regulate proliferation, migration, angiogenesis and vascular permeability of endothelial cells. VEGFR1 and VEGFR2 bind vascular endothelial growth factors (VEGFs), inducing receptor dimerisation and activation, characterised by phosphorylation of tyrosine ...
arxiv  

ADAPT NXT: Fixed Cycles or Every‐Other‐Week IV Efgartigimod in Generalized Myasthenia Gravis

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective This phase 3b, open‐label, randomized ADAPT NXT study investigated the efficacy, safety, and tolerability of efgartigimod administered in either a fixed cycles dosing regimen (3 cycles of 4 once‐weekly infusions, with 4 weeks between cycles) or a cycle followed by every‐other‐week (Q2W) dosing.
Ali A. Habib   +16 more
wiley   +1 more source

Elucidation of a four-site allosteric network in fibroblast growth factor receptor tyrosine kinases

open access: yeseLife, 2017
Receptor tyrosine kinase (RTK) signaling is tightly regulated by protein allostery within the intracellular tyrosine kinase domains. Yet the molecular determinants of allosteric connectivity in tyrosine kinase domain are incompletely understood. By means
Huaibin Chen   +10 more
doaj   +1 more source

Home - About - Disclaimer - Privacy