| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
KRAS gene mutations occur in approximately 40 % of colorectal cancers (CRCs) and are associated with resistance to anti-EGFR antibody therapy. We demonstrated FDG accumulation in positron emission tomography (PET) was significantly higher in CRCs with mutated KRAS than in those with wild-type KRAS in a clinical setting. Moreover, using paired isogenic human CRC cell lines that differ only in the mutational status of KRAS gene, we demonstrated that mutated KRAS caused higher FDG accumulation possibly by up-regulation of GLUT1; moreover, HIF-1α additively increased FDG accumulation in hypoxic lesions. FDG-PET might be useful for predicting the KRAS status noninvasively.
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