Results 81 to 90 of about 98,172 (269)

Anti-rheumatic agent auranofin induced apoptosis in chronic myeloid leukemia cells resistant to imatinib through both Bcr/Abl-dependent and -independent mechanisms

OncoTarget, 2014
Resistance to Imatinib mesylate (IM) is an emerging problem for patients with chronic myelogenous leukemia (CML). T315I mutation in the Bcr-Abl is the predominant mechanism of the acquired resistance to IM and second generation tyrosine kinase inhibitors
Xin Chen, Xianping Shi, Chong Zhao, Xiaofen Li, Xiaoying Lan, Shouting Liu, Hongbiao Huang, Ningning Liu, Siyan Liao, D. Zang, Wenbin Song, Quentin Liu, B. Carter, Q. Dou, Xuejun Wang, Jinbao Liu   +15 more
semanticscholar   +1 more source

TP‐0903 Suppresses Aurora A–PLK1 Signaling to Inhibit Proliferation of a Myelodysplastic Syndrome‐Derived Cell Line

Cancer Science, EarlyView.
TP‐0903 exerts the antitumor effects through diverse cell‐specific mechanisms, including apoptosis, ferroptosis, and cell cycle disruption. These insights underline the potential of TP‐0903 as a therapeutic agent for hematological malignancies and emphasize the need for further research to fully elucidate the molecular targets of TP‐0903 and optimize ...
Tomoko Kimura‐Hyoda, Mikuri Ryu, Ryosuke Yuta, Saori Fukumoto, Kentaro Hosokawa, Hisayuki Yao, Yoko Yasuda, Koichi Miura, Kaoru Tohyama, Fumio Arai, Takeshi Uchiumi   +10 more
wiley   +1 more source

Transferred BCR/ABL DNA from K562 Extracellular Vesicles Causes Chronic Myeloid Leukemia in Immunodeficient Mice

PLoS ONE, 2014
Our previous study showed that besides mRNAs and microRNAs, there are DNA fragments within extracellular vesicles (EVs). The BCR/ABL hybrid gene, involved in the pathogenesis of chronic myeloid leukemia (CML), could be transferred from K562 EVs to ...
Jin Cai, Gengze Wu, Xiaorong Tan, Yu Han, Caiyu Chen, Chuanwei Li, Na Wang, X. Zou, Xinjian Chen, Faying Zhou, D. He, Lin Zhou, P. Jose, C. Zeng   +13 more
semanticscholar   +1 more source

Role of STAT3 in transformation and drug resistance in CML

Frontiers in Oncology, 2012
Chronic Myeloid Leukemia (CML) is initially driven by the bcr-abl fusion oncoprotein. The identification of bcr-abl led to the discovery and rapid translation into the clinic of bcr-abl kinase inhibitors.
Rajesh R Nair, Joel H Tolentino, Lori A Hazlehurst   +2 more
doaj   +1 more source

CRISPR Technology in Disease Management: An Updated Review of Clinical Translation and Therapeutic Potential

Cell Proliferation, EarlyView.
CRISPR‐Cas systems offer transformative genome editing capabilities for precise manipulation of cellular genes. This enables two main therapeutic avenues: ex vivo modification of patient cells for re‐transplantation or direct in vivo gene targeting via advanced delivery methods.
Bahareh Farasati Far, Marziyeh Akbari, Mohammad Amin Habibi, Morteza Katavand, Sherko Nasseri   +4 more
wiley   +1 more source

Treatment‐Free Remission in Chronic Myeloid Leukemia: Revisiting the “W” Questions

European Journal of Haematology, EarlyView.
ABSTRACT Chronic myeloid leukemia (CML) has undergone a transformation from a fatal disease to a chronic, manageable condition with the advent of tyrosine kinase inhibitors (TKIs), particularly imatinib. This shift has significantly improved survival rates, and for some patients, achieving deep molecular response (DMR) has made treatment‐free remission
Antonella Bruzzese, Ernesto Vigna, Enrica Antonia Martino, Nicola Amodio, Caterina Labanca, Francesco Mendicino, Eugenio Lucia, Virginia Olivito, Fortunato Morabito, Massimo Gentile   +9 more
wiley   +1 more source

Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide through glutathione-depletion in imatinib-resistant cells

Haematologica, 2007
The development of resistance to imatinib mesylate may partly depend on high Bcr-Abl-expression levels. Arsenic trioxide (ATO) has Bcr-Abl suppressing activity in vitro.
Heiko Konig, Nicolai Härtel, Beate Schultheis, Michael Schatz, Christian Lorentz, Junia V. Melo, Rüdiger Hehlmann, Andreas Hochhaus, Paul La Rosée   +8 more
doaj   +1 more source

A computational dynamic model of combination treatment for type II inhibitors with asciminib

Protein Science, Volume 34, Issue 8, August 2025.
Abstract Despite continuous strides forward in drug development, resistance to treatment looms large in the battle against cancer as well as communicable diseases. Chronic myeloid leukemia (CML) is treated with targeted therapy and treatment is personalized when resistance arises.
J. Roadnight Sheehan, Astrid S. de Wijn, Ran Friedman   +2 more
wiley   +1 more source

Identification of novel tyrosine kinase inhibitors for drug resistant T315I mutant BCR-ABL: a virtual screening and molecular dynamics simulations study

Scientific Reports, 2014
BCR-ABL tyrosine kinase plays a major role in the pathogenesis of chronic myeloid leukemia (CML) and is a proven target for drug development. Currently available drugs in the market are effective against CML; however, side-effects and drug-resistant ...
H. N. Banavath, O. P. Sharma, Muthuvel Suresh Kumar, R. Baskaran   +3 more
semanticscholar   +1 more source

Long persistent bcr-abl positive transcript detected by polymerase chain reaction after marrow transplant for chronic myelogenous leukemia without clinical relapse: a study of 64 patients [PDF]

, 1993
K Miyamura, T Tahara, Masashi Tanimoto, Y Morishita, Kohei Kawashima, Y Morishima, Hajime Saito, Shinobu Tsuzuki, K. Takeyama, Y Kodera   +9 more
openalex   +3 more sources