2015 Fiscal Year Final Research Report
Development of treatment strategy for rhabdomyosarcoma based on control of cancer stem cell proliferation
Project/Area Number |
26670766
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Pediatric surgery
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Research Institution | Keio University |
Principal Investigator |
Kuroda Tatsuo 慶應義塾大学, 医学部, 教授 (60170130)
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Co-Investigator(Kenkyū-buntansha) |
HIYAMA Eisou 広島大学, 学内共同利用施設等, 教授 (00218744)
TAKITA Junko 東京大学, 医学部附属病院, 准教授 (00359621)
IKEDA Hitoshi 獨協医科大学, 医学部, 教授 (10326928)
FUCHIMOTO Yasushi 慶應義塾大学, 医学部, 講師(非常勤) (40219077)
MORIKAWA Yasuhide 慶應義塾大学, 医学部, 講師(非常勤) (90124958)
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Keywords | 小児外科学 / 小児腫瘍学 / 小児がん / 腫瘍幹細胞 / 横紋筋肉腫 |
Outline of Final Research Achievements |
Either PAX3-FKHR or PAX7-FKHR gene was positive in 76% of alveolar type rhabomyosarcoma, whereas never detected in embryonal type tumor. Survival rate was significantly lower in alveolar type cases with positive chimeric gene (44.2±7.3%) compared to those with negative chimeric gene (75.0±12.5%) , which was similar to that of embryonal cases (76.3±4.9%) . ALL mixed type cases were alive regardless of chimeric gene positivity. CD44, a stem cell marker, was positive in all rhabdomyosarcoma cell line examined, whereas, CD44v was negative in all the cell lines. Positivity rate of CD133 was 25% in RD cell line, whereas, less than 2% in other cell lines such as Rh30, KYM-1, RMS-YM. However, CD133 positive cells are chemotherapy resistant, and rapidly formed tumor after administrated in mice. Novel treatment strategy may be stratified according to the genotype and expression of the stem cell makers in rhabdomyosarcoma.
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Free Research Field |
小児外科学
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