Associated Papers
Proteomic subtypes enrich current acute myeloid leukemia nomenclature and reflect intrinsic pathogenesis alongside aging.
Cheng WY et al.
Blood, 2025
40829168 (PubMed )
Supplement: BLOOD_BLD-2024-027692-mmc5.xlsx › Sheet_1
Fusion oncoproteins and cooperating mutations define disease phenotypes in NUP98-rearranged leukemia.
Umeda M et al.
Blood, 2025
40700635 (PubMed )
Supplement: BLOOD_BLD-2025-028993-mmc2.xlsx › Supplementary_Table_6
Fusion oncoproteins and cooperating mutations define disease phenotypes in NUP98-rearranged leukemia.
Umeda M et al.
Medrxiv : the Preprint Server for Health Sciences, 2025
39974131 (PubMed )
Supplement: media-2.xlsx › Supplementary_Table_6
Aging and comprehensive molecular profiling in acute myeloid leukemia.
Li JF et al.
Proceedings of the National Academy of Sciences of the United States of America, 2024
38422020 (PubMed )
Supplement: pnas.2319366121.sd02.xlsx › Sheet_1
Transcriptome-based molecular subtypes and differentiation hierarchies improve the classification framework of acute myeloid leukemia.
Cheng WY et al.
Proceedings of the National Academy of Sciences of the United States of America, 2022
36442087 (PubMed )
Supplement: pnas.2211429119.sd02.xlsx › snv_indel
Integrated Genomic Analysis Identifies UBTF Tandem Duplications as a Recurrent Lesion in Pediatric Acute Myeloid Leukemia.
Umeda M et al.
Blood Cancer Discovery, 2022
35176137 (PubMed )
Supplement: bcd-21-0160_supplemental_tables_supp1-32.xlsx › Table_S12_SNV_indel
Genetic and Transcriptional Contributions to Relapse in Normal Karyotype Acute Myeloid Leukemia.
Petti AA et al.
Blood Cancer Discovery, 2022
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