| Project/Area Number |
08670666
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
HARA Nobuyuki Kyushu University Research Institute for Diseases of the Chest, Faculty of Medicine, Professor, 医学部, 教授 (90038802)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAVAMA Koichi Kyushu University Assistant, 医学部, 助手 (50274444)
KAWASAKI Masayuki Kyushu University Assistant, 医学部, 助手 (90264051)
KUWANO Kazuuvoshi Kyushu University Assistant Professor, 医学部, 講師 (40205266)
NAKANISHI Yoichi Kyushu University Assistant Professor, 医学部, 講師 (20172356)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | IIP / lung cancer / p53 / Fas / PCNA / apoptosis / 癌抑制遺伝子p53 / 肺線維症 / Fas・Fas Lシステム |
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| Research Abstract |
It is reported that 7% to 30% of patients with idiopathic interstitial pneumonia (IIP) are associated with lung cancer. Inversely, 8% of patients with lung cancer are associated with IIP,and 35%of patients with lung cancer have pulmonary interstitial changes. These facts indicate that pulmonary fibrosis has an important role as a background of lung carcinogenesis. We haveinvestigated the mechanisms of cell proliferation and carcinogenesis for the lung tissue from 20 patients with lung cancer associated with pulmonary interstitial changes.
In cancer tissue immunohistochemical expression of p53 was observed in 70% of the cases. while, in alveolar and bronchiolar epithelium of fibrosis area, it was observed in 45% of the cases. In fibrosis area, the staining intensity was lower, and the staining pattern was scattered. Positive ratio of PCNA was 90% in cancer area, and 60% in fibrosis area in which positive area was distributed unequally around bronchial epithelium. No expression of Fas was seen in cancer area. Positive ratio of TUNEL stain in fibrotic area was 50%. In the cases multiple area was anlyzed by step section for p53 expression, PCNA expression and TUNEL stain, co-expression of p53 and PCNA, and simultaneous DNA damage were foca11y observed.
These results indicate that both cell proliferatioh and cell damage (or apoptosis) occur simultaneously in tissue exhibiting pulmonary fibrosis. Thus, it is suggested that DNA damage and repair are seen in the tissue with pulmonary flbrosis, leading to luhg carcinogenesis. In order to clarify whether p53 expression in pulmonary fibrosis represents p53. mutation as precancerous lesion or expression of wild type p53 to preserve DNA stability, p53 gene analysis ln these area are now ongoing.
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