ArticleNature medicine2009
Hematopoietic colony-stimulating factors mediate tumor-nerve interactions and bone cancer pain.
Article in Nature medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 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
117 citing papers in PubMed, 185 citations in OpenAlex.
- Oral and Intestinal Bacterial Substances Associated with Disease Activities in Patients with Rheumatoid Arthritis: A Cross-Sectional Clinical Study.Journal of immunology research · 2022Trial
- Sensory innervation shapes cancer immunotherapy efficacy and adverse events.Journal for immunotherapy of cancer · 2026Review
- Chronic pain in Alzheimer disease and the role of neuroimmune interactions.Pharmacological reviews · 2026Review
- Cancer pain.Nature reviews. Disease primers · 2026Review
- Neural regulation of cancer: from microenvironmental hijacking to systemic circuit co-option.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Transcriptome of the human C2 dorsal root ganglia in C1-2 arthrodesis surgery: insight for neck pain.Brain : a journal of neurology · 2026Article
- Peripheral nerve remodeling in the tumor microenvironment: neuro-immune crosstalk, molecular mechanisms, and precision therapeutic.Frontiers in immunology · 2026Review
- Decoding Pancreatic Cancer Pain: From Tumor-Nerve Crosstalk to Targeted Analgesic Strategies.International journal of medical sciences · 2026Review
- Nociceptor neurons promote PDAC progression and cancer pain by interaction with cancer-associated fibroblasts and suppression of natural killer cells.Cell research · 2025Article
- Nerves, nodes, and neoplasia.Frontiers in immunology · 2025Review
- Cellular senescence in the innervated niche modulates cancer-associated pain: an emerging therapeutic target?Frontiers in immunology · 2025Review
- Neuroscience in peripheral cancers: tumors hijacking nerves and neuroimmune crosstalk.MedComm · 2024Review
- Bone transport induces the release of factors with multi-tissue regenerative potential for diabetic wound healing in rats and patients.Cell reports. Medicine · 2024Article
- Anatomo-physiological basis and applied techniques of electrical neuromodulation in chronic pain.Journal of anesthesia, analgesia and critical care · 2024Review
- From pain to tumor immunity: influence of peripheral sensory neurons in cancer.Frontiers in immunology · 2024Review
- Alleviative Effect ofPlants (Basel, Switzerland) · 2023Article
- Exploring the Novel Dimension of Immune Interactions in Pain: JAK Inhibitors' Pleiotropic Potential.Life (Basel, Switzerland) · 2023Review
- Review
- Activation of β2-Adrenergic Receptors in Microglia Alleviates Neuropathic Hypersensitivity in Mice.Cells · 2023Article
- Hypoxia-Inducible Factor-1: A Novel Therapeutic Target for the Management of Cancer, Drug Resistance, and Cancer-Related Pain.Cancers · 2022Review
57 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
13 authors at 4 institutions in 5 countries.
Funding
Abstract
Pain is one of the most severe and debilitating symptoms associated with several forms of cancer. Various types of carcinomas and sarcomas metastasize to skeletal bones and cause spontaneous bone pain and hyperalgesia, which is accompanied by bone degradation and remodeling of peripheral nerves. Despite recent advances, the molecular mechanisms underlying the development and maintenance of cancer-evoked pain are not well understood. Several types of non-hematopoietic tumors secrete hematopoietic colony-stimulating factors that act on myeloid cells and tumor cells. Here we report that receptors and signaling mediators of granulocyte- and granulocyte-macrophage colony-stimulating factors (G-CSF and GM-CSF) are also functionally expressed on sensory nerves. GM-CSF sensitized nerves to mechanical stimuli in vitro and in vivo, potentiated CGRP release and caused sprouting of sensory nerve endings in the skin. Interruption of G-CSF and GM-CSF signaling in vivo led to reduced tumor growth and nerve remodeling, and abrogated bone cancer pain. The key significance of GM-CSF signaling in sensory neurons was revealed by an attenuation of tumor-evoked pain following a sensory nerve-specific knockdown of GM-CSF receptors. These results show that G-CSF and GM-CSF are important in tumor-nerve interactions and suggest that their receptors on primary afferent nerve fibers constitute potential therapeutic targets in cancer pain.
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.