• Corpus ID: 14225678

Detection of BCR-ABL proteins in blood cells of benign phase chronic myelogenous leukemia patients.

@article{Guo1991DetectionOB,
  title={Detection of BCR-ABL proteins in blood cells of benign phase chronic myelogenous leukemia patients.},
  author={J. Q. Guo and J Y J Wang and Ralph B. Arlinghaus},
  journal={Cancer research},
  year={1991},
  volume={51 11},
  pages={
          3048-51
        }
}
More than 95% of patients with chronic myelogenous leukemia (CML) contain an abnormal chromosome termed the Philadelphia chromosome (Ph1). Ph1 and the resulting BCR-ABL fused genes are markers for this type of leukemia. The product of the fused BCR-ABL genes is a protein of about 2000 amino acids termed P210 BCR-ABL. Although the BCR-ABL protein can be routinely detected in blood cells from blast crisis CML patients by assaying for its activated tyrosine kinase activity, detection of P210 BCR… 
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BCR-ABL protein expression in peripheral blood cells of chronic myelogenous leukemia patients undergoing therapy.
TLDR
The results indicate that the BCR-ABL Western blotting assay has clinical applications for both diagnosis and prospective evaluation ofPh1-positive and Ph1-negative CML patients.
Comparison of bcr-abl protein expression and Philadelphia chromosome analyses in chronic myelogenous leukemia patients.
The Philadelphia chromosome (Ph) is found in most chronic myelogenous leukemia (CML) patients. The bcr-abl oncoprotein (P210 or P185), the product of the fused bcr-abl gene produced by the Ph, is…
Bcr-Abl expression levels determine the rate of development of resistance to imatinib mesylate in chronic myeloid leukemia.
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It is shown that cells expressing high amounts of Bcr-Abl are much less sensitive to imatinib and, more significantly, take a substantially shorter time for yielding a mutant subclone resistant to the inhibitor than cells with low expression levels, as in chronic phase.
Successful Preservation of Native BCR::ABL1 in Chronic Myeloid Leukemia Primary Leukocytes Reveals a Reduced Kinase Activity
TLDR
In vitro findings provide the first direct measure of BCR ::ABL1 kinase activity in primary CP-CML and reveal the presence of a still uncharacterized inhibitory mechanism that maintains BCR::ABL 1 in a low activity state in CP- CML despite its overexpression.
Myeloid Leukemia Development of Resistance to Imatinib Mesylate in Chronic Bcr-Abl Expression Levels Determine the Rate of Updated
TLDR
It is shown that cells expressing high amounts of Bcr-Abl are much less sensitive to imatinib and, more significantly, take a substantially shorter time for yielding a mutant subclone resistant to the inhibitor than cells with low expression levels, as in chronic phase.
Bcr‐abl protein detection in peripheral blood mononuclear cells for follow‐up of chronic myelogenous leukaemia patients
TLDR
Monitoring of CML patients by quantification of the bcr‐abl protein is a feasible and sensitive alternative to chromosomal analysis of bone marrow.
Inhibition of Rac GTPases in the Therapy of Chronic Myelogenous Leukemia
TLDR
It is shown that CML stem cells are the least vulnerable to ABL-targeted therapy and may serve as reservoirs for occult CML progression; and the relatively low impact of imatinib therapy on the outcome of BP CML patients.
Molecular biology of bcr-abl1-positive chronic myeloid leukemia.
TLDR
Primordial aspects of the pathogenesis of CML, such as the mechanisms responsible for the transition from chronic phase to blast crisis, the causes of genomic instability and faulty DNA repair, the phenomenon of stem cell quiescence, the role of tumor suppressors in TKI resistance and CML progression, still remain poorly understood are synthesized.
Selective Expression and Constitutive Phosphorylation of SHC Proteins in the CD34 1 Fraction of Chronic Myelogenous Leukemias 1
TLDR
Investi-gated the expression and phosphorylation of Src-homology-2 and col-lagen-Homology domains (Shc) proteins in subpopulations of CML primary cells to investigate the role of Shc in normal hemopoiesis and CML leukemogenesis.
Identification of CRKL as the constitutively phosphorylated 39-kD tyrosine phosphoprotein in chronic myelogenous leukemia cells.
TLDR
The results suggest that pp39 CRKL in CML neutrophils may be stably tyrosine-phosphorylated by the BCR/ABL kinase at an early stage of myeloid differentiation when the ABL kinase is active.
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References

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TLDR
Different morphological types of leukocytes directly obtained from patients at the blast crisis stage of CML for expression of P210bcr-abl tyrosine protein kinase activity are examined and a novel Mr 53,000 protein was found to undergo phosphorylation at serine and tyosine in immune complex kinase assays of two blast crisis CML cell lines and in samples from blast crisis patients in which P210 bcr-rab was detected.
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TLDR
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TLDR
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  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
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TLDR
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