2009 Fiscal Year Final Research Report
Clinical research for disease mechanisms associated with TFL gene dysfunction in malignant lymphoid tumors
| Project/Area Number |
20790674
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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 |
Hematology
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| Research Institution | Kobe University |
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Principal Investigator |
MINAGAWA Kentaro Kobe University, 医学部附属病院, 医員 (80432574)
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| Project Period (FY) |
2008 – 2009
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| Keywords | TFL / ZC3H12D / Tumor suppressor gene / FISH / 6q- / Rb / Apoptosis |
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| Research Abstract |
We recently identified a novel gene with a similar CCCH-type zinc finger domain as a possible tumor suppressor gene that is involved in a cryptic breakpoint translocation found in human transformed follicular lymphoma. To clarify clinical significance for the gene, we analyzed the gene defect of 84 lymphoma patients. Eleven patients (15.3%) lose at least one allele. TFL protein inhibited cell growth and provoked apoptosis. As for its subcellular localization, it localized in the cytoplasmic granules called P-bodies. The inhibitory activity of TFL for lymphocyte proliferation highlights the potential utility of TFL as therapeutic targets for leukemia and/or lymphoma.
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