2014 Fiscal Year Final Research Report
Verification of hypoxia independent activation of glucose metabolism in oral cancer
| Project/Area Number |
24792166
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Surgical dentistry
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| Research Institution | Hokkaido University (2013-2014)
Nagasaki University (2012) |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 低酸素 / 糖代謝 / 口腔癌 |
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| Outline of Final Research Achievements |
Cancer cells have extremely high growth activity. Previously, it was understood that the activity is supported by activated HIF1 via glucose metabolic mechanism under tumor specific hypoxic condition. But, clinical study comparing FDG-PET to FMISO-PET showed the cases that had highly activated metabolic capacity even without hypoxia.
In this study, we stained HIF1, Ki67, GLUT1 in all the metastatic lymph nodes from over 2000 of operative enucleated cervical lymph nodes.
All three factors expressed abundantly in tumor specific manor. HIF1 expression pattern was unrelated to oxygen gradient from blood vessels. These results suggest that tumor specific hyper-activation of HIF1 is partially regulate glucose transporter expression and has more direct relation to cancer cell's special growth activity.
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| Free Research Field |
口腔癌
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