ArticleBlood advances2022
Transcriptomic analysis reveals proinflammatory signatures associated with acute myeloid leukemia progression.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- Epigenetics and In Silico Transcriptome Analysis of Pediatric Acute Myeloid Leukemia.European journal of haematology · 2026Review
- Hierarchical lineage tracing reveals diverse pathways of cytarabine resistance.Nature communications · 2026Article
- Discovery of BEND4 as a novel single-gene prognostic marker and therapeutic target for adverse AML.NPJ precision oncology · 2026Article
- The novel ETV6::RARA fusion gene, identified in acute promyelocytic leukemia, is sensitive to invitro all-tans retinoic acid and arsenic trioxide administrations.Annals of hematology · 2026Article
- Targeting IL-1/IRAK1/4 signaling in acute myeloid leukemia stem cells following treatment and relapse.Leukemia · 2026Article
- Isocitrate dehydrogenase 1 mutations drive downregulation of IL1R1 and dysregulated inflammatory response in acute myeloid leukemia.Blood cancer journal · 2026Article
- Immune monitoring for relapse of acute myeloid leukemia after allogeneic stem cell transplantation in clinical laboratories.Frontiers in immunology · 2026Review
- High IL1R1 expression predicts poor survival and benefit from stem cell transplant in intermediate-risk acute myeloid leukemia from the Leucegene cohort.Biomarker research · 2025Article
- Characteristics and prognosis of paediatric normal karyotype acute myeloid leukaemia: A NOPHO-DBH AML study.British journal of haematology · 2025Article
- Shared genetic association between inflammatory bowel disease and acute myeloid leukemia: insights from mendelian randomization and transcriptomic analyses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Inflammatory signaling pathways play a role in SYK inhibitor resistant AML.Scientific reports · 2025Article
- Hierarchical Lineage Tracing Reveals Diverse Pathways of AML Treatment Resistance.bioRxiv : the preprint server for biology · 2025Article
- Transcriptomic signature can distinguish chronic neutrophilic leukemia from ambiguous neutrophilic leukemias.Frontiers in genetics · 2025Article
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- Transcriptome Analysis in Mexican Adults with Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024Article
- Large-scale genome-wide association studies reveal the genetic causal etiology between ankylosing spondylitis and risk of leukemia and lymphocytic malignancies.Frontiers in oncology · 2024Article
Corrections and comments
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Authors and funding
20 authors at 9 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous studies have been performed over the last decade to exploit the complexity of genomic and transcriptomic lesions driving the initiation of acute myeloid leukemia (AML). These studies have helped improve risk classification and treatment options. Detailed molecular characterization of longitudinal AML samples is sparse, however; meanwhile, relapse and therapy resistance represent the main challenges in AML care. To this end, we performed transcriptome-wide RNA sequencing of longitudinal diagnosis, relapse, and/or primary resistant samples from 47 adult and 23 pediatric AML patients with known mutational background. Gene expression analysis revealed the association of short event-free survival with overexpression of GLI2 and IL1R1, as well as downregulation of ST18. Moreover, CR1 downregulation and DPEP1 upregulation were associated with AML relapse both in adults and children. Finally, machine learning-based and network-based analysis identified overexpressed CD6 and downregulated INSR as highly copredictive genes depicting important relapse-associated characteristics among adult patients with AML. Our findings highlight the importance of a tumor-promoting inflammatory environment in leukemia progression, as indicated by several of the herein identified differentially expressed genes. Together, this knowledge provides the foundation for novel personalized drug targets and has the potential to maximize the benefit of current treatments to improve cure rates in AML.
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