1995 Fiscal Year Final Research Report Summary
Genetic analysis of tumor-dormant mice
| Project/Area Number |
05454687
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory animal science
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| Research Institution | Niigata University |
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Principal Investigator |
SATO Norimitsu Niigata University Sch.of Med.Assoc.Professor, 医学部, 助教授 (00111716)
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| Co-Investigator(Kenkyū-buntansha) |
FUJISAWA Nobuyosi Niigata University Sch.of Med.Assistant, 医学部, 助手 (50199311)
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| Project Period (FY) |
1993 – 1995
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| Keywords | Tumor dormance / Adoptive immunotherapy against cancer / ddY substrain / Tumor-dormant mice / Tumor-resistant gene / Ehrlich tumor |
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| Research Abstract |
We concluded the following results.
1)Ehrlich ascites tumor (EAT) cells lack H-2 surface antigens.
2)However, non-MHC antigens may remain on the cell surface and some host defense mechanisms will be induced agaist EAT.
3)Some inbred strains of mice might have EAT-resistant genes, linkaged near H-2 gene locus. Number of EAT-resistant genes seem to be one or two.
4)Adoptive immune transfer of the EAT-dormant disposition of ddY-drm mice is possible by the EAT-activated spleen cells inoculation to ddY-prg mice. Cellular immunno-resistance, therefore, is involved in the mechanism.
5)Adoptive immunotherapy agaist EAT is only possible between ddY-drm and ddY-prg mice which may share a common genetic background other than H-2 or Ia loci through the history of two-way selection starting from the same basal stock colony .
6)Gene analysis of N2 mice will provide interesting results . In future, identification of EAT-resistant (EAT-dormant) gene, production of the Tg ddY-prg mice, and the gene transfer therapy against EAT will be interesting research objects .
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