Source:http://linkedlifedata.com/resource/pubmed/id/15659796
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2005-1-20
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pubmed:abstractText |
Although radiotherapy is highly effective in relieving bone pain from cancer invasion, the mechanism of pain relief remains unclear. To explore the mechanism of radiotherapy-induced analgesia, we have developed an animal model of bone pain resulting from cancer invasion. Using this animal model system, radiation-induced pain response and pain-related signals in the spinal cord were analyzed. The hind paw model of bone pain from cancer invasion was developed by injecting transplantable hepatocellular carcinoma, HCa-1, into the periosteal membrane of the foot dorsum in C3H/HeJ mice. Bony invasion from HCa-1 cells was confirmed by histopathological examinations. We also measured the development of pain-associated behaviors. In this model, changes in the objective level of pain response after irradiation of the tumor were analyzed. Expression of pain-related host signals in the spinal cord, such as calcitonin gene-related peptide (CGRP), substance P, and c-fos, was investigated with immunohistochemical staining. In the histopathological examinations, bone invasion from HCa-1 cells was seen from day 7 and was evident at day 14 after injection. Measurable pain-associated behaviors were developed from day 7. In this model, mice treated with radiotherapy showed decreased objective levels of pain with a higher threshold to graded mechanical stimulation than did control mice from day 3 after irradiation. After irradiation of tumors, significant decreases in the expression of CGRP were shown in the spinal cord, whereas neither substance P nor c-fos showed any alteration. We developed a novel hind paw model of bone pain from cancer invasion that was confirmed by histopathological examination and measurable pain-associated behaviors. Radiotherapy decreased the objective level of pain and the underlying mechanism involved in the alteration of pain-related host signal, CGRP, in the spinal cord.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0077-8923
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
1030
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
179-86
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15659796-Animals,
pubmed-meshheading:15659796-Bone Neoplasms,
pubmed-meshheading:15659796-Calcitonin Gene-Related Peptide,
pubmed-meshheading:15659796-Carcinoma, Hepatocellular,
pubmed-meshheading:15659796-Liver Neoplasms,
pubmed-meshheading:15659796-Mice,
pubmed-meshheading:15659796-Pain,
pubmed-meshheading:15659796-Signal Transduction,
pubmed-meshheading:15659796-Spinal Cord,
pubmed-meshheading:15659796-Substance P
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pubmed:year |
2004
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pubmed:articleTitle |
Radiation-induced alteration of pain-related signals in an animal model with bone invasion from cancer.
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pubmed:affiliation |
Department of Radiation Oncology, Yonsei University College of Medicine, CPO Box 8044, Seoul, Republic of Korea. jsseong@yumc.yonsei.ac.kr
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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