ArticleMolecular pain2011
Inhibition of p38-MAPK signaling pathway attenuates breast cancer induced bone pain and disease progression in a murine model of cancer-induced bone pain.
Article in Molecular pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- ANA-12 Targets and Inhibits BDNF/TrkB Signaling to Alleviate Pain Behaviors in Rheumatoid Arthritis Mice.Neurochemical research · 2025Article
- TRPC4 Mediates Trigeminal Neuropathic Pain via CaCNS neuroscience & therapeutics · 2025Article
- Microglia and p38 MAPK Inhibitors Suppress Development of Mechanical Allodynia in Both Sexes in a Mouse Model of Antiretroviral-Induced Neuropathic Pain.International journal of molecular sciences · 2023Article
- MicroRNA-4500 Inhibits Migration, Invasion, and Angiogenesis of Breast Cancer Cells via RRM2-Dependent MAPK Signaling Pathway.Molecular therapy. Nucleic acids · 2020Article
- Article
- The Endocannabinoid System Alleviates Pain in a Murine Model of Cancer-Induced Bone Pain.The Journal of pharmacology and experimental therapeutics · 2020Article
- Substance P modulates electroacupuncture analgesia in humanized mice with sickle cell disease.Journal of pain research · 2019Article
- The Src family kinase inhibitor dasatinib delays pain-related behaviour and conserves bone in a rat model of cancer-induced bone pain.Scientific reports · 2017Article
- PINTnet: construction of condition-specific pathway interaction network by computing shortest paths on weighted PPI.BMC systems biology · 2017Article
- Effects of Src-kinase inhibition in cancer-induced bone pain.Molecular pain · 2016Article
- The Analgesic and Antineuroinflammatory Effect of Baicalein in Cancer-Induced Bone Pain.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Quercetin reduces Ehrlich tumor-induced cancer pain in mice.Analytical cellular pathology (Amsterdam) · 2015Article
- Use of Animal Models in Understanding Cancer-induced Bone Pain.Cancer growth and metastasis · 2015Review
- Tumor cell p38 MAPK: A trigger of cancer bone osteolysis.Cancer cell & microenvironment · 2015Article
- Article
- Ubiquitin-conjugating enzyme Ubc13 controls breast cancer metastasis through a TAK1-p38 MAP kinase cascade.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Eukaryotic elongation factor 2 controls TNF-α translation in LPS-induced hepatitis.The Journal of clinical investigation · 2013Article
- Network and data integration for biomarker signature discovery via network smoothed T-statistics.PloS one · 2013Article
- Disease modification of breast cancer-induced bone remodeling by cannabinoid 2 receptor agonists.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMechanisms driving cancer-induced bone pain are poorly understood. A central factor implicated to be a key player in the process of tumorigenesis, osteoclastogenesis and nociception is p38 MAPK. We determined the role of p38 MAPK in a mouse model of breast cancer induced bone pain in which mixed osteolytic and osteoblastic remodeling occurs.
resultsIn cancer-treated mice, acute as well as chronic inhibition of p38 MAPK with SB203580 blocked flinching and guarding behaviors in a dose-dependent manner whereas no effect on thresholds to tactile stimuli was observed. Radiographic analyses of bones demonstrated that chronic inhibition of p38 MAPK reduced bone loss and incidence of spontaneous fracture in cancer-treated mice. Histological analysis of bones collected from mice treated with the p38 MAPK inhibitor showed complete absence of osteoblastic growth in the intramedullary space as well as significantly reduced tumor burden.
conclusionsBlockade of non-evoked pain behaviors but not hypersensitivity suggests differences in the underlying mechanisms of specific components of the pain syndrome and a possibility to individualize aspects of pain management. While it is not known whether the role of p38 MAPK signaling can be expanded to other cancers, the data suggest a need for understanding molecular mechanisms and cellular events that initiate and maintain cancer-induced bone pain for effective management for both ongoing pain as well as breakthrough pain.
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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.