Results 41 to 50 of about 9,645 (157)
CGP 57148, a Tyrosine Kinase Inhibitor, Inhibits the Growth of Cells Expressing BCR-ABL, TEL-ABL, and TEL-PDGFR Fusion Proteins [PDF]
CGP 57148 is a compound of the 2-phenylaminopyrimidine class that selectively inhibits the tyrosine kinase activity of the ABL and the platelet-derived growth factor receptor (PDGFR) protein tyrosine kinases. We previously showed that CGP 57148 selectively kills p210BCR-ABL–expressing cells. To extend these observations, we evaluated the ability of CGP
Martin Carroll+23 more
openaire +4 more sources
Constitutive association of BRCA1 and c-Abl and its ATM-dependent disruption after irradiation [PDF]
BRCA1 plays an important role in mechanisms of response to double-strand breaks, participating in genome surveillance, DNA repair, and cell cycle checkpoint arrests.
Favaudon, V.+7 more
core +2 more sources
Chronic Myeloid Leukemia (CML) is characterized by a balanced translocation juxtaposing the Abelson (ABL) and breakpoint cluster region (BCR) genes.
Anna Grazia Recchia+20 more
doaj +1 more source
Assembling defenses against therapy-resistant leukemic stem cells: Bcl6 joins the ranks [PDF]
The resistance of leukemic stem cells in response to targeted therapies such as tyrosine kinase inhibitors (TKIs) relies on the cooperative activity of multiple signaling pathways and molecules, including TGFβ, AKT, and FOXO transcription factors ...
Austin+30 more
core +2 more sources
STK25 Loss Augments Anti‐PD‐1 Therapy Efficacy by Regulating PD‐L1 Stability in Colorectal Cancer
This study demonstrates that STK25 depletion facilitates CRC immune escape through the inhibition of PD‐L1 Ser283 phosphorylation‐mediated ubiquitination, and promotes tumor growth. Furthermore, these findings identify STK25 as a potential therapeutic target to trigger antitumor immunity and promote immunotherapy efficacy. Abstract Tumor immune evasion
Xiaowen Qiao+20 more
wiley +1 more source
Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I [PDF]
Background: Chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive (Ph+) acute lymphatic leukemia (Ph + ALL) are caused by the t(9;22), which fuses BCR to ABL resulting in deregulated ABL-tyrosine kinase activity.
Badura, Susanne+8 more
core +1 more source
OBJECTIVE: This study aimed to verify the association between human leukocyte antigens and the bcr-abl fusion protein resulting from t(9;22)(q34;q11) in chronic leukemia myeloid and acute lymphoblastic leukemia patients.
Daiana Landenberger de Carvalho+3 more
doaj +1 more source
Relapsed and refractory multiple myeloma remains a major clinical challenge. This study shows that FOXM1 contributes to resistance against BH3 mimetics in multiple myeloma cells. The FOXM1 inhibitor NB73 enhances the effectiveness of BH3 mimetics by reducing FOXM1 expression and suppressing the MYC pathway.
Zhi Wen+16 more
wiley +1 more source
Therapeutic targeting of chromatin alterations in leukemia and solid tumors
Abstract Alterations in chromatin conformation and post‐translational modification of histones have become increasingly recognized as critical drivers of cancer development, progression, and therapy resistance. Recent advances in drug development have led to the establishment of several highly selective small molecule inhibitors, several of which are ...
Florian Perner+7 more
wiley +1 more source
Nanosensors in Leukemia Management: Pioneering Real‐Time Biomarker Detection for Precision Oncology
This review highlights pioneering nanosensors designed for real‐time leukemia biomarker detection, integrating advanced nanomaterials such as liposomes, polymeric nanoparticles and quantum dots. It examines electrochemical, optical and magnetic detection mechanisms, the applications across AML, ALL, CML, and CLL subtypes, and clinical translation ...
Hamed Soleimani Samarkhazan+5 more
wiley +1 more source