ArticlePloS one2021
A B-cell developmental gene regulatory network is activated in infant AML.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- DNA Methylation of Pharmacologic and Leukemia-Related Genes Predicts Clinical Outcomes in Pediatric Acute Myeloid Leukemia.Cancers · 2026Article
- Statistical Inference of Phenotype-Specific Molecular Mechanisms from Cell Line-Specific Gene Regulatory Networks with Application to Quizartinib Sensitivity.International journal of molecular sciences · 2026Article
- Age-specific mutation profiles and their prognostic implications in pediatricHaematologica · 2026Article
- Integrating transcriptomic profiling and machine learning: A clinically actionable prognostic model for infant acute myeloid leukemia.HemaSphere · 2025Article
- Epigenomic diagnosis and prognosis of Acute Myeloid Leukemia.Nature communications · 2025Article
- Indoleamine 2,3-dioxygenase 1 alters the proportions of B cell subpopulations in the microenvironment of acute myeloid leukemia.Molecular biomedicine · 2025Article
- The E3 ubiquitin ligase Herc1 modulates the response to nucleoside analogs in acute myeloid leukemia.Blood advances · 2024Article
- Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024Review
- Differential co-expression network analysis elucidated genes associated with sensitivity to farnesyltransferase inhibitor and prognosis of acute myeloid leukemia.Cancer medicine · 2023Article
- Inflammatory bone marrow signaling in pediatric acute myeloid leukemia distinguishes patients with poor outcomes.Nature communications · 2022Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Infant Acute Myeloid Leukemia (AML) is a poorly-addressed, heterogeneous malignancy distinguished by surprisingly few mutations per patient but accompanied by myriad age-specific translocations. These characteristics make treatment of infant AML challenging. While infant AML is a relatively rare disease, it has enormous impact on families, and in terms of life-years-lost and life limiting morbidities. To better understand the mechanisms that drive infant AML, we performed integrative analyses of genome-wide mRNA, miRNA, and DNA-methylation data in diagnosis-stage patient samples. Here, we report the activation of an onco-fetal B-cell developmental gene regulatory network in infant AML. AML in infants is genomically distinct from AML in older children/adults in that it has more structural genomic aberrations and fewer mutations. Differential expression analysis of ~1500 pediatric AML samples revealed a large number of infant-specific genes, many of which are associated with B cell development and function. 18 of these genes form a well-studied B-cell gene regulatory network that includes the epigenetic regulators BRD4 and POU2AF1, and their onco-fetal targets LIN28B and IGF2BP3. All four genes are hypo-methylated in infant AML. Moreover, micro-RNA Let7a-2 is expressed in a mutually exclusive manner with its target and regulator LIN28B. These findings suggest infant AML may respond to bromodomain inhibitors and immune therapies targeting CD19, CD20, CD22, and CD79A.
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