Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I [PDF]
BMC Cancer, 2012 Background Chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive (Ph+) acute lymphatic leukemia (Ph + ALL) are caused by the t(9;22), which fuses BCR to ABL resulting in deregulated ABL-tyrosine kinase activity.
Mian Afsar +8 more
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New type of Bcr/Abl junction in Philadelphia chromosome-positive chronic myelogenous leukemia [PDF]
Blood, 1990 A new and rare type of Bcr/Abl junction between exon C3 of the 3′ portion of the Bcr gene and Abl exon 2 has been identified in the leukemic cells of two Ph1-positive chronic myelogenous leukemia patients in chronic phase. This is the fourth type of Bcr/Abl junction so far identified in Ph1-positive hematologic malignancies and is a consequence of an ...
Felice Gavosto +16 more
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BCR-ABL rearrangements in children with Philadelphia chromosome- positive chronic myelogenous leukemia [PDF]
Blood, 1991 Abstract Leukemia cells from adults with Philadelphia (Ph1)-chromosome positive chronic myelogenous leukemia (CML) have a characteristic molecular rearrangement between the BCR and ABL genes whereby major breakpoint cluster region (Mbcr) exons 2 or 3 are joined to ABL exon II.
Robert Peter Gale +2 more
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PLoS ONE, 2022 Chronic myelogenous leukemia (CML) is a hematopoietic stem cell malignancy that accounts for 15-20% of all cases of leukemia. CML is caused by a translocation between chromosomes 9 and 22 which creates an abnormal fusion gene, BCR::ABL1.
Dawne N Shelton +7 more
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CDK8/19 inhibition attenuates G1 arrest induced by BCR-ABL antagonists and accelerates death of chronic myelogenous leukemia cells [PDF]
Cell Death DiscoveryImatinib mesylate (IM) and other BCR-ABL tyrosine kinase inhibitors (BCR-ABLi) are the mainstay of chronic myelogenous leukemia (CML) treatment. However, activation of circumventing signaling pathways and quiescence may limit BCR-ABLi efficacy.
Alvina I. Khamidullina +17 more
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Long circulating lectin conjugated paclitaxel loaded magnetic nanoparticles: a new theranostic avenue for leukemia therapy. [PDF]
PLoS ONE, 2011 Amongst all leukemias, Bcr-Abl positive chronic myelogenous leukemia (CML) confers resistance to native drug due to multi drug resistance and also resistance to p53 and fas ligand pathways.
Abhalaxmi Singh +2 more
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Leukemic infiltration of the ovary as an initial presentation of chronic myeloid leukemia in chronic phase [PDF]
Vojnosanitetski Pregled, 2022 Introduction. Extramedullary sites of leukemic proliferation, harboring an adverse outcome, are rare and usually found in the blastic phase of chronic myeloid leukemia.
Sekulić Borivoj +4 more
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Combination of bortezomib and mitotic inhibitors down-modulate Bcr-Abl and efficiently eliminates tyrosine-kinase inhibitor sensitive and resistant Bcr-Abl-positive leukemic cells. [PDF]
PLoS ONE, 2013 Emergence of resistance to Tyrosine-Kinase Inhibitors (TKIs), such as imatinib, dasatinib and nilotinib, in Chronic Myelogenous Leukemia (CML) demands new therapeutic strategies.
Octavian Bucur +7 more
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Isolated monocytosis was the flag preceding abnormalities in other parameters of complete blood counts in chronic myeloid leukemia with e1a2 (minor, P190) chimeric transcripts [PDF]
Precision and Future Medicine, 2019 Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm with the molecular hallmark of BCR-ABL1 chimeric transcripts from t(9;22)(q24;q22). In more than 95% of CML, the fusion occurs in the major breakpoint cluster region (M-bcr) of BCR, most ...
Jae Won Yun +5 more
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Several different cytogenetic clones arising during treatment of Philadelphia positive chronic myeloid leukemia with tyrosine kinase inhibitors lead to the progression into Philadelphia negative acute myeloid leukemia [PDF]
Vojnosanitetski Pregled, 2021 Introduction. Additional karyotype abnormalities in the Philadelphia-positive (Ph+) clone can emerge during the progression of chronic myeloid leukemia (CML) and are of-ten associated with the resistance to treatment with tyrosine kinase inhibitors (TKI).
Denčić-Fekete Marija +6 more
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