1999 Fiscal Year Final Research Report Summary
Functional analysis of cyclin D1 alternative transcript b
Project/Area Number |
10670980
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Hematology
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Research Institution | AICHI CANCER CENTER |
Principal Investigator |
HOSOKAWA Yoshitaka LABORATORY OF CHEMOTHERAPY, SECTION CHIEF, 化学療法部, 室長 (60229193)
|
Co-Investigator(Kenkyū-buntansha) |
SETO Masao LABORATORY OF CHEMOTHERAPY, CHIEF, 化学療法部, 部長 (80154665)
|
Project Period (FY) |
1998 – 1999
|
Keywords | Lymphoma / chromosome translocation / cyclin D1 |
Research Abstract |
The cyclin D1/PRAD1 oncogene, a key regulator of the G1 phase progression of the cell cycle has been identified as the long-sought BCL-1 oncogene in B-cell malignancies with t(11;14)(q13;q32) translocation. Recently, a novel alternative spliced cyclin D1 transcript, called transcript [b], has been identified by ourselves. The level of the variant transcript [b] was lower than that of the originally reported cyclin D1 transcript, called transcript [a], in several human non-lymphoid cancer cell lines but the endogenous cellular expression of transcript [b] products has not yet been determined. Northern blot analysis and reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that the transcript [b] mRNAs are well expressed in B-lymphoid cell lines with t(11;14)(q13;q32) translocation and at much lower or undetectable levels in other cells. Western blot analysis using a human cyclin D1-specific monoclonal antibody, which can recognize and distinguish the products of transcripts [a] and [b], strongly suggested that the transcript [b] protein is indeed expressed in these B-cell lines. The present study provides the first identification of the endogenous cellular expression of the cyclin D1 transcript [b] protein and strongly suggests that this alternative form of cyclin D1 may play a significant role in the molecular pathogenesis of B-lymphoid malignancies with t(11;14)(q13;q32) translocation. Further studies are warranted to study the biological function of transcript [b] and its role in cell cycle control.
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[Publications] Joh, T., Hosokawa, Y., Suzuki, R., Takahashi, T., and Seto, M.: "Establishment of an inducible expression system of chimeric MLL-LTG9 protein and inhibition of Hox a7, Hox b7 and Hox c9 expression by MLL-LTG9 in 32Dc13 cells."Oncogene. 18. 1125-1130 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] Akagi, T., Tamura, A., Motegi, M., Suzuki, R., Hosokawa, Y., Nakamura, S., Morishima, Y., Seto, M., and Taniwaki, M.: "Molecular cytogenetic delineation of the breakpoint at 18q21.1 in low-grade B-cell lymphoma of mucosa-associated lymphoid tissue."Genes Chrom. & Cancer. 24. 315-321 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] Akagi, T., Motegi, M., Tamura, A., Suzuki, R., Hosokawa, Y., Suzuki, H., Ota, H., Nakamura, S., Morishima, M., Taniwaki, M., Seto, M.: "A novel gene, MALT1 at 18q21, is involved in t(11;18)(q21;q21) found in low-grade B-cell lymphoma of mucosa-associated lymphoid tissue."Oncogene,. 18. 5785-5794 (1999)
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「研究成果報告書概要(欧文)」より
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[Publications] Hosokawa, Y., Maeda, Y., Ichinohasama, R., Miura, I., Taniwaki, M. and Seto, M.: "The Ikaros gene, a central regulator of lymphoid differentiation, fuese to the BCL6 gene as a result of t(3;7)(q27;q12) translocation in a patient with diffuse large B-cell lymphoma."Blood. (in press).
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「研究成果報告書概要(欧文)」より
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[Publications] Motegi, M., Yonequmi, M., Suzuki, H., suzuki, R., Hosokawa, Y., Hosaka, S., Kodera, Y., Morishima, M., Nakamura, S. and Seto, M.: "API2-MALT1 chimeric transcripts involved in mucosa-associated lymphoid tissue type lymphoma predict heterogenous products."Am. J. Pathol.. (in press).
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「研究成果報告書概要(欧文)」より
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