Detection of derivative 9 deletion by BCR-ABL fluorescence in-situ hybridization signal pattern to evaluate treatment response in CML patients [PDF]
Background: To evaluate prognostic effect of submicroscopic deletions involving breakage and fusion points of the derivative chromosome 9 and 22 in chronic myeloid leukemia in untreated patients and their follow up samples to correlate with disease ...
Bakshi Sonal R. +8 more
doaj +1 more source
Epigenetic dysregulation in chronic myeloid leukaemia: A myriad of mechanisms and therapeutic options [PDF]
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
Targeting quiescent leukemic stem cells using second generation autophagy inhibitors [PDF]
In chronic myeloid leukemia (CML), tyrosine kinase inhibitor (TKI) treatment induces autophagy that promotes survival and TKI-resistance in leukemic stem cells (LSCs).
A Hamilton +42 more
core +2 more sources
Activation of tyrosine kinases by mutation of the gatekeeper threonine. [PDF]
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 +4 more
core +1 more source
Targeting self-renewal pathways in myeloid malignancies [PDF]
A fundamental property of hematopoietic stem cells (HSCs) is the ability to self-renew. This is a complex process involving multiple signal transduction cascades which control the fine balance between self-renewal and differentiation through ...
Copland, M., Sands, W.A., Wheadon, H.
core +2 more sources
Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I [PDF]
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.
Badura, Susanne +8 more
core +1 more source
BCR ABL Fusion Protein Detection by a Modern Approach: Fluroscent Immuno Bead Assay
ABSTRACT Introduction Chronic Myeloid Leukemia (CML) is probably the most extensively studied human malignancy. CML patients (90-95%) harbor the Philadelphia (Ph) chromosome, a shortened chromosome 22, resulting from a reciprocal translocation t (9; 22) (q34; q11) between the long arms of chromosome 9 and 22, fusion ABL proto-oncogene on chromosome ...
S. Dasgupta +4 more
openaire +1 more source
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]
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 +11 more
core +1 more source
Transcriptional activation of the miR-17-92 cluster is involved in the growth-promoting effects of MYB in human Ph-positive leukemia cells. [PDF]
MicroRNAs, non-coding regulators of gene expression, are likely to function as important downstream effectors of many transcription factors including MYB. Optimal levels of MYB are required for transformation/maintenance of BCR-ABL-expressing cells.
Blandino, Giovanni +15 more
core +3 more sources
Prognosis of acute myeloid leukemia relies heavily on the cytogenetic and molecular abnormalities. AML1-ETO fusion protein resulting from t(8;21), a recurring cytogenetic abnormality, is known to be associated with favorable prognosis.
Manish K. Singh +5 more
doaj +1 more source

