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Bolouri, Hamid; Ries, Rhonda E; Wiedeman, Alice E; Hylkema, Tiffany; Scheiding, Sheila; Gersuk, Vivian H; O'Brien, Kimberly; Nguyen, Quynh-Anh; Smith, Jenny L; Alice Long, S; Meshinchi, Soheil
Nature communications, 11/2022, Letnik: 13, Številka: 1Journal Article
High levels of the inflammatory cytokine IL-6 in the bone marrow are associated with poor outcomes in pediatric acute myeloid leukemia (pAML), but its etiology remains unknown. Using RNA-seq data from pre-treatment bone marrows of 1489 children with pAML, we show that > 20% of patients have concurrent IL-6, IL-1, IFNα/β, and TNFα signaling activity and poorer outcomes. Targeted sequencing of pre-treatment bone marrow samples from affected patients (n = 181) revealed 5 highly recurrent patterns of somatic mutation. Using differential expression analyses of the most common genomic subtypes (~60% of total), we identify high expression of multiple potential drivers of inflammation-related treatment resistance. Regardless of genomic subtype, we show that JAK1/2 inhibition reduces receptor-mediated inflammatory signaling by leukemic cells in-vitro. The large number of high-risk pAML genomic subtypes presents an obstacle to the development of mutation-specific therapies. Our findings suggest that therapies targeting inflammatory signaling may be effective across multiple genomic subtypes of pAML.
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Vir: Osebne bibliografije
in: SICRIS
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