| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Research Abstract |
Pancreatic ductal adenocarcinoma (PDA) is characterised by aggressive tumor spread, early metastasis and a poor prognosis. Standard therapy for PDA patients includes not only surgery and chemotherapy but also radiotherapy. However, there have been few detailed molecular biological studies to investigate about the effect of radiotherapy on PDA. It was reported that histone deacetylase 1 (HDAC1) is responsible for DNA repair of double strand breaks after irradiation in human fibroblasts. Here, we examined HDAC1 is involved in the mechanism of radioresistance of PDA. The irradiated pancreatic cancer cell lines reduced the radiosensitivity and increased the HDAC1 mRNA expression. The radioresistance was decreased after the addition of low-concentration TSA or knockdown of HDAC1 in pancreatic cancer cell lines. The present data suggested that HDAC1 is invoved in the mechanism of the radioresistance of pancreatic cancer cells.
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