Results 1 to 10 of about 118,885 (322)

Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I [PDF]

BMC Cancer, 2012
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.
Mian Afsar, Metodieva Anna, Badura Susanne, Khateb Mamduh, Ruimi Nili, Najajreh Yousef, Ottmann Oliver, Mahajna Jamal, Ruthardt Martin   +8 more
doaj   +9 more sources

Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-κB signaling and depleting Bcr-Abl [PDF]

Molecular Cancer, 2010
Background Chronic myelogenous leukemia (CML) is characterized by the chimeric tyrosine kinase Bcr-Abl. Bcr-Abl-T315I is the notorious point mutation that causes resistance to imatinib and the second generation tyrosine kinase inhibitors, leading to poor
Jingxuan Pan
exaly   +6 more sources

Pterostilbene downregulates BCR/ABL and induces apoptosis of T315I-mutated BCR/ABL-positive leukemic cells [PDF]

Scientific Reports, 2022
In this study, we examined the antileukemic effects of pterostilbene, a natural methylated polyphenol analog of resveratrol that is predominantly found in berries and nuts, using various human and murine leukemic cells, as well as bone marrow samples ...
Shohei Kawakami, Mitsuyo Tsuma-Kaneko, Masakazu Sawanobori, Tomoko Uno, Yoshihiko Nakamura, Hideyuki Matsuzawa, Rikio Suzuki, Makoto Onizuka, Takashi Yahata, Kazuhito Naka, Kiyoshi Ando, Hiroshi Kawada   +11 more
doaj   +5 more sources

Direct Binding of CRKL to BCR-ABL Is Not Required for BCR-ABL Transformation [PDF]

Blood, 1997
AbstractCRKL has previously been shown to be a major tyrosine phosphorylated protein in neutrophils of patients with BCR-ABL+ chronic myelogenous leukemia and in cell lines expressing BCR-ABL. CRKL and BCR-ABL form a complex as demonstrated by coimmunoprecipitation and are capable of a direct interaction in a yeast two-hybrid assay.
Conor Heaney, Kathryn S. Kolibaba, Arun Bhat, Tsukasa Oda, Sayuri Ohno, Shane Fanning, Brian J. Druker   +6 more
openalex   +5 more sources

I13 overrides resistance mediated by the T315I mutation in chronic myeloid leukemia by direct BCR-ABL inhibition [PDF]

Frontiers in Pharmacology, 2023
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm caused by a BCR-ABL fusion gene. Imatinib has significantly improved the treatment of CML as a first-generation tyrosine kinase inhibitor (TKIs). The T315I mutant form of BCR-ABL is the most
Congying Gao, Lei Zhang, Yun Xu, Xiangyu Ma, Peilei Chen, Zhe-Sheng Chen, Liuya Wei   +6 more
doaj   +2 more sources

BCR-ABL affects STAT5A and STAT5B differentially. [PDF]

PLoS ONE, 2014
Signal transducers and activators of transcription (STATs) are latent cytoplasmic transcription factors linking extracellular signals to target gene transcription. Hematopoietic cells express two highly conserved STAT5-isoforms (STAT5A/STAT5B), and STAT5
Michael Schaller-Schönitz, David Barzan, Andrew J K Williamson, John R Griffiths, Iris Dallmann, Karin Battmer, Arnold Ganser, Anthony D Whetton, Michaela Scherr, Matthias Eder   +9 more
doaj   +5 more sources

An In-house Method for Molecular Monitoring of BCR-ABL [PDF]

Turkish Journal of Hematology, 2012
OBJECTIVE: At present in Turkey, centers that are able to give reliable RQ-PCR BCR-ABL results are limited in number. We aimed to describe a cost-effective, in-house method for BCR-ABL quantification and to illustrate an example for RQ-PCR validation ...
Hakkı Ogun Sercan, Ilgın Öztürk, Ceyda Çalışkan, Melek Pehlivan, Zeynep Sercan   +4 more
doaj   +4 more sources

New Inhibitors of Bcr-Abl Based on 2,6,9-Trisubstituted Purine Scaffold Elicit Cytotoxicity in Chronic Myeloid Leukemia-Derived Cell Lines Sensitive and Resistant to TKIs [PDF]

Pharmaceutics
Bcr-Abl is an oncoprotein with aberrant tyrosine kinase activity involved in the progression of chronic myeloid leukemia (CML) and has been targeted by inhibitors such as imatinib and nilotinib.
Thalia Delgado, Denisa Veselá, Hana Dostálová, Vladimír Kryštof, Veronika Vojáčková, Radek Jorda, Alejandro Castro, Jeanluc Bertrand, Gildardo Rivera, Mario Faúndez, Miroslav Strnad, Christian Espinosa-Bustos, Cristian O. Salas   +12 more
doaj   +2 more sources

Targeted disruption of the BCR-ABL fusion gene by Cas9/dual-sgRNA inhibits proliferation and induces apoptosis in chronic myeloid leukemia cells [PDF]

Acta Biochimica et Biophysica Sinica
The BCR-ABL fusion gene, formed by the fusion of the breakpoint cluster region protein (BCR) and the Abl Oncogene 1, Receptor Tyrosine Kinase (ABL) genes, encodes the BCR-ABL oncoprotein, which plays a crucial role in leukemogenesis.
Zeng Jianling, Liang Xinquan, Duan Lili, Tan Fenghua, Chen Liujie, Qu Jiayao, Li Jia, Li Kai, Luo Dixian, Hu Zheng   +9 more
doaj   +2 more sources

A Small Molecule Inhibitor, OGP46, Is Effective against Imatinib-Resistant BCR-ABL Mutations via the BCR-ABL/JAK-STAT Pathway

Molecular Therapy - Oncolytics, 2020
Chronic myeloid leukemia (CML) is caused by the Philadelphia (Ph+) chromosome carrying the BCR-ABL oncogene, a constitutively active tyrosine kinase. The discovery of imatinib represents a major success story in the treatment against CML.
Luca Vincenzo Ballestra, Yu Ke, Xin Xu
exaly   +2 more sources