Achievement of MR4.5 (BCR-ABL1 ≤ 0.0032% on international scale) is an important goal of tyrosine kinase inhibitor (TKI) treatment for patients with chronic myeloid leukemia (CML).
Accurate detection of <i>BCR-ABL</i> fusion transcripts at and below molecular response (MR) 4 (0.01% International Scale [IS]) is required for disease monitoring in patients with chronic myeloid leukemia (CML).
It remains unknown whether the administration of tyrosine kinase inhibitors (TKIs) targeting BCR-ABL1 after allogeneic hematopoietic cell transplantation (HCT) is associated with improved outcomes for patients with chronic myelogenous leukemia (CML).
Asciminib is a potent, specific BCR-ABL1 inhibitor being developed for the treatment of patients with chronic myelogenous leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (Ph + ALL).
A total of 77 of 101 (76.24%) <i>Tg(hsp70:p210<sup>BCR/ABL1</sup>)</i> adult transgenic zebrafish (age 6 months to 1 year) developed chronic myeloid leukemia.
Chronic myelogenous leukemia (CML) is a myeloproliferative disorder defined by the presence of the fusion gene BCR-ABL1 in primitive hematopoietic progenitors.
The availability of several <i>BCR-ABL1</i> tyrosine kinase inhibitor (TKI) options means physicians and patients can select the most appropriate treatment for a patient with chronic myeloid leukemia (CML).
In this study, we investigated the reliability of multiple <i>BCR-ABL1</i> thresholds in predicting treatment outcomes for 184 subjects diagnosed with CML and treated with standard-dose imatinib mesylate (IM).
<i>BCR/ABL1</i> gene fusion is the hallmark of chronic myeloid leukemia (CML), and is generated in 5-10% of patients by a variant translocation involving 9q34, 22q11.2 and one or more additional genomic regions.
Chronic myeloid leukemia (CML) is a myeloid clonal proliferation disease defining by the presence of the Philadelphia chromosome that shows the movement of BCR-ABL1.
Combined MDM2 and BCR-ABL1 inhibition targets chronic myeloid leukemia stem/progenitor cells and has the potential to improve cure rates for chronic myeloid leukemia.
The studies were conducted by using (i) primary CML-CP stem/early progenitor cells and normal hematopoietic counterparts isolated from the bone marrow of newly diagnosed patients with CML-CP and from healthy donors, respectively, (ii) CML-blast phase cell lines (K562 and KCL-22), and (iii) from <i>BCR-ABL1</i>-transformed 32Dcl3 cell line.
The development of mutations in the BCR-ABL1 fusion gene transcript causes resistance to tyrosine kinase inhibitors (TKIs) based therapy in chronic myeloid leukemia (CML).
The <i>BCR-ABL1</i> fusion gene is the driver oncogene in chronic myeloid leukemia (CML) and Philadelphia-chromosome positive (Ph+) acute lymphoblastic leukemia (ALL).
The resistance for the tyrosine kinase inhibitors in chronic myeloid leukemia (CML) occurs mainly due to BCR/ABL1 dependent and independent mechanisms.
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm the hallmark of which, the breakpoint cluster region-Abelson (BCR-ABL) oncogene, has been the target of tyrosine kinase inhibitors (TKIs), which have significantly improved the survival of patients with CML.
Chronic myeloid leukaemia (CML) is a myeloproliferative disorder characterized by the presence of breakpoint cluster region-Abelson murine leukemia (BCR-ABL1) gene fusion as a hallmark that is expressed as two major transcripts b2a2 and b3a2.