ArticleJCI insight2019
Angiocrine signals regulate quiescence and therapy resistance in bone metastasis.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.
- Consequences of Aging on Bone.Aging and disease · 2023Pooled it
- Insights into the mechanism of vascular endothelial cells on bone biology.Bioscience reports · 2021Pooled it
- Osteocyte-vascular Interactions in Bone Physiology and Pathology.Current osteoporosis reports · 2026Review
- Breaking the immune "cold niche" in bone metastasis: core mechanisms of the multidimensional interwoven regulatory network and precision breakthrough strategies.Molecular cancer · 2026Review
- Removal of aging microenvironment of bone defects can effectively promote bone defect repair.Journal of translational medicine · 2026Article
- Tumour endothelial cell reprogramming orchestrates angiocrine signalling to drive chemoresistance in breast cancer.Angiogenesis · 2026Article
- From complexity to clarity: aging bone marrow niche in bone and blood regeneration and malignancy.Bone research · 2026Review
- Crosstalk between bone and vasculature within bone.Fundamental research · 2026Review
- Enhancing Cancer Therapy with Hyperthermia: Synergistic Effects with Natural Compounds and Conventional Treatments.International journal of molecular sciences · 2026Review
- Remodeling the tumor dormancy ecosystem to prevent recurrence and metastasis.Signal transduction and targeted therapy · 2026Review
- Rapid 3D Immunolabeling and Light Sheet Microscopy for Quantitative Analysis of Intact Tissues.Computational and structural biotechnology journal · 2026Article
- Review
- Lung endothelial PEAR1 induces tumor cell dormancy.Molecular cancer · 2025Article
- Degeneration and Impaired Resilience of Skull Bone and Hematopoietic Bone Marrow.bioRxiv : the preprint server for biology · 2025Article
- Review
- Cancer-on-a-chip for precision cancer medicine.Lab on a chip · 2025Review
- Towards understanding cancer dormancy over strategic hitching up mechanisms to technologies.Molecular cancer · 2025Review
- Bone marrow adipocytes: key players in vascular niches, aging, and disease.Frontiers in cell and developmental biology · 2025Review
- Prognostic and Immunological Implications of Telomere Maintenance-Related Genes in Breast Cancer: A Mechanistic Exploration.Breast cancer (Dove Medical Press) · 2025Article
- Nanocarriers based therapy and diagnosis of brain diseases: cross the blood-brain barrier.Science and technology of advanced materials · 2025Review
4 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
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Bone provides supportive microenvironments for hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs) and is a frequent site of metastasis. While incidences of bone metastases increase with age, the properties of the bone marrow microenvironment that regulate dormancy and reactivation of disseminated tumor cells (DTCs) remain poorly understood. Here, we elucidate the age-associated changes in the bone secretome that trigger proliferation of HSCs, MSCs, and DTCs in the aging bone marrow microenvironment. Remarkably, a bone-specific mechanism involving expansion of pericytes and induction of quiescence-promoting secretome rendered this proliferative microenvironment resistant to radiation and chemotherapy. This bone-specific expansion of pericytes was triggered by an increase in PDGF signaling via remodeling of specialized type H blood vessels in response to therapy. The decline in bone marrow pericytes upon aging provides an explanation for loss of quiescence and expansion of cancer cells in the aged bone marrow microenvironment. Manipulation of blood flow - specifically, reduced blood flow - inhibited pericyte expansion, regulated endothelial PDGF-B expression, and rendered bone metastatic cancer cells susceptible to radiation and chemotherapy. Thus, our study provides a framework to recognize bone marrow vascular niches in age-associated increases in metastasis and to target angiocrine signals in therapeutic strategies to manage bone metastasis.
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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.