Additional file 8 of The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency

Additional file 8 of The small inhibitor WM-1119 effectively targets KAT6A-rearranged AML, but not KMT2A-rearranged AML, despite shared KAT6 genetic dependency

Supplementary Material 8

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Bibliographic Details
Main Author:	Mathew Sheridan (19821431) (author)
Other Authors:	Muhammad Ahmad Maqbool (15079162) (author), Anne Largeot (10860732) (author), Liam Clayfield (19821434) (author), Jingru Xu (5711219) (author), Natalia Moncaut (11267376) (author), Robert Sellers (14949664) (author), Jessica Whittle (19821437) (author), Jerome Paggetti (11183457) (author), Mudassar Iqbal (274750) (author), Romain Aucagne (18222759) (author), Laurent Delva (19821440) (author), Syed Murtuza Baker (9767712) (author), Michael Lie-a-Ling (19821443) (author), Valerie Kouskoff (848348) (author), Georges Lacaud (848349) (author)
Published:	2024
Subjects:	Biophysics Biochemistry Medicine Cell Biology Genetics Molecular Biology Pharmacology Cancer Hematology myeloid differentiation program primary patient amls models allowed us appropriate therapeutic approach aml using cellular epigenetic factors kat6a class kat6a inhibitor small inhibitor wm genetic results indicate critical differentiation pathways 1119 completely abrogated kat6ar aml patients common kmt2ar aml kmt2a rearranged amls rearranged aml kmt2ar amls therapeutic approaches murine models critical regulators conditionally abrogated kmt2a rearranged kat6a plays whole protein transcriptome level targeted degradation study indicates shrna knock recurrently translocated normal hematopoiesis may represent malignant cells limited role leukemia pathways kmt2ar leukemogenicity kat6ar cells fusion protein flow cytometry dramatic increase crispr knock complete deletion cell rna catalytic activity also tested 1119 treatment
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