2010 Fiscal Year Final Research Report
The analysis of myeloid antigens expressed in acute lymphoblastic leukemia
| Project/Area Number |
21790976
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | University of Yamanashi |
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Principal Investigator |
AKAHANE Koshi University of Yamanashi, 医学部附属病院, 助教 (90377531)
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| Project Period (FY) |
2009 – 2010
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| Keywords | 急性リンパ性白血病 / 骨髄球系抗原 / CD33 / CD13 |
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| Research Abstract |
We previously reported frequent expression of myeloid antigen CD33 on t(17;19)-ALL, which shows the poorest outcome in childhood ALL, and that E2A-HLF fusion transcriptional factor derived from t(17;19) induces CD33 expression. In this study, we analyzed the mechanism of CD33 expression induced by E2A-HLF and found that the PEA3 binding sites located downstream of the start site of CD33 gene is important for the induction by E2A-HLF. We also confirmed that PEA3 binding sites are essential for CD33 expression in both Philadelphia chromosome-positive ALL and ALL with 11q23 chromosomal translocations, which are representative refractory childhood ALLs. These observations indicate the possibility that CD33 expression in refractory ALLs was induced by the common mechanism mediated by activation of PEA3 binding sites.
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