| Project/Area Number |
24791148
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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 |
Dermatology
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | Connexin 26 / コネキシン26 / 発癌 / Connexin26 |
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| Research Abstract |
The aim of this study was to clarify the mechanism of carcinogenesis in KID (Keratitis-ichthyosis-defness) syndrome by model mouse. The model mouse expressed mutated Connexin 26(Cx26) gene in the epidermis. The mutation was from a patient with KID syndrome with skin cancer. Some of the mice had unusual phenotype, but none of them had progressed skin cancer before they died. We irradiated UVB on the mice. Although no skin cancer was induced by UVB irradiation, the irradiated skin developed ulceration and persisted for several months. Some of the mice had multiple abscess, indicating the complication of immunodeficiency. Although the T cell function seemed normal, some immunodeficiency can be associated with carcinogenesis.
We transfected the mutated gene to the HaCaT cells, and irradiated UVB. The cell death by UVB irradiation was decreased by the gene transfection. This result suggested that mutated Cx26 gene can be related to the UV associated carcinogenesis.
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