Results 21 to 30 of about 101,700 (245)

Effects of imatinib on vascular insulin sensitivity and free fatty acid transport in early weight gain.

open access: yesPLoS ONE, 2021
BackgroundVascular endothelial dysfunction is an essential part of the pathophysiology of type 2 diabetes and its complications. In type 2 diabetes, endothelial dysfunction is characterized by reduced insulin signaling and increased transendothelial ...
Camiel V J Box   +6 more
doaj   +1 more source

Imatinib-Induced Psoriasis

open access: yesTurkish Journal of Hematology, 2013
Imatinib is a signal transduction regulator that selectively inhibits the tyrosine kinase family, including bcr-abl and c-kit, and the platelet-derived growth factor (PDGF) receptor. It is currently the fi rst-line therapy for newly diagnosed chronic myeloid leukemia (CML) patients [1].
Atalay, Figen   +2 more
openaire   +4 more sources

Imatinib

open access: yesJapanese Journal of Clinical Immunology, 2009
The progress in molecular targeting therapy includes two tides, namely, small molecule compounds and large molecule biological agents. Although the latter prevails in the field of clinical immunology, the former attracts more and more attention in these few years.
openaire   +4 more sources

Impact of Rechallenge with Imatinib in Patients with Advanced Gastrointestinal Stromal Tumor after Failure of Imatinib and Sunitinib

open access: yesGastroenterology Research and Practice, 2014
Purpose. This retrospective, nonrandomized study investigated the effect of imatinib rechallenge plus best supportive care (BSC) on overall survival after imatinib and sunitinib treatment for patients with locally advanced or metastatic gastrointestinal ...
Akira Sawaki   +3 more
doaj   +1 more source

Epigenetic dysregulation in chronic myeloid leukaemia: A myriad of mechanisms and therapeutic options [PDF]

open access: yes, 2018
The onset of global epigenetic changes in chromatin that drive tumor proliferation and heterogeneity is a hallmark of many forms cancer. Identifying the epigenetic mechanisms that govern these changes and developing therapeutic approaches to modulate ...
Koschmieder, Steffen, Vetrie, David
core   +1 more source

Inhibition of MDR1 does not sensitize primitive chronic myeloid leukemia CD34+ cells to imatinib [PDF]

open access: yes, 2009
<p><b>Objective:</b> To investigate the interaction of imatinib mesylate (IM) with the clinically relevant adenosine triphosphate-binding cassette efflux transporter MDR1 (ABCB1) in cells from patients with chronic myeloid leukemia (CML)
Hatziieremia, S.   +4 more
core   +1 more source

CAQ Corner: Basic concepts of transplant immunology

open access: yes, 2022
Liver Transplantation, EarlyView.
Amanda Cheung, Josh Levitsky
wiley   +1 more source

Imatinib inhibits VEGF-independent angiogenesis by targeting neuropilin 1-dependent ABL1 activation in endothelial cells. [PDF]

open access: yes, 2014
To enable new blood vessel growth, endothelial cells (ECs) express neuropilin 1 (NRP1), and NRP1 associates with the receptor tyrosine kinase VEGFR2 after binding the vascular endothelial growth factor A (VEGF) to enhance arteriogenesis.
Alessandro Fantin   +74 more
core   +4 more sources

Dual gene activation and knockout screen reveals directional dependencies in genetic networks. [PDF]

open access: yes, 2018
Understanding the direction of information flow is essential for characterizing how genetic networks affect phenotypes. However, methods to find genetic interactions largely fail to reveal directional dependencies. We combine two orthogonal Cas9 proteins
Biton, Anne   +12 more
core   +2 more sources

Protein kinase Cδ and c-Abl kinase are required for transforming growth factor β induction of endothelial-mesenchymal transition in vitro. [PDF]

open access: yes, 2011
OBJECTIVE: The origin of the mesenchymal cells responsible for the intimal fibrosis in systemic sclerosis (SSc) has not been fully identified. The present study was undertaken to investigate whether subendothelial mesenchymal cells may emerge through ...
Jimenez, Sergio A., Li, zhaodong
core   +2 more sources

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