Results 11 to 20 of about 60,584 (224)

Reciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment. [PDF]

PLoS ONE, 2009
BACKGROUND:t(9;22) is a balanced translocation, and the chromosome 22 breakpoints (Philadelphia chromosome--Ph+) determine formation of different fusion genes that are associated with either Ph+ acute lymphatic leukemia (Ph+ ALL) or chronic myeloid ...
Xiaomin Zheng, Claudia Oancea, Reinhard Henschler, Malcolm A S Moore, Martin Ruthardt   +4 more
doaj   +1 more source

The functional interplay between the t(9;22)-associated fusion proteins BCR/ABL and ABL/BCR in Philadelphia chromosome-positive acute lymphatic leukemia. [PDF]

PLoS Genetics, 2015
The hallmark of Philadelphia chromosome positive (Ph(+)) leukemia is the BCR/ABL kinase, which is successfully targeted by selective ATP competitors. However, inhibition of BCR/ABL alone is unable to eradicate Ph(+) leukemia.
Anahita Rafiei, Afsar Ali Mian, Claudia Döring, Anna Metodieva, Claudia Oancea, Frederic B Thalheimer, Martin Leo Hansmann, Oliver Gerhard Ottmann, Martin Ruthardt   +8 more
doaj   +1 more source

Target Inhibition of CBP Induced Cell Senescence in BCR-ABL- T315I Mutant Chronic Myeloid Leukemia

Frontiers in Oncology, 2021
The treatment of chronic myeloid leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKIs), such as imatinib, has yielded clinical success. However, the direct targeting of BCR-ABL does not eradicate CML cells expressing mutant BCR-ABL, especially ...
Ke Yang, Fang Wang, Hong Zhang, Xiaokun Wang, Likun Chen, Xiaodong Su, Xingping Wu, Qianqian Han, Zhen Chen, Zhe-Sheng Chen, Liwu Fu   +10 more
doaj   +1 more source

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.
Liuya Wei, Yang Yang, Pranav Gupta, Aihong Wang, Min Zhao, Yao Zhao, Mei Qu, Yu Ke, Ying Liu, Hong-Min Liu, Xin Xu, Yanli Sun, Zhe-Sheng Chen, Zhenbo Hu   +13 more
doaj   +1 more source

Small interfering RNA against BCR-ABL transcripts sensitize mutated T315I cells to nilotinib

Haematologica, 2010
Background Selective inhibition of the BCR-ABL tyrosine kinase by RNA interference has been demonstrated in leukemic cells. We, therefore, evaluated specific BCR-ABL small interfering RNA silencing in BCR-ABL-positive cell lines, including those ...
Michael Koldehoff, Lambros Kordelas, Dietrich W. Beelen, Ahmet H. Elmaagacli   +3 more
doaj   +1 more source

p185(BCR/ABL) has a lower sensitivity than p210(BCR/ABL) to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia [PDF]

, 2011
Background: The t(9;22) translocation leads to the formation of the chimeric breakpoint cluster region/c-abl oncogene 1 (BCR/ABL) fusion gene on der22, the Philadelphia chromosome.
Mahajna, Jamal, Metodieva, Anna, Mian, Afsar Ali, Najajreh, Yousef, Ottmann, Oliver G., Ruthardt, Martin   +5 more
core   +2 more sources

Sensitive detection of pre-existing BCR-ABL kinase domain mutations in CD34+ cells of newly diagnosed chronic-phase chronic myeloid leukemia patients is associated with imatinib resistance: implications in the post-imatinib era. [PDF]

PLoS ONE, 2013
BACKGROUND: BCR-ABL kinase domain mutations are infrequently detected in newly diagnosed chronic-phase chronic myeloid leukemia (CML) patients. Recent studies indicate the presence of pre-existing BCR-ABL mutations in a higher percentage of CML patients ...
Zafar Iqbal, Aamer Aleem, Mudassar Iqbal, Mubashar Iqbal Naqvi, Ammara Gill, Abid Sohail Taj, Abdul Qayyum, Najeeb ur-Rehman, Ahmad Mukhtar Khalid, Ijaz Hussain Shah, Muhammad Khalid, Riazul Haq, Mahwish Khan, Shahid Mahmood Baig, Abid Jamil, Muhammad Naeem Abbas, Muhammad Absar, Amer Mahmood, Mahmood Rasool, Tanveer Akhtar   +19 more
doaj   +1 more source

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

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   +1 more source

Expression of BCR/ABL p210 from a Knockin Allele Enhances Bone Marrow Engraftment without Inducing Neoplasia

Cell Reports, 2013
Chronic myeloid leukemia (CML) and some acute lymphoblastic leukemias are characterized by the t(9;22) chromosome, which encodes the BCR/ABL oncogene. Multiple mouse models of CML express BCR/ABL at high levels from non-Bcr promoters, resulting in the ...
Samantha B. Foley, Zacariah L. Hildenbrand, Abigail A. Soyombo, Jeffery A. Magee, Yipin Wu, Katherine I. Oravecz-Wilson, Theodora S. Ross   +6 more
doaj   +1 more source

Effect of HSP90AB1 and CC domain interaction on Bcr-Abl protein cytoplasm localization and function in chronic myeloid leukemia cells

Cell Communication and Signaling, 2021
Background The fusion oncoprotein Bcr-Abl is mostly located in the cytoplasm, which causes chronic myeloid leukemia (CML). After moving into the nucleus, the fusion protein can induce apoptosis of CML cells.
Yuhang Peng, Zhenglan Huang, Fangzhu Zhou, Teng Wang, Ke Mou, Wenli Feng   +5 more
doaj   +1 more source