Author

V. Zaberezhnyy

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 3

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 3 Research Focus:cell signaling & trafficking· 3 Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell type annotation· 2 Research Focus:drug response / drug discovery· 2 Organism:human· 2 Organism:mouse· 2

Frequent Co-Authors

J. DeGregori· 3 shared A. Goodspeed· 2 shared H. J. Park· 2 shared M. A. Gregory· 2 shared A. D Alessandro· 1 shared C. T. Jordan· 1 shared D. G. Tenen· 1 shared E. M. Pietras· 1 shared

Activity by Year

2018-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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3 shared papersCancer Biology

J. DeGregori

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3 papers

Recent·Most cited

Therapeutic resistance in acute myeloid leukemia cells is mediated by a novel ATM/mTOR pathway regulating oxidative phosphorylation

H. J. Park, M. A. Gregory, V. Zaberezhnyy, A. Goodspeed, C. T. Jordan, J. S. Kieft, J. DeGregori

The paper shows that marrow-mediated activation of ATM and mTOR increases oxidative phosphorylation, leading to resistance in FLT3 mutant AML cells, and that combining mTOR and FLT3 inhibitors reduces tumor burden.

bioRxiv · Feb 14, 2022Cancer Biology

Chronic Interleukin-1 exposure triggers selective expansion of Cebpa-deficient multipotent hematopoietic progenitors

K. C. Higa, A. Goodspeed, J. S. Chavez, V. Zaberezhnyy, J. L. Rabe, D. G. Tenen, E. M. Pietras, J. DeGregori

This study shows chronic IL-1β exposure selects for Cebpa-deficient HSPC by promoting myeloid differentiation and repressing stem cell programs, linking chronic inflammation to hematologic disorders.

bioRxiv · Mar 25, 2020Cancer Biology

Targeting glutamine metabolism and redox state for leukemia therapy

M. A. Gregory, T. Nemkov, V. Zaberezhnyy, H. J. Park, S. Gehrke, K. C. Hansen, A. D Alessandro, J. DeGregori

This study shows that inhibiting glutaminase with CB-839 reduces glutathione and increases mitochondrial ROS in AML, leading to apoptosis, and that combining it with pro-oxidant drugs enhances cell death in AML and ALL.

bioRxiv · Apr 18, 2018Cancer Biology