| Project/Area Number |
06454320
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
KUBOTA Kazuo Institute for Development, Aging and Cancer, Tohoku University Associate Professor, 加齢医学研究所, 助教授 (40161674)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Susumu Institute for Development, Aging and Cancer, Tohoku University Assistant Profess, 加齢医学研究所, 講師 (70182532)
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| Project Period (FY) |
1994 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1994: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Keywords | Nuclear medicine / Tumor diagnosis / Tumor recurrence / Radiotherapy / Positron emission tomography / ^<11>C-L-methionine / ^<18>F-fluorodexyglucose / ^<18>Fフルオロフェニルアラニン / ^<14>Cメチオニン(Met) / ^3Hチミジン(Thd) / ^<18>Fフルオロデオキシグルコース(FDG) |
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| Research Abstract |
This is a basic research project fot the detection of metabolic increase in recurrent cancer tissue using positron emission tomography that may be earlier than the volumetric increase in cancer tissue at the recurrence.
We have performed autoradiographic studies to elucidate the intratumoral distribution of FDG and 14Cmethionine (Met). In a tumor tissue, FDG uptake was observed not only in cancer cells but also in non-neoplastic tissue (stroma). Especially high FDG uptake is seen in activated macrophages and young granlation tissue. That may be a cause of false positive FDG uptake by post-therapy inflammation. FDG uptake both by cancer cells and by non-neoplastic tissues may contribute to the activity seen in PET images. Comparison of rapid and slow growing tumors showed that FDG uptake ratio of the rapid to the slow was higher than the uptake ratio with Met and thymidine. FDG may be an excellent tracer for the evaluation of differences among tumors, that is pre-treatment siagnosis.
While, tumor uptake of Met is largely achieved by viable cancer cells. Granulation tissue and macrophages showed low Met uptake and were lower than that of FDG.Met uptake by whole tumor will arrive at plateau early. It is pooled inside tumor tissue as free Met. Then, time related incorporation of cellularly pooled free Met into macromolecules, protein, lipids, RNA and DNA will be continued. Met uptake changes after tumor radiotherapy is close to the uptake changes of thymidine that is a marker of proliferation. FDG uptake showed a linear correlation to the percentage of viable tissue in vivo. Autoradiography study of post-radiotherapy tumor shows the highest methionine and thymidine uptake in residual viable cancer cells, whereas FDG uptake did not differ between viable cancer cells and macrophages. Met is a tracer that represents extension of proliferating cancer, cells, and may be suitable for predictive diagnosis of cancer recurrence using positron emission tomography.
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