Results 1 to 10 of about 199,448 (250)

Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I [PDF]

open access: yesBMC 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
doaj   +3 more sources

Association of HLA Class I and Class II genes with bcr-abl transcripts in leukemia patients with t(9;22) (q34;q11) [PDF]

open access: yesBMC Cancer, 2004
Background Based on the site of breakpoint in t(9;22) (q34;q11), bcr-abl fusion in leukemia patients is associated with different types of transcript proteins.
Cano Pedro   +2 more
doaj   +5 more sources

Performance characteristics of the first Food and Drug Administration (FDA)-cleared digital droplet PCR (ddPCR) assay for BCR::ABL1 monitoring in chronic myelogenous leukemia.

open access: yesPLoS 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
doaj   +3 more sources

Long circulating lectin conjugated paclitaxel loaded magnetic nanoparticles: a new theranostic avenue for leukemia therapy. [PDF]

open access: yesPLoS 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
doaj   +1 more source

Leukemic infiltration of the ovary as an initial presentation of chronic myeloid leukemia in chronic phase [PDF]

open access: yesVojnosanitetski 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
doaj   +1 more source

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]

open access: yesPLoS 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
doaj   +1 more source

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]

open access: yesPrecision 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
doaj   +1 more source

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]

open access: yesVojnosanitetski 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
doaj   +1 more source

Identification of small molecules that disrupt signaling between ABL and its positive regulator RIN1. [PDF]

open access: yesPLoS ONE, 2015
Constitutively active BCR-ABL kinase fusions are causative mutations in the pathogenesis of hematopoietic neoplasias including chronic myelogenous leukemia (CML).
Pamela Y Ting   +12 more
doaj   +1 more source

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

open access: yes, 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

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