ReviewFrontiers in immunology2025
Innate immune-inflammatory signaling milieu in myeloid leukemia and aging-associated clonal hematopoiesis pathologies.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Clonal Hematopoiesis in Colorectal Cancer: Mechanisms and Implications.Cancer medicine · 2026Review
- Covalent Organic Framework Bispecific Nanosystem for the Combined Treatment of Acute Myeloid Leukemia.Materials (Basel, Switzerland) · 2026Article
- Inflammatory signatures in the spectrum of myeloid diseases.HemaSphere · 2026Article
- Evolving Management Approaches Toward Personalized Therapy in Acute Myeloid Leukemia: A Narrative Review.Journal of personalized medicine · 2026Review
- Leukemic Transdifferentiation: From Pathological Plasticity to Dendritic Cell-Based Immunotherapy.Biomedicines · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related accumulation of somatic mutations in hematopoietic stem and progenitor cells (HSPCs), causing clonal hematopoiesis (CH), often precedes the development of hematologic malignancies. Chronic inflammation and aberrant cytokine expression that are common in aging, contribute to clonal expansion and genomic instability. Acute myeloid leukemia (AML) is an (epi)genetically and physiologically diverse malignancy, characterized by clonal proliferation and incomplete differentiation of HSPCs. The innate immune system, with pattern recognition receptors (PRRs), plays a pivotal role in maintaining hematopoietic homeostasis. Dysregulated signaling through PRRs disrupts hematopoiesis, fostering malignant cell proliferation. In addition, cytokines and interferons exert multifaceted effects on HSPCs, impacting their proliferation, differentiation, and survival. Therapeutic approaches targeting innate immune pathways, offer promising avenues for treating hematologic malignancies. Understanding the intricate crosstalk between innate immunity and hematopoiesis would provide insights into novel therapeutic strategies for combating hematologic malignancies, offering hope for improved patient outcomes and survival. In this review, we discuss about the malfunctioning innate immune-inflammatory axes in the context of abnormal hematopoiesis and the therapeutic approaches that are utilizing/targeting these pathways with efficacy. This review delves into the derangements of innate immune and inflammatory pathways implicated in the development of AML and myelodysplastic syndromes (MDS), shedding light on the therapeutic strategies targeting these pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.