1998 Fiscal Year Final Research Report Summary
Study on the inhibition of chemical carcinogenesis of buccal mucosa with a macrophage activating factor
| Project/Area Number |
09672086
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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 |
Surgical dentistry
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| Research Institution | Hyogo College of Medicine |
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Principal Investigator |
URADE Masahiro Hyogo College of Medicine, School of Medicine, Professor and Chair, 医学部, 教授 (70104883)
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| Co-Investigator(Kenkyū-buntansha) |
KISHIMOTO Hiromitsu Hyogo College of Medicine, School of Medicine, Associate, 医学部, 助手 (30291818)
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| Project Period (FY) |
1997 – 1998
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| Keywords | hamster buccal pouch carcinogenesis / dimethylbenzanthracene / macrophage activating factor (GcMAF) / inhibition of carcinogenesis |
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| Research Abstract |
This study was designed to investigate the inhibitory effects of a new macrophage activating factor (GcMAF) on hamster buccal pouch carcinogenesis with 9,1O-dimethyl-1,2-benzanthracene (DMBA) and on the growth of DMBA-induced tumor. GcMAF newly discovered by N.Yamamoto is a glycoprotein derived from serum Gc protein (vitamin D_3-binding protein) as precursor. The results obtained were as follows.
1)Twenty-nine Syrian hamsters (5 week-old) were divided into 15 with GcMAF administration (100 pg i.m. injection twice a week) and 14 without administration, and were painted a buccal pouch 3 times a week with 1% DMBA-acetone solution. Consequently, all hamsters of the group without GcMAF administration developed squamous cell carcinoma at the 9th to 10th week after DMBA application, and died of tumor within 20 weeks. On the other hand, two of 14 hamsters with GcMAF administration did not produce tumors, and the remaining 12 hamsters showed a delay of tumor development and growth and were alive
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until the 20th week of the experimental period. Also, their weight loss by tumor burden was slight.
2)Five tumor-bearing hamsters in the group without GcMAF administration showed the inhibition of tumor growth and weight loss by starting GcMAF from the 13th week. Four tumor-bearing hamsters in the group with GcMAF administration showed acceleration of tumor growth by stopping GcMAF from the 13th week.
3)Treatment of hamster peritoneal macrophages with GcMAF in vitro or in vivo demonstrated increased superoxide generation indicating the macrophage activation. The GcMAF-activated peritoneal macrophages revealed a significant cytocidal effect against hamster kidney BHK21 cells and human oral floor carcinoma KB cells as compared to non-activated macrophages.
From these findings, it was indicated that GcMAF inhibited or delayed the DMBA-induced hamster buccal pouch carcinogenesis and tumor growth via macrophage activation, This investigation suggested the possibility of immunotherapy for oral cancer with GcMAF. Less
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