ArticlePloS one2012
Contribution of an aged microenvironment to aging-associated myeloproliferative disease.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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.
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Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- Molecular and phenotypic blueprint of human hematopoiesis links proliferation stress to stem cell aging.The Journal of experimental medicine · 2026Article
- Cardiac cell senescence: molecular mechanisms, key proteins and therapeutic targets.Cell death discovery · 2024Review
- Effects of Systemic Peroxisome Proliferator-Activated Receptor Gamma Inhibition on Bone and Immune Cells in Aged Female Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- The sculpting of somatic mutational landscapes by evolutionary forces and their impacts on aging-related disease.Molecular oncology · 2022Review
- In Vitro and In Vivo Modeling of Normal and Leukemic Bone Marrow Niches: Cellular Senescence Contribution to Leukemia Induction and Progression.International journal of molecular sciences · 2022Review
- Article
- Senescent bone marrow microenvironment promotes Nras-mutant leukemia.Journal of molecular cell biology · 2021Article
- The three dimensions of somatic evolution: Integrating the role of genetic damage, life-history traits, and aging in carcinogenesis.Evolutionary applications · 2020Article
- Endothelial mTOR maintains hematopoiesis during aging.The Journal of experimental medicine · 2020Article
- Context-dependent selection as the keystone in the somatic evolution of cancer.Scientific reports · 2020Article
- Time-restricted feeding delays the emergence of the age-associated, neoplastic-prone tissue landscape.Aging · 2019Article
- Decoy fitness peaks, tumor suppression, and aging.Aging cell · 2019Article
- Article
- Mixing old and young: enhancing rejuvenation and accelerating aging.The Journal of clinical investigation · 2019Review
- Review
- Signaling Pathways Regulating Hematopoietic Stem Cell and Progenitor Aging.Current stem cell reports · 2018Article
- Heterodimerization of AML1/ETO with CBFβ is required for leukemogenesis but not for myeloproliferation.Leukemia · 2017Article
- Endothelial transplantation rejuvenates aged hematopoietic stem cell function.The Journal of clinical investigation · 2017Article
- Angelica sinensis Polysaccharides Ameliorate Stress-Induced Premature Senescence of Hematopoietic Cell via Protecting Bone Marrow Stromal Cells from Oxidative Injuries Caused by 5-Fluorouracil.International journal of molecular sciences · 2017Article
- The aging hematopoietic stem cell niche: Phenotypic and functional changes and mechanisms that contribute to hematopoietic aging.Seminars in hematology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
The molecular and cellular mechanisms of the age-associated increase in the incidence of acute myeloid leukemia (AML) remain poorly understood. Multiple studies support that the bone marrow (BM) microenvironment has an important influence on leukemia progression. Given that the BM niche itself undergoes extensive functional changes during lifetime, we hypothesized that one mechanism for the age-associated increase in leukemia incidence might be that an aged niche promotes leukemia progression. The most frequent genetic alteration in AML is the t(8;21) translocation, resulting in the expression of the AML1-ETO fusion protein. Expression of the fusion protein in hematopoietic cells results in mice in a myeloproliferative disorder. Testing the role of the age of the niche on leukemia progression, we performed both transplantation and in vitro co-culture experiments. Aged animals transplanted with AML1-ETO positive HSCs presented with a significant increase in the frequency of AML-ETO positive early progenitor cells in BM as well as an increased immature myeloid cell load in blood compared to young recipients. These findings suggest that an aged BM microenvironment allows a relative better expansion of pre-leukemic stem and immature myeloid cells and thus imply that the aged microenvironment plays a role in the elevated incidence of age-associated leukemia.
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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.