1991 Fiscal Year Final Research Report Summary
Genetic and molecular studies on the oncogenesis of hematopoietic malignancies
| Project/Area Number |
01480301
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | KUMAMOTO UNIVERSITY |
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Principal Investigator |
TAKATSUKI Kiyoshi Kumamoto University, Medical School, Professor, 医学部, 教授 (80026830)
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| Co-Investigator(Kenkyū-buntansha) |
ASOU Norio Kumamoto University, Medical School, Assistant, 医学部, 助手 (50175171)
MATSUZAKI Hiromitsu Kumamoto Universiry, Medical School Hospital, Assistant Professor, 医学部附属病院, 講師 (30136725)
HATTORI Toshio Kyoto Univ., Virus Institute, Associate Professor, ウイルス研究所, 助教授 (30172935)
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| Project Period (FY) |
1989 – 1991
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| Keywords | Oncogene / Adult T-Cell Leukemia / Multiple myeloma / Chromosome / Cell line / Cytokine / Immunoglobulin / T-cell receptor |
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| Research Abstract |
We tried to clarify the oncogenesis of hematopoietic maliganancies, especially lymphocytic maliganancies such as adult T-cell leukemia (ATL) and multiple myeloma. We also tried to establish the cell line from the patients with chromosome abnormalities.
1) We established amylase-producing myeloma cell line (KHM-1) from a patient with hyperamyalasemia. Chromosome analysis showed a translocation between near the amylase gene locus and the abl oncogene locus. This cell line operates under an autocrine growth mechanism with respect of these two cytokines, IL-6 and TNF-alpha.
2) The cell line (KHM-2B) expressing two oncogene products, c-myc and bcl-2, was established from a patient with acute lymphocytic leukemia with an 8 ; 14 and 14 ; 18 chromosome translocation. In this cell line, two oncogenes were activated by two translocations to immunoglobulin genes.
3) We studied the rearrangement and expression of the immunoglobulin (Ig) and T-cell receptor (TCR) genes in 12 patients with acute unclassified leukemia (AUL). Our results suggest that AUL may generally originate from undifferentiated cells with an aberrant rearrangement and/or expression of the Ig and TCR genes.
4) We showed that p53 tumor suppressor gene was frequently mutated in the acute phase of ATL. These results suggests that p53 mutations may be associated with the transition from chronic to acute ATL. On the other hand, cell surface expression of the TCR/CD3 complex were very low on the cells from acute type ATL, but not from chronic type ATL.
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