| Project/Area Number |
12670974
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Hematology
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
OGAWA Seishi Faculty of Medicin, The University of Tokyo, assistant professor, 医学部・附属病院, 助手 (60292900)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KUROKAWA Mineo Faculty of Medicin, The University of Tokyo, assistant professor, 医学部・附属病院, 助手 (80312320)
AOKI Katsumi Faculty of Medicin, The University of Tokyo, assistant professor, 医学部・附属病院, 助手 (40291322)
|
|---|
| Project Period (FY) |
2000 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2000: ¥2,100,000 (Direct Cost: ¥2,100,000)
|
|---|
| Keywords | t(l ; 7) (q10 ; p10) / myelodysplastic syndrome / breakpoint / alphoid sequence / centromere / FISH / chromosome 1 / chromosome 7 / 二次性白血病 / alphoid反復配列 / 二動原体染色体 |
|---|
| Research Abstract |
The unbalanced translocation t(l ; 7)(qlO ; plO) is a recurrent chromosomal abnormality found in myelodysplastic syndrome (MDS) and acute myelocytic leukemia with prior histories of chemoradiotherapy. We investigated the breakpoints of this translocation using two-color FISH analysis in order to clarify its roles in pathogenesis of MDS. It was revealed that the translocation occurred between two clusters of centromere alphoid sequences recognized by D1Z7 on chromosome 1 and D7Z1 on chromosome 7. Based on the large variations of relative intensities of FISH signals of these alphoid signals on the derivative chromosome and the corresponding normal chromosome, however, the location the breakpoint within each alphoid cluster may largely differs among patients, indicating that it is loss of 7q and/or gain of 1q materials, rather than the abnormalities of a specific gene near the breakpoint, that might be important for the pathogenesis of MDS/AML harboring this translocation.
|
