Author

I. Todorovski

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:drug response / drug discovery· 3 Approach:statistical model· 3 Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Organism:human· 2 Organism:mouse· 2 Research Focus:cell type annotation· 1

Frequent Co-Authors

R. W. Johnstone· 3 shared S. J. Vervoort· 3 shared G. Mir Arnau· 2 shared M. Zethoven· 2 shared S. Bjelosevic· 2 shared A. H. Wei· 1 shared A. Newbold· 1 shared A. T. Papenfuss· 1 shared

Activity by Year

2020-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 32 mutual co-author links

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3 shared papersCancer Biology

R. W. Johnstone

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3 papers

Recent·Most cited

RNA decay defines the therapeutic response to transcriptional perturbation in leukaemia

I. Todorovski, B. Feran, Z. Fan, S. Gadipally, D. Yoannidis, I. Y. Kong, S. Bjelosevic, M. Zethoven, E. D. Hawkins, K. J. Simpson, G. Mir Arnau, A. T. Papenfuss, R. W. Johnstone, S. J. Vervoort

The paper shows that mRNA decay rates determine the effectiveness of transcriptional inhibitors in leukemia, with short-lived mRNAs being more responsive and long-lived ones being modulated by RNA-binding proteins.

bioRxiv · Apr 6, 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

Epigenetic reprogramming of plasmacytoid dendritic cells drives type I interferon-dependent differentiation of acute myeloid leukemias for therapeutic benefit

J. Salmon, I. Todorovski, S. J. Vervoort, K. L. Stanley, C. J. Kearney, L. Martelotto, F. Rossello, T. Semple, G. Mir Arnau, M. Zethoven, M. Bots, E. Vidacs, K. McArthur, E. Gressier, N. De Weerd, , R. W. Johnstone

The paper shows that inhibiting HDACs in AML promotes type I IFN production by pDCs, enhancing anti-tumor immunity and therapeutic benefit.

bioRxiv · Aug 23, 2020 · PreprintCancer Biology