Results 51 to 60 of about 125,674 (260)
Inhibition of interleukin-1 signaling enhances elimination of tyrosine kinase inhibitor treated CML stem cells [PDF]
Treatment of chronic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKI) fails to eliminate leukemia stem cells (LSC). Patients remain at risk for relapse, and additional approaches to deplete CML LSC are needed to enhance the ...
Agarwal, Puneet +9 more
core +1 more source
Treatment of BCR-ABL+ human leukemia has been significantly improved by ABL tyrosine kinase inhibitors (TKIs), but they are not curative for most patients and relapses are frequently associated with BCR-ABL mutations, warranting new targets for improved treatments.
Chen, Min +5 more
openaire +3 more sources
This study successfully establishes adamantinomatous craniopharyngioma (ACP) patient‐derived organoids (PDOs) that preserve the histopathological and genetic features of the original tumors. Through drug sensitivity assays and subsequent mechanistic analyses, the study demonstrates that Ceritinib exerts its inhibitory effects on ACP PDO growth by ...
Huarong Zhang +15 more
wiley +1 more source
Sphingomyelin synthase 1 activity is regulated by the BCR-ABL oncogene[S]
Sphingomyelin synthase (SMS) produces sphingomyelin while consuming ceramide (a negative regulator of cell proliferation) and forming diacylglycerol (DAG) (a mitogenic factor). Therefore, enhanced SMS activity could favor cell proliferation.
Tara Ann Burns +9 more
doaj +1 more source
Targeting the oligomerization of BCR/ABL by membrane permeable competitive peptides inhibits the proliferation of Philadelphia Chromosome positive leukemic cells [PDF]
The BCR/ABL fusion protein is the hallmark of Philadelphia Chromosome positive (Ph+) leukemia. The constitutive activation of the ABL-kinase in BCR/ABL cells induces the leukemic phenotype.
Beißert, Tim +8 more
core
The chimeric RNA ERCC1‐iASPP possesses dual coding and non‐coding functions, synergistically accelerating the process of cellular malignant transformation. Abstract Genetic variation at 19q13.3 critically modulates chemical carcinogen‐induced lung carcinogenesis, particularly in mediating the activity of benzo[a]pyrene (B[a]P), a major polycyclic ...
Mingming Shan +9 more
wiley +1 more source
Background The bcr-abl fusion gene is the pathological origin of chronic myeloid leukemia (CML) and plays a critical role in the resistance of imatinib. Thus, bcr-abl disruption-based novel therapeutic strategy may warrant exploration.
Ningshu Huang +8 more
doaj +1 more source
Aleukemic bcr-abl positive granulocytic sarcoma [PDF]
Granulocytic sarcoma (GS) can occur de novo or in association with intramedullary myeloid disorders. With the advent of sophisticated molecular detection techniques to detect diagnostic genes such as bcr-abl, PML-RARA and CBFB/MYH11 in bone marrow or peripheral blood, many cases of the so called 'primary' GS are questionable.
Kuan, Jew-Win +3 more
openaire +3 more sources
T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities
T cell exhaustion limits immunotherapy efficacy. This article delineates its progression from stem‐like to terminally exhausted states, governed by persistent antigen, transcription factors, epigenetics, and metabolism. It maps the exhaustion landscape in the TME and proposes integrated reversal strategies, providing a translational roadmap to overcome
Yang Yu +7 more
wiley +1 more source
Evaluation of Morpholino Antisense Oligos’ Role on BCR-ABL Gene Silencing in the K562 Cell Line [PDF]
Objective: Chronic myeloid leukemia (CML) develops when a hematopoietic stem cellacquires the BCR/ABL fusion gene. This causes these transformed hematopoietic cellsto have a greater than normal proliferation rate.
Bahman Delalat +6 more
doaj

