Results 41 to 50 of about 98,172 (269)

Targeting BCR-ABL+ stem/progenitor cells and BCR-ABL-T315I mutant cells by effective inhibition of the BCR-ABL-Tyr177-GRB2 complex

Oncotarget, 2017
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.
Kun Meng, Min Chen, Ali G. Turhan, Hongxia Ding, Qingcong Lin, Xiaoyan Jiang   +5 more
openaire   +4 more sources

Combination therapy of BCR-ABL-positive B cell acute lymphoblastic leukemia by tyrosine kinase inhibitor dasatinib and c-JUN N-terminal kinase inhibition

Journal of Hematology & Oncology, 2020
Background The Philadelphia chromosome (Ph), which leads to the creation and expression of the fusion gene product BCR-ABL, underlines the pathogenesis of chronic myelogenous leukemia (CML) and a fraction of adult and pediatric acute B-lymphoblastic ...
Xinhua Xiao, Ping Liu, Donghe Li, Zhizhou Xia, Peihong Wang, Xiuli Zhang, Mingzhu Liu, Lujian Liao, Bo Jiao, Ruibao Ren   +9 more
doaj   +1 more source

Interactions of p62 with p210 and Bcr-Abl-associated Proteins [PDF]

Journal of Biological Chemistry, 1998
A 62-kDa Ras GTPase-activating protein (RasGAP)-associated protein is tyrosine-phosphorylated under a variety of circumstances including growth factor stimulation and in cells transformed by activated tyrosine kinases. A cDNA for p62(dok), reported to be the RasGAP-associated 62-kDa protein, was recently cloned from Abl-transformed cells. In this study,
Kara Johnson, Brian J. Druker, Tsukasa Oda, Amie S. Corbin, Arun Bhat   +4 more
openaire   +3 more sources

Pharmacological difference between degrader and inhibitor against oncogenic BCR-ABL kinase

Scientific Reports, 2018
Chronic myelogenous leukemia (CML) is characterized by the oncogenic fusion protein, BCR-ABL protein kinase, against which clinically useful inhibitors have been developed. An alternative approach to treat CML is to degrade the BCR-ABL protein. Recently,
N. Shibata, K. Shimokawa, Katsunori Nagai, Nobumichi Ohoka, T. Hattori, Naoki Miyamoto, O. Ujikawa, Tomoya Sameshima, H. Nara, N. Cho, M. Naito   +10 more
semanticscholar   +1 more source

Potential role of Notch signalling in CD34+ chronic myeloid leukaemia cells: cross-talk between Notch and BCR-ABL. [PDF]

PLoS ONE, 2015
Notch signalling is critical for haemopoietic stem cell (HSC) self-renewal and survival. The role of Notch signalling has been reported recently in chronic myeloid leukaemia (CML) - a stem cell disease characterized by BCR-ABL tyrosine kinase activation.
Abdullah Aljedai, Anne-Marie Buckle, Prashant Hiwarkar, Farhatullah Syed   +3 more
doaj   +1 more source

Simultaneous inhibition of TRIM24 and TRIM28 sensitises prostate cancer cells to antiandrogen therapy, decreasing VEGF signalling and angiogenesis

Molecular Oncology, EarlyView.
TRIM24 and TRIM28 are androgen receptor (AR) coregulators which exhibit increased expression with cancer progression. Both TRIM24 and TRIM28 combine to influence the response of castrate‐resistant prostate cancer (CRPC) cells to AR inhibitors by mediating AR signalling, regulation of MYC and upregulating VEGF to promote angiogenesis. Castrate‐resistant
Damien A. Leach, Nilesh Chatterjee, Kellie Spahr, Gilberto Serrano de Almeida, Anabel Varela‐Carver, Taimur T. Shah, Mathias Winkler, Hashim U. Ahmed, Charlotte L. Bevan   +8 more
wiley   +1 more source

Induction of autophagy by Imatinib sequesters Bcr‐Abl in autophagosomes and down‐regulates Bcr‐Abl protein [PDF]

American Journal of Hematology, 2013
Chronic Myeloid Leukemia (CML) is a disease of hematopoietic stem cells which harbor the chimeric gene Bcr‐Abl. Expression levels of this constitutively active tyrosine kinase are critical for response to tyrosine kinase inhibitor treatment and also disease progression, yet the regulation of protein stability is poorly understood.
Elzinga, Baukje M., Nyhan, Michelle J., Crowley, Lisa C., O'Donovan, Tracey R., Cahill, Mary R., McKenna, Sharon L.   +5 more
openaire   +3 more sources

Induction of apoptosis in imatinib sensitive and resistant chronic myeloid leukemia cells by efficient disruption of bcr-abl oncogene with zinc finger nucleases

Journal of Experimental & Clinical Cancer Research, 2018
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, Zhenglan Huang, Miao Gao, Zhenhong Luo, Fangzhu Zhou, Lin Liu, Qing Xiao, Xin Wang, Wenli Feng   +8 more
doaj   +1 more source

A Novel C19orf47‐AKT2 Chimeric RNA Generated by Cis‐Splicing of Adjacent Genes Is Associated With Glioblastoma Prognosis

Annals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective Malignant gliomas pose significant therapeutic challenges. This study aimed to identify and characterize a novel chimeric RNA in glioma and assess its clinical and functional significance for precision treatment. Methods The C19orf47‐AKT2 chimeric RNAs were identified through RNA sequencing and validated by polymerase chain reaction.
Zihan Wang, Bowen Ni, Kezhi Wu, Qi Zhang, Jinglin Guo, Runwei Yang, Ziyu Wang, Guozhong Yi, Guanglong Huang, Minyi He, Yimin Xu, Yawei Liu   +11 more
wiley   +1 more source

Regulation of hTERT by BCR-ABL at multiple levels in K562 cells

BMC Cancer, 2011
Background The cytogenetic characteristic of Chronic Myeloid Leukemia (CML) is the formation of the Philadelphia chromosome gene product, BCR-ABL. Given that BCR-ABL is the specific target of Gleevec in CML treatment, we investigated the regulation of ...
Chai Juin Hsien, Zhang Yong, Tan Wei Han, Chng Wee Joo, Li Baojie, Wang Xueying   +5 more
doaj   +1 more source