Results 111 to 120 of about 45,526 (248)

Immune System and Hepatic Stellate Cells’ Crosstalk in Liver Fibrosis: Pathways and Therapeutic Potential

open access: yesJournal of Immunology Research, Volume 2026, Issue 1, 2026.
Liver fibrosis, characterized by the excessive deposition of extracellular matrix (ECM) driven by hepatic stellate cells (HSCs) activation, remains a critical challenge due to its progression to cirrhosis and hepatocellular carcinoma (HCC). This review clarifies the complex crosstalk between the immune system and HSCs, highlighting key cellular players
Wahyu Widowati   +10 more
wiley   +1 more source

Transcriptional activation of the miR-17-92 cluster is involved in the growth-promoting effects of MYB in human Ph-positive leukemia cells. [PDF]

open access: yes, 2018
MicroRNAs, non-coding regulators of gene expression, are likely to function as important downstream effectors of many transcription factors including MYB. Optimal levels of MYB are required for transformation/maintenance of BCR-ABL-expressing cells.
Blandino, Giovanni   +15 more
core   +3 more sources

Acute lymphoblastic B‐cell leukemia or CAR‐T cell related skin changes – a relevant diagnostic challenge

open access: yes
JDDG: Journal der Deutschen Dermatologischen Gesellschaft, EarlyView.
Farzan Solimani   +9 more
wiley   +1 more source

Molecular Insights Into Repurposed Drug Interactions With HDAC11 for Advancing Epigenetic Therapeutics in Cancer and Neurodegenerative Diseases

open access: yesJournal of Chemistry, Volume 2026, Issue 1, 2026.
Histone deacetylase 11 (HDAC11) is a member of the HDAC family that plays a crucial role in epigenetic regulation, influencing key cellular processes like transcription, differentiation, and proliferation. Abnormal expressions and functions of HDAC11 have been described in various diseases, including neurodegenerative diseases and cancer, highlighting ...
Yinsheng Yang   +5 more
wiley   +1 more source

Treating Imatinib-Resistant Leukemia: The Next Generation Targeted Therapies

open access: yesThe Scientific World Journal, 2006
Imatinib (Gleevec/STI-571/CGP57148B, Novartis) is a small-molecule, tyrosine kinase inhibitor developed to target BCR-ABL, c-Kit, and PDGF-R. Through inhibition of these oncogenic kinases, imatinib is effective in the treatment of BCR-ABL–positive ...
Michael R. Burgess, Charles L. Sawyers
doaj   +1 more source

In Vivo Eradication of Human BCR/ABL-Positive Leukemia Cells With an ABLKinase Inhibitor [PDF]

open access: yes, 2017
BACKGROUND: The leukemia cells of approximately 95% of patients with chronic myeloid leukemia and 30%-50% of adult patients with acute lymphoblastic leukemia express the Bcr/Abl oncoprotein, which is the product of a fusion gene created by a chromosomal ...
Buchdunger, Elisabeth   +7 more
core  

The mechanisms of taxodione-induced apoptosis in BCR-ABL-positive leukemia cells

open access: yesFolia Pharmacologica Japonica, 2019
Chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) are caused by a fusion protein, BCR-ABL, which induces cellular transformation by activating the signaling molecules, STAT5 and Akt. The specific BCR-ABL inhibitors including imatinib, nilotinib, and dasatinib, are clinically utilized in the treatment with CML and ALL patients ...
Yuki, Uchihara   +2 more
openaire   +3 more sources

Disease Progression Mediated by Egr-1 Associated Signaling in Response to Oxidative Stress [PDF]

open access: yes, 2012
When cellular reducing enzymes fail to shield the cell from increased amounts of reactive oxygen species (ROS), oxidative stress arises. The redox state is misbalanced, DNA and proteins are damaged and cellular transcription networks are activated.
Abdulkadir   +99 more
core   +2 more sources

Nilotinib treatment in mouse models of P190 Bcr/Abl lymphoblastic leukemia

open access: yesMolecular Cancer, 2007
Background Ph-positive leukemias are caused by the aberrant fusion of the BCR and ABL genes. Nilotinib is a selective Bcr/Abl tyrosine kinase inhibitor related to imatinib, which is widely used to treat chronic myelogenous leukemia.
Groffen John   +7 more
doaj   +1 more source

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