ArticleThe Journal of clinical investigation2015
Aging-associated inflammation promotes selection for adaptive oncogenic events in B cell progenitors.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 154 citations in OpenAlex.
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- The complex role of IL-37 in cancer pathogenesis: exploring its influence on hallmarks of cancer.Frontiers in immunology · 2026Review
- Immunosenescence and organoids: pathophysiology and therapeutic opportunities.Immunity & ageing : I & A · 2025Review
- Modelling the ageing dependence of cancer evolutionary trajectories.Nature reviews. Cancer · 2025Review
- Endoplasmic Reticulum Stress-Induced triggering Receptor Expressed on Myeloid Cells 2 (TREM2) Downregulation Exacerbates Platelet Activation and Myocardial Infarction in Patients With Coronary Artery Disease.Journal of the American Heart Association · 2025Article
- Periarteriolar niches become inflamed in aging bone marrow, remodeling the stromal microenvironment and depleting lymphoid progenitors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Inflammation Promotes Aging-Associated Oncogenesis in the Lung.Aging and cancer · 2025Article
- The Role of Senescence, its Therapeutic Relevance and Clinical Implications in the Tumor Microenvironment.Theranostics · 2025Review
- A distinct metabolic and epigenetic state drives trained immunity in HSC-derived macrophages from autoimmune mice.Cell stem cell · 2024Article
- The evolutionary theory of cancer: challenges and potential solutions.Nature reviews. Cancer · 2024Review
- The impact of the senescent microenvironment on tumorigenesis: Insights for cancer therapy.Aging cell · 2024Review
- The nuclear cytokine IL-37a controls lethal cytokine storms primarily via IL-1R8-independent transcriptional upregulation of PPARγ.Cellular & molecular immunology · 2023Article
- ETV6 represses inflammatory response genes and regulates HSPC function during stress hematopoiesis in mice.Blood advances · 2023Article
- Foxm1 haploinsufficiency drives clonal hematopoiesis and promotes a stress-related transition to hematologic malignancy in mice.The Journal of clinical investigation · 2023Article
- The regulation roles of miRNAs in Helicobacter pylori infection.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Panhematopoietic RNA barcoding enables kinetic measurements of nucleate and anucleate lineages and the activation of myeloid clones following acute platelet depletion.Genome biology · 2023Article
- The 'omics of obesity in B-cell acute lymphoblastic leukemia.Journal of the National Cancer Institute. Monographs · 2023Article
- Reversal of aging-associated increase in myelopoiesis and expression of alarmins by angiotensin-(1-7).Scientific reports · 2023Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
The incidence of cancer is higher in the elderly; however, many of the underlying mechanisms for this association remain unexplored. Here, we have shown that B cell progenitors in old mice exhibit marked signaling, gene expression, and metabolic defects. Moreover, B cell progenitors that developed from hematopoietic stem cells (HSCs) transferred from young mice into aged animals exhibited similar fitness defects. We further demonstrated that ectopic expression of the oncogenes BCR-ABL, NRAS(V12), or Myc restored B cell progenitor fitness, leading to selection for oncogenically initiated cells and leukemogenesis specifically in the context of an aged hematopoietic system. Aging was associated with increased inflammation in the BM microenvironment, and induction of inflammation in young mice phenocopied aging-associated B lymphopoiesis. Conversely, a reduction of inflammation in aged mice via transgenic expression of α-1-antitrypsin or IL-37 preserved the function of B cell progenitors and prevented NRAS(V12)-mediated oncogenesis. We conclude that chronic inflammatory microenvironments in old age lead to reductions in the fitness of B cell progenitor populations. This reduced progenitor pool fitness engenders selection for cells harboring oncogenic mutations, in part due to their ability to correct aging-associated functional defects. Thus, modulation of inflammation--a common feature of aging--has the potential to limit aging-associated oncogenesis.
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