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

Authors
 JINSIL SEONG  ;  HEE CHUL PARK  ;  BAE WHAN LEE  ;  UN JUNG KIM  ;  JIYOUNG KIM 
Citation
 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, Vol.1030 : 179-186, 2004 
Journal Title
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES
ISSN
 0077-8923 
Issue Date
2004
MeSH
Animals ; Bone Neoplasms/complications ; Bone Neoplasms/radiotherapy* ; Bone Neoplasms/secondary* ; Calcitonin Gene-Related Peptide/metabolism ; Carcinoma, Hepatocellular/pathology ; Liver Neoplasms/pathology ; Mice ; Pain/etiology ; Pain/physiopathology* ; Signal Transduction/radiation effects* ; Spinal Cord/physiopathology
Keywords
pain in the bone ; animal model ; bone metastasis ; radiation
Abstract
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.
Full Text
http://onlinelibrary.wiley.com/doi/10.1196/annals.1329.023/abstract
DOI
10.1196/annals.1329.023
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
Yonsei Authors
Kim, Un Jeng(김은정) ORCID logo https://orcid.org/0000-0003-0968-0252
Seong, Jin Sil(성진실) ORCID logo https://orcid.org/0000-0003-1794-5951
Lee, Bae Hwan(이배환) ORCID logo https://orcid.org/0000-0003-4719-9021
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/111397
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