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Novel Treatment Strategies for Chronic Myeloid Leukemia.
Blood
December 2024
Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.
Starting with imatinib, tyrosine kinase inhibitors (TKIs) have turned chronic myeloid leukemia (CML) from a lethal blood cancer into a chronic condition. As patients with access to advanced CML care have an almost normal life expectancy, there is a perception that CML is a problem of the past, and one should direct research resources elsewhere. However, a closer look at the current CML landscape reveals a more nuanced picture.
View Article and Find Full Text PDFEffect of imatinib on lipopolysaccharide‑induced acute lung injury and endothelial dysfunction through the P38 MAPK and NF-κB signaling pathways in vivo and in vitro.
Respir Physiol Neurobiol
December 2024
Department of Emergency Medicine, The Second Hospital of Tianjin Medical University, Tianjin 300211, China. Electronic address:
Background: The primary purpose of this study was to demonstrate the preventive effects of imatinib (IMA) on lipopolysaccharide (LPS)-induced inflammation in a mouse model of acute lung injury (ALI) and human umbilical vascular endothelial cells.
Methods: LPS stimulation for 24 h induced ALI and cell inflammation. The pathological results of the lungs were evaluated using the wet/dry weight ratio, pulmonary vascular permeability measurements, and myeloperoxidase immunohistochemistry.
Stretching the structural envelope of imatinib to reduce β-amyloid production by modulating both β- and γ-secretase cleavages of APP.
Front Chem
October 2024
Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY, United States.
We previously showed that the anticancer drug imatinib mesylate (IMT, trade name: Gleevec) and a chemically distinct compound, DV2-103 (a kinase-inactive derivative of the potent Abl and Src kinase inhibitor, PD173955) lower Aβ levels at low micromolar concentrations primarily through a lysosome-dependent mechanism that renders APP less susceptible to proteolysis by BACE1 without directly inhibiting BACE1 enzymatic activity, or broadly inhibiting the processing of other BACE1 substrates. Additionally, IMT indirectly inhibits γ-secretase and stimulates autophagy, and thus may decrease Aβ levels through multiple pathways. In two recent studies we demonstrated similar effects on APP metabolism caused by derivatives of IMT and DV2-103.
View Article and Find Full Text PDFBCAT1 contributes to the development of TKI-resistant CML.
Cell Oncol (Dordr)
October 2024
Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, China.
Purpose: Although most of chronic myeloid leukemia (CML) patients can be effectively treated by the tyrosine kinase inhibitors (TKIs), such as Imatinib, TKI-resistance still occurs in approximately 15-17% of cases. Although many studies indicate that branched chain amino acid (BCAA) metabolism may contribute to the TKI resistance in CML, the detailed mechanisms remains largely unknown.
Method: The cell proliferation, colony formation and in vivo transplantation were used to determined the functions of BCAT1 in leukemogenesis.
Sustained antiviral response against HIV-1 infection in peripheral blood mononuclear cells from people with chronic myeloid leukemia treated with ponatinib.
Front Pharmacol
September 2024
Immunopathology and Viral Reservoir Unit, National Center of Microbiology, Instituto de Salud Carlos III, Madrid, Spain.
Article Synopsis
- - HIV-1 infection persists due to long-term viral reservoirs in latently infected CD4 T cells, prompting the need for strategies to stimulate cytotoxic immunity, including the "Shock and Kill" approach.
- - Ponatinib, a tyrosine kinase inhibitor used for chronic myeloid leukemia, has shown effectiveness against HIV-1 and may enhance the immune response against both cancer and viral infections.
- - In a study of patients with chronic myeloid leukemia who switched from imatinib to ponatinib, results indicated that ponatinib treatment significantly reduced HIV-1 infection rates and increased the cytotoxic response from peripheral blood mononuclear cells, with effects lasting at least 12 months post-treatment.
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