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Radiation-induced alteration of pain-related signals in an animal model with bone invasion from cancer

DC FieldValueLanguage
dc.contributor.author김은정-
dc.contributor.author성진실-
dc.contributor.author이배환-
dc.date.accessioned2015-07-14T16:41:32Z-
dc.date.available2015-07-14T16:41:32Z-
dc.date.issued2004-
dc.identifier.issn0077-8923-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/111397-
dc.description.abstractAlthough 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.-
dc.description.statementOfResponsibilityopen-
dc.format.extent179~186-
dc.relation.isPartOfANNALS OF THE NEW YORK ACADEMY OF SCIENCES-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHBone Neoplasms/complications-
dc.subject.MESHBone Neoplasms/radiotherapy*-
dc.subject.MESHBone Neoplasms/secondary*-
dc.subject.MESHCalcitonin Gene-Related Peptide/metabolism-
dc.subject.MESHCarcinoma, Hepatocellular/pathology-
dc.subject.MESHLiver Neoplasms/pathology-
dc.subject.MESHMice-
dc.subject.MESHPain/etiology-
dc.subject.MESHPain/physiopathology*-
dc.subject.MESHSignal Transduction/radiation effects*-
dc.subject.MESHSpinal Cord/physiopathology-
dc.titleRadiation-induced alteration of pain-related signals in an animal model with bone invasion from cancer-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Physiology (생리학)-
dc.contributor.googleauthorJINSIL SEONG-
dc.contributor.googleauthorHEE CHUL PARK-
dc.contributor.googleauthorBAE WHAN LEE-
dc.contributor.googleauthorUN JUNG KIM-
dc.contributor.googleauthorJIYOUNG KIM-
dc.identifier.doi10.1196/annals.1329.023-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.relation.journalcodeJ00181-
dc.identifier.eissn1749-6632-
dc.identifier.pmid15659796-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1196/annals.1329.023/abstract-
dc.subject.keywordpain in the bone-
dc.subject.keywordanimal model-
dc.subject.keywordbone metastasis-
dc.subject.keywordradiation-
dc.contributor.alternativeNameKim, Un Jeng-
dc.contributor.alternativeNameSeong, Jin Sil-
dc.contributor.alternativeNameLee, Bae Hwan-
dc.rights.accessRightsnot free-
dc.citation.volume1030-
dc.citation.startPage179-
dc.citation.endPage186-
dc.identifier.bibliographicCitationANNALS OF THE NEW YORK ACADEMY OF SCIENCES, Vol.1030 : 179-186, 2004-
dc.identifier.rimsid35790-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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