| Budget Amount *help |
¥47,450,000 (Direct Cost: ¥36,500,000、Indirect Cost: ¥10,950,000)
Fiscal Year 2016: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2015: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2014: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2013: ¥9,360,000 (Direct Cost: ¥7,200,000、Indirect Cost: ¥2,160,000)
Fiscal Year 2012: ¥26,910,000 (Direct Cost: ¥20,700,000、Indirect Cost: ¥6,210,000)
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| Outline of Final Research Achievements |
Because p53 plays an important role in the transcriptional regulation of genes encoding proteins involved in DNA repair and apoptosis, the modification of p53 may appear to be a pivotal determinant of cells fate. During carcinogenic progression, p53 is mutated or deleted in nearly half of all human cancers and fails to function normally. Both PTEN and BRCA1 also regulate the expression of several genes identified as key roles in affecting breast and ovarian cancer risk. They also participate in DNA repair and recombination processes related to maintenance of genomic integrity and control of cell proliferation. Genetic defects in DNA repair and DNA damage response genes often lead to an increase in cancer incidence. The role of defects is also associated with modulation of signaling pathways. Furthermore, mutations or epigenetic silencing in DNA repair genes have been associated with a phenotype of sensitivity of cancers to the therapy.
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