Results 171 to 180 of about 52,225 (202)
Some of the next articles are maybe not open access.
Evaluation of deoxyhypusine synthase inhibitors targeting BCR-ABL positive leukemias
Investigational New Drugs, 2012Effective inhibition of BCR-ABL tyrosine kinase activity with Imatinib represents a breakthrough in the treatment of patients with chronic myeloid leukemia (CML). However, more than 30 % of patients with CML in chronic phase do not respond adequately to Imatinib and the drug seems not to affect the quiescent pool of BCR-ABL positive leukemic stem and ...
Ziegler, P +14 more
openaire +2 more sources
The cytotoxicity of a Grb2-SH3 inhibitor in Bcr-Abl positive K562 cells
Biochemical Pharmacology, 2008Chronic myelogenous leukemia (CML) is characterized by the presence of Bcr-Abl oncoprotein. Gleevec has been designed to treat many CML patients by specifically targeting Bcr-Abl, but resistance to it is already apparent in many cases. In CML cells, Bcr-Abl activates several signaling pathways, including the Ras-dependent pathway, in which growth ...
Yun-Bin, Ye +8 more
openaire +2 more sources
Optimization of methods for the detection of BCR-ABL activity in Philadelphia-positive cells
Experimental Hematology, 2009The recent success in treating chronic myeloid leukemia (CML) with tyrosine kinase inhibitors (TKI), such as imatinib mesylate (IM), has created a demand for reproducible methods to accurately assess inhibition of BCR-ABL activity within CML cells, including rare stem and progenitor cells, either in vitro or in vivo.
Ashley, Hamilton +4 more
openaire +3 more sources
Blood, 2005
Abstract AMN107 is a new, highly potent and selective BCR-ABL inhibitor currently in clinical development for the treatment of imatinib-resistant chronic myelogenous leukemia (CML) or Philadelphia positive acute lymphoblastic leukemia ALL (Ph+ALL).
Andreas Hochhaus +14 more
openaire +1 more source
Abstract AMN107 is a new, highly potent and selective BCR-ABL inhibitor currently in clinical development for the treatment of imatinib-resistant chronic myelogenous leukemia (CML) or Philadelphia positive acute lymphoblastic leukemia ALL (Ph+ALL).
Andreas Hochhaus +14 more
openaire +1 more source
Tyrosine kinase inhibitors in BCR/ABL positive ALL.
Journal of Clinical Oncology, 20116536 Background: The treatment of acute lymphocytic leukemia (ALL) represents a success for chemotherapy treatments developed in the early 70’s.
openaire +1 more source
Journal of Clinical Oncology, 2005
3015 Background: AMN107, a novel aminopyrimidine ATP-competitive inhibitor of Bcr-Abl. AMN107, is 10- to 50-fold more potent than imatinib against Bcr-Abl expressing cell lines, and is effective against most cell lines expressing imatinib-resistant Bcr-Abl mutants.
O. Ottmann +9 more
openaire +1 more source
3015 Background: AMN107, a novel aminopyrimidine ATP-competitive inhibitor of Bcr-Abl. AMN107, is 10- to 50-fold more potent than imatinib against Bcr-Abl expressing cell lines, and is effective against most cell lines expressing imatinib-resistant Bcr-Abl mutants.
O. Ottmann +9 more
openaire +1 more source
BCR/ABL-Positive Chronic Myeloid Leukemia in Children: Current Treatment Approach
Current Oncology ReportsThe purpose of this review is to summarize the most updated treatment recommendations for pediatric CML, and to discuss current areas of investigation.There is new phase 1 data to support the safety of the non-ATP competitive tyrosine kinase inhibitor (TKI) asciminib in the pediatric cohort.
Jenna M, Menger +3 more
openaire +2 more sources
Advances in BCR/ABL positive ALL
ADVANCES IN CELL AND GENE THERAPY, 2019Netanel A. Horowitz, Jacob M. Rowe
openaire +1 more source
Implicating the bcr/abl Gene in the Pathogenesis of Philadelphia Chromosome-Positive Human Leukemia
1991Publisher Summary The hypothesis that the Philadelphia chromosome might have a causative role in human chronic myelogenous leukemia (CML) was validated by the discovery that the human homologue of the v -abl oncogene of Abelson murine leukemia virus (A-MuLV) mapped to chromosome 9q34, precisely the locus disrupted in the formation of the ...
G Q, Daley, Y, Ben-Neriah
openaire +2 more sources

