ArticleNature communications2022
Inflammatory bone marrow signaling in pediatric acute myeloid leukemia distinguishes patients with poor outcomes.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- Inflammation as a central driver in AML pathogenesis and therapy resistance.Science China. Life sciences · 2026Review
- Exploring the Role of Macrophage Marker CD68 in Pediatric Acute Myeloid Leukemia.International journal of molecular sciences · 2026Article
- Regulatory role of mTORC1 signaling in osteoblasts in acute myeloid leukemia progression and steady-state hematopoiesis.iScience · 2026Article
- Development of an interpretable machine learning model to predict complete remission and first adverse event in pediatric acute myeloid leukemia using routine clinical data.Frontiers in oncology · 2026Article
- Constitutive systemic inflammation in Shwachman-Diamond Syndrome.Molecular medicine (Cambridge, Mass.) · 2025Article
- Leukemic Cells Infiltrate the Ovaries Without Damaging Ovarian Reserve in an Acute Myeloid Leukemia Mouse Model.Endocrinology · 2025Article
- Relationship Between anJournal of clinical medicine · 2025Article
- Interleukin-6 as the preferred prognostic factor in infection-complicated acute myeloid leukemia.Contemporary oncology (Poznan, Poland) · 2025Article
- Alternative splicing and genetic variation of mhc-e: implications for rhesus cytomegalovirus-based vaccines.Communications biology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.