Results 41 to 50 of about 45,526 (248)

Activation of tyrosine kinases by mutation of the gatekeeper threonine. [PDF]

, 2008
Protein kinases targeted by small-molecule inhibitors develop resistance through mutation of the gatekeeper threonine residue of the active site. Here we show that the gatekeeper mutation in the cellular forms of c-ABL, c-SRC, platelet-derived growth ...
Azam, Mohammad, Daley, George, Gray, Nathanael, KURIYAN, John, Seeliger, Markus   +4 more
core   +1 more source

The chronic myeloid leukemia stem cell: stemming the tide of persistence [PDF]

, 2017
Chronic myeloid leukaemia (CML) is caused by the acquisition of the tyrosine kinase BCR-ABL1 in a haemopoietic stem cell (HSC), transforming it into a leukaemic stem cell (LSC) that self-renews, proliferates and differentiates to give rise to a ...
Holyoake, Tessa L., Vetrie, David
core   +1 more source

Multifaceted actions of 8-amino-adenosine kill BCR–ABL positive cells [PDF]

Leukemia & Lymphoma, 2012
Survival of chronic myelogenous leukemia (CML) cells is dependent on BCR-ABL kinase, the activity of which is contingent on the level of BCR-ABL protein and the availability of adenosine triphosphate (ATP). We hypothesized that 8-amino-adenosine (8-amino-Ado)-mediated reduction in cellular ATP level and inhibition of mRNA synthesis leading to a ...
Rathi N, Pillai, Lisa S, Chen, Mary L, Ayres, Billie J, Nowak, Michael W, Thomas, Elizabeth J, Shpall, Michael J, Keating, Varsha, Gandhi   +7 more
openaire   +2 more sources

Real-World Outcomes With Low-Dose Dasatinib (50 mg) in Imatinib-Resistant Chronic Myeloid Leukemia in Chronic Phase: A Retrospective Analysis of Efficacy and Safety. [PDF]

Cancer Rep (Hoboken)
ABSTRACT Background Dasatinib, a potent second‐generation tyrosine kinase inhibitor (TKI), is highly effective in chronic myeloid leukemia in chronic phase (CML‐CP) resistant to imatinib at standard dosing (100 mg daily), but is often limited by adverse events.
Gangadaran N, Mamlekar H, Saha S, Kashyap R, Yadav S, Rahman K, Gupta R, Vijayaran M, Singh M, Chandra D.   +9 more
europepmc   +2 more sources

Epigenetic dysregulation in chronic myeloid leukaemia: A myriad of mechanisms and therapeutic options [PDF]

, 2018
The onset of global epigenetic changes in chromatin that drive tumor proliferation and heterogeneity is a hallmark of many forms cancer. Identifying the epigenetic mechanisms that govern these changes and developing therapeutic approaches to modulate ...
Koschmieder, Steffen, Vetrie, David
core   +1 more source

Quinacrine Depletes BCR-ABL and Suppresses Ph-Positive Leukemia Cells

Cancer Investigation, 2019
Drug resistance to TKIs and the existance of CML leukemia stem cells is an urgent problem. In this study, we demonstrate that quinacrine (QC) induces apoptosis in BCR-ABL positive CML and acute lymphoblastic leukemia (ALL) cells. Interestingly, QC inhibits the colony formation of primary CD34+ progenitor/stem leukemia cells from CML patients.
Hu Lei, Yaoyao Tu, Li Yang, Jin Jin, Hao Luo, Hanzhang Xu, Jingwu Kang, Li Zhou, Yingli Wu   +8 more
openaire   +2 more sources

CREB is a critical regulator of normal hematopoiesis and leukemogenesis [PDF]

, 2008
The cAMP-responsive element binding protein (CREB) is a 43-kDa nuclear transcription factor that regulates cell growth, memory, and glucose homeostasis. We showed previously that CREB is amplified in myeloid leukemia blasts and expressed at higher levels
Akashi, Akashi, Bai, Bottazzi, Bruserud, Cheng, Christensen, Conkright, Crans-Vargas, Deepa B. Shankar, Dejah R. Judelson, Desdouets, Deshpande, Elliot M. Landaw, Fried, Fu, Hestdal, Impey, Ingrid Schmid, Jamieson, Jenny Chang, Jerry C. Cheng, Kathleen M. Sakamoto, Kentaro Kinjo, Kim, Kinjo, Kohn, Kondo, Koschmieder, Koya, Krishan, Kwon, Lee, Mayr, Mendoza, Miyoshi, Montminy, Ninomiya, Noriyuki Kasahara, Passegué, Ravi Bhatia, Rehemtulla, Renata Stripecke, Scherr, Shah, Shankar, Shankar, Shaywitz, Stripecke, Traver, Tuschl, Van Etten, Ventura, Winston S. Wu, Wong, Yuan   +55 more
core   +3 more sources

Deletions of the derivative chromosome 9 occur at the time of the Philadelphia translocation and provide a powerful and independent prognostic indicator in chronic myeloid leukemia [PDF]

, 2001
Chronic myeloid leukemia (CML) is characterized by formation of the BCR-ABL fusion gene, usually as a consequence of the Philadelphia (Ph) translocation between chromosomes 9 and 22.
Bench, AJ, Campbell, LJ, Grace, C, Green, AR, Huntly, BJP, Nacheva, EP, Prince, HM, Reid, AG, Shepherd, P, Szer, J, Telford, N, Turner, P   +11 more
core   +1 more source

Detection of BCR-ABL Positive Cells in an Asymptomatic Patient: A Case Report and Literature Review

Case Reports in Medicine, 2010
We report a case of an asymptomatic 39-year-old male who was incidentally found to have a white blood cell count of 15 000/mm3 associated with a positive BCR-ABL/t(9;22)(q34;q11) chromosomal translocation detected in 51/300 of cells by FISH and RT-PCR ...
Soley Bayraktar, Mark Goodman
doaj   +1 more source

Follow-up of Chronic Myeloid Leukemia Patients whose Tyrosine Kinase Treatment Was Stopped: Case Series

Hematology, Transfusion and Cell Therapy, 2022
İntroduction: Chronic Myeloid Leukemia (CML) is a myeloproliferative disease characterized by the formation of the BCR ABL1 fusion protein with translocation t(9;22) (Philadelphia chromosome-Ph).
Kemal Fidan, Ali Unal
doaj   +1 more source