ArticleBlood2019
Acute myeloid leukemia induces protumoral p16INK4a-driven senescence in the bone marrow microenvironment.
Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 102 citations in OpenAlex.
- Stromal cell senescence augments haematopoietic cell fitness in clonal haematopoiesis.Nature cell biology · 2026Article
- Bone marrow mesenchymal stem cells are functionally remodeled after complete remission of acute myeloid leukemia.Journal of translational internal medicine · 2026Article
- Prognostic significance of therapy-induced senescence and SASP dynamics in acute myeloid leukemia: a retrospective cohort study.BMC cancer · 2026Article
- Exploiting cellular senescence in hematologic malignancies.Translational oncology · 2026Review
- Accelerated senescence of bone marrow erythrocyte precursors in myelodysplastic syndrome.Annals of medicine · 2025Article
- The mitochondria as an emerging target of self-renewal in T-cell acute lymphoblastic leukemia.Cancer biology & therapy · 2025Review
- Cell cycle regulator MYBL2 is a distinct vulnerability in acute myeloid leukemia.Cell death discovery · 2025Article
- ISENICS: a model for identifying senescent immune cells and samples and characterization of their roles in tumor microenvironment.Briefings in bioinformatics · 2025Article
- Review
- Age-related mesenchymal stromal cell senescence is associated with progression from MGUS to multiple myeloma.Leukemia · 2025Article
- Leukemia cells remodel bone marrow stromal cells to generate a protumoral microenvironment via the S100A8-NOX2-ROS signaling pathway.Scientific reports · 2025Article
- SenNet recommendations for detecting senescent cells in different tissues.Nature reviews. Molecular cell biology · 2024Review
- A View of Myeloid Transformation through the Hallmarks of Cancer.Blood cancer discovery · 2024Review
- Construction and validation of a SASP-related prognostic signature in patients with acute myeloid leukaemia.Journal of cellular and molecular medicine · 2024Article
- HIF-1α is an important regulator of IL-8 expression in human bone marrow stromal cells under hypoxic microenvironment.Protoplasma · 2024Article
- Acute myeloid leukemia-driven IL-3-dependent upregulation of BCL2 in non-malignant hematopoietic stem and progenitor cells increases venetoclax-induced cytopenias.Haematologica · 2024Article
- Transforming the Niche: The Emerging Role of Extracellular Vesicles in Acute Myeloid Leukaemia Progression.International journal of molecular sciences · 2024Review
- Article
- RAB27B-regulated exosomes mediate LSC maintenance via resistance to senescence and crosstalk with the microenvironment.Leukemia · 2024Article
- Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is an age-related disease that is highly dependent on the bone marrow (BM) microenvironment. With increasing age, tissues accumulate senescent cells, characterized by an irreversible arrest of cell proliferation and the secretion of a set of proinflammatory cytokines, chemokines, and growth factors, collectively known as the senescence-associated secretory phenotype (SASP). Here, we report that AML blasts induce a senescent phenotype in the stromal cells within the BM microenvironment and that the BM stromal cell senescence is driven by p16INK4a expression. The p16INK4a-expressing senescent stromal cells then feed back to promote AML blast survival and proliferation via the SASP. Importantly, selective elimination of p16INK4a
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.