| Project/Area Number |
04044073
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Institution | Cancer Research Institute Kanazawa University |
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Principal Investigator |
OHNO Shinsuke Cancer Research Institute, Kanazawa University, がん研究所, 助教授 (70019868)
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| Co-Investigator(Kenkyū-buntansha) |
WIENER Francis Department of Tumorbiology, Karolinska Institute, 腫瘍生物部, 教授
MATSUSHIMA Kouji Cancer Research Institute, Kanazawa University, がん研究所, 教授 (50222427)
MURAKAMI Seishi Cancer Research Institute, Kanazawa University, がん研究所, 教授 (90019878)
HAYAKAWA Jun-ichiro School of Medicine, Kanazawa University, 医学部, 教授 (50110622)
FRANCIS Wien カロリンスカ研究所, 腫瘍生物部, 教授
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥11,700,000 (Direct Cost: ¥11,700,000)
Fiscal Year 1994: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1993: ¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 1992: ¥4,700,000 (Direct Cost: ¥4,700,000)
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| Keywords | SCID mouse / Plasmacytoma / Cytogenetics / Chromosomal translocation / Abelson leukemia virus / Abelson白血病ウィルス |
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| Research Abstract |
In order to determine the timing of the chromosomal translocations specific for murine plasmacytomas (t (12 ; 15) or t (6 ; 15) ) with respect to the stages of B-cell development, C.B-17 scid/scid mice were reconstituted with SRBC-immunized or normal BALB/c6.15 mouse spleen and bone marrow cells. Plasmacytomas were induced by i.p.injection of pristane alone or of pristane + Abelson murine leukemia virus (A-MuLV).
Five plasmacytomas developed in 19 SCID mice. Karyotype analysis showed that 3 were of donor (BALB/c6.15) origin and 2 were of host (C.B-17scid/scid) origin. Plasmacytomas originated in SCID mice (ABPC-SCID-IM-B and IM-D) had a・ t (6 ; 15) chromosomal translocation. Precursor cells from which the plasmacaytomas carrying t (6 ; 15) chromosomal translocation developed might be in a pro-, pre-B cell stage, because no functional B-cells develop in SCID mice by the defect of V- (D) -J recombination system. Ig allotype of C.B-17scid/scid mouse is "b". However, both IM-B and IM-D were
… More
IgA-producers of "a" allotype. This indicates that IM-B and IM-D did not develop from "leaky" SCID cells. SSLP (Simple Sequarance Repeat Length Polymorphism) analysis using several microsatellite DNAs of known chromosomal locations suggested that the Igh-C regions of chromosome 12 of IM-B and IM-D were replaced by those of chromosome 12 of BALB/c6.15 cells, therefore synthesizing IgA of "a" allotype.
In the next series of experiments, C.B-17scid/scid mice were reconstituted with surface Ig-positive cells (immature and mature B) obtained from BALB/c6.15 mouse spleens. Plasmacytomas were induced as mentioned above. Six plasmacytomas were induced by pristane + A-MuLV in 80 SCID mice. Four plasmacytomas developed by pristane alone in 40 SCID mice, so far. Karyotype analysis revealed that all the plasmacytomas developed were of donor mouse (BALB/c6.15) cell origin. Interestingly, all the plasmacytomas developed so far carried t (12 ; Rb (6.del 15) ) chromosomal translocation irrespective of the inducing agents. Therefore, precursor cells from which the plasmacytomas carrying a t (12 ; 15) chromosomal translocation develop are suggested to be sIg-positive, immature and/or mature B cells. Less
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