What question did this study set out to answer?

Determine whether the BCR/ABL oncogene stimulates reactive oxygen species production in hematopoietic cells and evaluate how this oxidative stress impacts downstream phosphatase activity and signaling.

August 1, 2000Journal of Biological ChemistryOpen Access

The BCR/ABL Tyrosine Kinase Induces Production of Reactive Oxygen Species in Hematopoietic Cells

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Authors

MSMartin SattlerCity Of Hope National Medical Center SVShalini VermaAcharya Narendra Deva University of Agriculture and Technology GSGautam ShrikhandeNorthwell Health

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Implication

In vitro study reveals BCR-ABL elevates reactive oxygen species to inhibit phosphatases in hematopoietic cells, suggesting antioxidant therapies could counteract leukemia transformation.

Key Points

Determine whether the BCR/ABL oncogene stimulates reactive oxygen species production in hematopoietic cells and evaluate how this oxidative stress impacts downstream phosphatase activity and signaling.
Transformed hematopoietic cell lines (Ba/F3, 32Dcl3, and MO7e) with BCR/ABL and tested kinase dependence using the selective inhibitor STI571.
Treated untransformed cells with exogenous hydrogen peroxide or the phosphatase inhibitor pervanadate to model constitutive oxidative stress.
Administered reducing agents (pyrrolidine dithiocarbamate or N-acetylcysteine) to BCR/ABL-expressing MO7/p210 cells to assess changes in reactive oxygen species and tyrosine phosphorylation.
BCR/ABL transformation increased intracellular reactive oxygen species compared with quiescent, untransformed cells, an effect entirely reversed by STI571 kinase inhibition.
Hydrogen peroxide exposure markedly suppressed total cellular protein-tyrosine phosphatase activity to levels comparable with pervanadate and elevated tyrosine phosphorylation of BCR/ABL substrates, including c-ABL, c-CBL, SHC, and SHP-2.
Antioxidant treatment with reducing agents decreased reactive oxygen species accumulation and reduced substrate tyrosine phosphorylation in BCR/ABL-positive cells.

Cite This Study

Sattler et al. (2000) studied this question.

synapsesocial.com/papers/6a898b650e4958e0bcf7c8ad https://doi.org/10.1074/jbc.m002094200

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Implication

In vitro study reveals BCR-ABL elevates reactive oxygen species to inhibit phosphatases in hematopoietic cells, suggesting antioxidant therapies could counteract leukemia transformation.

The BCR/ABL Tyrosine Kinase Induces Production of Reactive Oxygen Species in Hematopoietic Cells

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Implication

Key Points

Cite This Study

The BCR/ABL Tyrosine Kinase Induces Production of Reactive Oxygen Species in Hematopoietic Cells

Discussion

Member takes

Implication

Key Points

Cite This Study

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