Article in Nature cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
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.
2 · The registry
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.
Inés Fernández MaestreMemorial Sloan Kettering Cancer Center, Louis V. Gerstner Jr Graduate School of Biomedical Sciences, New York, NY, USA.
Sheng F CaiHuman Oncology and Pathogenesis Program, Center for Hematologic Malignancies and Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-2708-887X
Ross L LevineHuman Oncology and Pathogenesis Program, Center for Hematologic Malignancies and Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-7884-1905
X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI Paul Robson · 1985 to 2026
$61.9M
Developing Effective Approaches to Extend Hematopoietic Healthspan by Targeting Cell-Extrinsic and Cell-Intrinsic Alterations at Middle AgeR01DK118072 · NIDDK · JACKSON LABORATORY · PI Jennifer Jean Trowbridge · 2018 to 2026
$4.2M
Inflammatory Signaling in DNMT3A-Mutated Human Hematopoietic Stem CellsU01AG077925 · NIA · JACKSON LABORATORY · PI LEVINE, ROSS L, TROWBRIDGE, JENNIFER JEAN · 2021 to 2025
$2.9M
Discovery of Aging-Associated Mechanisms Causing Expansion and Progression of Clonal Hematopoiesis of Indeterminant Potential (CHIP)R01AG069010 · NIA · JACKSON LABORATORY · PI TROWBRIDGE, JENNIFER JEAN · 2020 to 2024
$2.4M
Identifying Inflammatory Mediators of Clonal HematopoiesisF99CA284253 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI FERNANDEZ MAESTRE, INES · 2023 to 2024
$75k
Canada Research Chairs (Chaires de recherche du Canada) Tier II CRCEC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) 953407Edward P. Evans Foundation EvansMDS DRGGouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada) PJT-203948, PJT-180406Jackson Laboratory (JAX) Scholar AwardLeukemia and Lymphoma Society (Leukemia & Lymphoma Society) CDP Fellow AwardLeukemia and Lymphoma Society (Leukemia & Lymphoma Society) Scholar AwardNCI NIH HHS F99 CA284253NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA034196NIA NIH HHS R01 AG069010NIA NIH HHS U01 AG077925NIDDK NIH HHS R01 DK118072U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) F99CA284253U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) P30CA008748U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) P30CA034196U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) R01DK118072U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) R01AG069010, U01AG077925
6 · The paper itself
Abstract
Microenvironment remodelling impacts tumour growth and metastasis, but whether remodelling promotes pre-malignant clonal fitness remains unknown. Here, using single-cell RNA-sequencing of the bone-marrow microenvironment in a mouse model of DNMT3A-mutant clonal haematopoiesis (CH), we identify mesenchymal stromal cells (MSCs) in a molecular state of cellular senescence. Elevated bone-marrow MSC senescence is also observed in humans with CH driven by several common somatic mutations. MSC senescence is induced by mutant haematopoietic cells in a contact-independent manner through production of soluble factors including TNF-α and IL-6. These cytokines activate a Stat3-driven pathway that is necessary and sufficient for MSC senescence induction. Genetic or pharmacological depletion of senescent non-haematopoietic cells reduces the burden of CH and delays progression to myeloid neoplasia. Our findings show that microenvironment remodelling modifies pre-malignant clonal fitness and identifies disruption of the crosstalk between pre-malignant cells and their niche as a cancer prevention strategy.
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.
Stromal cell senescence augments haematopoietic cell fitness in clonal haematopoiesis. · full record | OpenQuestion