Author

A. H. Wei

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· 2

Signature Assays, Organisms & Methods

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Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:drug response / drug discovery· 1 Organism:mouse· 1

Frequent Co-Authors

A. K. Enjeti· 1 shared A. M. Douglas· 1 shared A. Mannan· 1 shared A. Newbold· 1 shared B. Nixon· 1 shared C. de Bock· 1 shared C. Shembrey· 1 shared D. A. Skerrett-Byrne· 1 shared

Activity by Year

2021-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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1 shared paperCancer Biology

A. K. Enjeti

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Blockade of redox second messengers inhibits JAK/STAT and MEK/ERK signaling sensitizing FLT3-mutant acute myeloid leukemia to targeted therapies

Z. P. Germon, J. R. Sillar, A. Mannan, R. J. Duchatel, D. Staudt, H. C. Murray, I. J. Findlay, E. R. Jackson, H. P. McEwen, A. M. Douglas, T. Mclachlan, J. E. Schjenken, D. A. Skerrett-Byrne, H. Huang, M. N. Melo-Braga, , M. D. Dun

This study identifies the Rac-NOX2 complex as a driver of redox signaling in FLT3-mutant AML, showing that inhibiting NOX2 reduces key signaling pathways and enhances response to FLT3 inhibitors.

bioRxiv · Mar 9, 2022 · PreprintCancer Biology

Reprogramming of serine metabolism is an actionable vulnerability in FLT3-ITD driven acute myeloid leukaemia

S. Bjelosevic, E. Gruber, A. Newbold, L. M. Kats, C. Shembrey, T. C. Abrehart, I. Todorovski, G. Pomilio, A. H. Wei, G. P. Gregory, S. J. Vervoort, K. K. Brown, R. W. Johnstone

This study identifies serine metabolism as a vulnerability in FLT3-ITD AML, showing that targeting serine synthesis enhances chemotherapy efficacy.

Cancer Discovery · Jan 12, 2021Peer-reviewedCancer Biology