Results 31 to 40 of about 128,389 (322)

Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia.

New England Journal of Medicine, 2001
BACKGROUND BCR-ABL is a constitutively activated tyrosine kinase that causes chronic myeloid leukemia (CML). Since tyrosine kinase activity is essential to the transforming function of BCR-ABL, an inhibitor of the kinase could be an effective treatment ...
B. Druker, M. Talpaz, D. Resta, B. Peng, E. Buchdunger, J. Ford, N. Lydon, H. Kantarjian, R. Capdeville, Sayuri Ohno-Jones, C. Sawyers   +10 more
semanticscholar   +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

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

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

Suppression of autophagy by BCR ABL

Frontiers in Bioscience, 2012
Imatinib and second generation BCR/ABL tyrosine kinase inhibitors (TKIs) serve now as standard therapies for patients with chronic myelogenous leukemia (CML); however, CML stem cells are intrinsically insensitive to the cell death-inducing effects of TKIs, allowing the persistence of a "reservoir" of BCR/ABL-expressing CML-initiating cells potentially ...
CALABRETTA, Bruno, SALOMONI, Paolo
openaire   +5 more sources

Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival [PDF]

, 2012
Recent evidence suggests CML stem cells are insensitive to kinase inhibitors and responsible for minimal residual disease in treated patients. We investigated whether CML stem cells, in a transgenic mouse model of CML-like disease or derived from ...
Anderson, Ashley Hamilton, Bhatia, Bin Zhang, Branford, Carsten Müller-Tidow, Chen, Chomel, Chu, Copland, Corbin, Daley, Druker, Druker, Druker, Elaine K. Allan, Felsher, Franck E. Nicolini, G. Vignir Helgason, Gabert, Gorre, Gothert, Graham, Hamilton, Hayette, Holyoake, Hughes, Hurtz, Jiang, Jordan, Jordanides, Jorgensen, Konig, Konig, Konig, Koschmieder, Li, Lombardo, Lugo, Mirle Schemionek, Myssina, Notta, Pellicano, Ravi Bhatia, Samanta, Samanta, Schemionek, Scott, Shachaf, Shah, Sharma, Sharma, Sobrinho-Simoes, Steffen Koschmieder, Svetlana Myssina, Talpaz, Tessa L. Holyoake, Valerie G. Brunton, Wang, Weinstein, Weisberg, White   +61 more
core   +1 more source

Modular PROTAC Design for the Degradation of Oncogenic BCR-ABL.

Angewandte Chemie, 2016
Proteolysis Targeting Chimera (PROTAC) technology is a rapidly emerging alternative therapeutic strategy with the potential to address many of the challenges currently faced in modern drug development programs.
Ashton C Lai, M. Toure, D. Hellerschmied, J. Salami, S. Jaime-Figueroa, Eunhwa Ko, J. Hines, C. Crews   +7 more
semanticscholar   +1 more source

Contributions of the RhoGEF activity of p210 BCR/ABL to disease progression [PDF]

, 2014
We have previously identified a tyrosine kinase-independent, guanine nucleotide exchange factor (GEF) activity that is contained within the region of p210 BCR/ABL that distinguishes it from p190 BCR/ABL.
Chen, Ru, Fitzpatrick, Ethan R, Hu, Tinghui, Tala, Ilona, Whitehead, Ian P, Williams, David A   +5 more
core   +1 more source

Management of imatinib-resistant CML patients [PDF]

, 2007
Imatinib has had marked impact on outcomes in chronic myelogenous leukemia (CML) patients for all stages of the disease and is endorsed by international treatment guidelines as the first line option.
Branford S, Burger H, Burgess MR, Cortes J, Crossman LC, Donato NJ, Druker BJ, Gambacorti-Passerini C, Giles F, Hochhaus A, Hughes TP, Iacobucci I, Kantarjian H, Lahaye T, Mahon FX, Melo JV, O'Hare T, Quintas-Cardama A, Rousselot P, Sleijfer S, Soverini S, Weisberg E   +21 more
core   +1 more source

MTSS1 is a critical epigenetically regulated tumor suppressor in CML [PDF]

, 2015
Chronic myeloid leukemia (CML) is driven by malignant stem cells that can persist despite therapy. We have identified Metastasis suppressor 1 (Mtss1/MIM) to be downregulated in hematopoietic stem and progenitor cells from leukemic transgenic SCLtTA/Bcr ...
Braunschweig, T., Brümmendorf, T. H., Chatain, N., Copland, M., Costa, I. G., Gusmao, E. G., Haenzelmann, S., Hamilton, A., Helgason, G.V., Herrmann, O., Holyoake, T. L., Kintsler, S., Koschmieder, S., Li, S., Merle Reher, M., Müller-Tidow, C., Schemionek, M., Schubert, C., Schwab, A.   +18 more
core   +1 more source