دورية أكاديمية
أعرض في EDS

Cancer-induced bone pain: Mechanisms and models.

التفاصيل البيبلوغرافية
العنوان: Cancer-induced bone pain: Mechanisms and models.
المؤلفون: Lozano-Ondoua AN; Department of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ, USA., Symons-Liguori AM, Vanderah TW
المصدر: Neuroscience letters [Neurosci Lett] 2013 Dec 17; Vol. 557 Pt A, pp. 52-9. Date of Electronic Publication: 2013 Sep 25.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Elsevier Scientific Publishers Ireland Country of Publication: Ireland NLM ID: 7600130 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-7972 (Electronic) Linking ISSN: 03043940 NLM ISO Abbreviation: Neurosci Lett Subsets: MEDLINE
أسماء مطبوعة: Publication: Limerick : Elsevier Scientific Publishers Ireland
Original Publication: Amsterdam, Elsevier/North-Holland.
مواضيع طبية MeSH: Bone Neoplasms/*complications , Pain/*etiology , Pain/*metabolism, Acid Sensing Ion Channels/metabolism ; Animals ; Bone Neoplasms/metabolism ; Bone Neoplasms/secondary ; Cytokines/metabolism ; Disease Models, Animal ; Humans ; Mice ; Nerve Growth Factors/metabolism ; Oxidative Stress/physiology ; Rats
مستخلص: Cancerous cells can originate in a number of different tissues such as prostate, breast and lung, but often go undetected and are non-painful. Many types of cancers have a propensity to metastasize to the bone microenvironment first. Tumor burden within the bone causes excruciating breakthrough pain with properties of ongoing pain that is inadequately managed with current analgesics. Part of this failure is due to the poor understanding of the etiology of cancer pain. Animal models of cancer-induced bone pain (CIBP) have revealed that the neurochemistry of cancer has features distinctive from other chronic pain states. For example, preclinical models of metastatic cancer often result in the positive modulation of neurotrophins, such as NGF and BDNF, that can lead to nociceptive sensitization. Preclinical cancer models also demonstrate nociceptive neuronal expression of acid-sensing receptors, such as ASIC1 and TRPV1, which respond to cancer-induced acidity within the bone. CIBP is correlated with a significant increase in pro-inflammatory mediators acting peripherally and centrally, contributing to neuronal hypersensitive states. Finally, cancer cells generate high levels of oxidative molecules that are thought to increase extracellular glutamate concentrations, thus activating primary afferent neurons. Knowledge of the unique neuro-molecular profile of cancer pain will ultimately lead to the development of novel and superior therapeutics for CIBP.
(Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)
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معلومات مُعتمدة: R01 CA142115 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: ASIC; Cytokines; Glutamate; NGF; Oxidative Stress; Syngenic tumor model
المشرفين على المادة: 0 (Acid Sensing Ion Channels)
0 (Cytokines)
0 (Nerve Growth Factors)
تواريخ الأحداث: Date Created: 20131001 Date Completed: 20140711 Latest Revision: 20211021
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC4542064
DOI: 10.1016/j.neulet.2013.08.003
PMID: 24076008
قاعدة البيانات: MEDLINE
الوصف
تدمد:1872-7972
DOI:10.1016/j.neulet.2013.08.003