ReviewNeuroscience bulletin2024
Peripheral Mechanism of Cancer-Induced Bone Pain.
Review in Neuroscience bulletin, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled 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.
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
34 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Risk factors and clinical significance of refractory pain in patients with bone metastases: a comprehensive meta-analysis.Frontiers in neurology · 2025Pooled it
- Bone metastasis and pain research through the dual lens of bibliometrics and bioinformatics: knowledge structure, frontiers, and core pathway analysis (2015-2024).Frontiers in medicine · 2025Pooled it
- Single-cell RNA sequencing analysis of bone cancer pain model induced by Lewis lung cancer cells in male mice.Annals of medicine · 2026Article
- CaNeuroscience bulletin · 2026Article
- Cancer-related pain: A bidirectional modulator of cancer progression.Clinical and translational medicine · 2026Review
- Applications of micro/nano drug delivery systems in cancer pain management.Bioactive materials · 2026Review
- Downregulation of ClC-3 chloride channels in dorsal root ganglia neurons contributes to bone metastasis-induced pain.The Journal of biological chemistry · 2026Article
- Prelimbic cortex-basolateral amygdala glutamatergic circuit drives cancer-induced bone pain in mice.iScience · 2026Article
- Spinal KCC2 Mediates the Modulation Effect of HDAC2 on Bone Cancer Pain in Rats.Current cancer drug targets · 2026Article
- Mechanism of BMSCs Inhibiting Microglia Activation and Neuroinflammatory Response to Alleviate BCP by Regulating TLR4/ NF-κB Signaling Pathway.Journal of inflammation research · 2026Article
- The excitatory neurotransmitter glutamate and its receptors: the culprits behind neuropathic pain?Frontiers in aging neuroscience · 2026Review
- Chemokine CCL2 Mediates Neuroglial Crosstalk and Drives Chronic Pain Pathogenesis.Neuroscience bulletin · 2025Review
- Cancer pain: molecular mechanisms and management.Molecular biomedicine · 2025Review
- Prognostic and therapeutic potential of disulfidptosis-related genes in colon adenocarcinoma: a comprehensive multi-omics study.Cancer cell international · 2025Article
- Lidocaine-A Promising Candidate for the Treatment of Cancer-Induced Bone Pain: A Narrative Review.Advances in therapy · 2025Review
- Spinal TREM2/PI3K/Akt signal axis elicits microglial activation and aggravates bone cancer pain.Journal of anesthesia and translational medicine · 2025Article
- Chinese acupoint therapies in cancer pain management: research advances and future perspectives.Pain management · 2025Review
- Key developments and hotspots in programmed cell death in liver cancer pain: a bibliometric study.Discover oncology · 2025Article
- Cancer-nervous system crosstalk: from biological mechanism to therapeutic opportunities.Molecular cancer · 2025Review
- GluR2 overexpression in ACC glutamatergic neurons alleviates cancer-induced bone pain in rats.Molecular medicine (Cambridge, Mass.) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-induced bone pain (CIBP) is a type of ongoing or breakthrough pain caused by a primary bone tumor or bone metastasis. CIBP constitutes a specific pain state with distinct characteristics; however, it shares similarities with inflammatory and neuropathic pain. At present, although various therapies have been developed for this condition, complete relief from CIBP in patients with cancer is yet to be achieved. Hence, it is urgent to study the mechanism underlying CIBP to develop efficient analgesic drugs. Herein, we focused on the peripheral mechanism associated with the initiation of CIBP, which involves tissue injury in the bone and changes in the tumor microenvironment (TME) and dorsal root ganglion. The nerve-cancer and cancer-immunocyte cross-talk in the TME creates circumstances that promote tumor growth and metastasis, ultimately leading to CIBP. The peripheral mechanism of CIBP and current treatments as well as potential therapeutic targets are discussed in this review.
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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.