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Acute myeloid leukemia

Distinct and overlapping mechanisms of resistance to azacytidine and guadecitabine in acute myeloid leukemia

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Fig. 1: Identification of AZA and GDAC resistance mechanisms in THP1 cells using a genome-wide CRISPR screen.
Fig. 2: Loss of SLC29A1, DCK and UCK2 mediate distinct resistance patterns to AZA, GDAC, and cytarabine.


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This work was supported by a grant in aid from the Cancer Council of Victoria to JS and LMK. LMK was supported by a fellowship from the Victorian Cancer Agency, JS was supported by a fellowship from the Australian Medical Research Future Fund, RWJ was supported by a fellowship from the National Health and Medical Research Council of Australia and EG was supported by the Australian Postgraduate Award.

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Correspondence to Lev M. Kats.

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The laboratory of JS has received research funding from Astex Pharmaceuticals. JS, LMK and RWJ served on the scientific advisory board of Celgene Corp.

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Gruber, E., Franich, R.L., Shortt, J. et al. Distinct and overlapping mechanisms of resistance to azacytidine and guadecitabine in acute myeloid leukemia. Leukemia 34, 3388–3392 (2020).

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