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Träfflista för sökning "WFRF:(Klein C) srt2:(1990-1994)"

Sökning: WFRF:(Klein C) > (1990-1994)

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1.
  • Axelson, H, et al. (författare)
  • A new variant 15; 16 translocation in mouse plasmacytoma leads to the juxtaposition of c-myc and immunoglobulin lambda
  • 1991
  • Ingår i: Oncogene. - : Nature Publishing Group. - 0950-9232. ; 6:12, s. 70-2263
  • Tidskriftsartikel (refereegranskat)abstract
    • Mouse plasmacytomas (MPCs) induced by pristane oil, or by a combination of pristane oil and Abelson virus, carry one of two chromosomal translocations. The typical 12; 15 translocation leads to the juxtaposition of c-myc and immunoglobulin heavy-chain sequences, whereas the 6; 15 translocation links the kappa light-chain locus with the pvt-1 (plasmacytoma variant translocation) locus, located at least 75kb 3' of c-myc [Cory, S., Graham, M., Webb, E., Corcoran, L. & Adams, J. (1985). EMBO J., 4, 675-681]. Unlike the human Burkitt's lymphoma-associated translocation, the lambda/myc juxtaposed variant translocation has not been found previously in MPCs. Using unconventional MPC induction systems in which the tumor precursor cell was induced to proliferate in a secondary host, we have recently identified a 15; 16 translocation in six of the derived MPCs [Wiener, F., Silva, S., Sugiyama, H., Babonits, M. & Klein, G. (1990). Genes Chromosomes Cancer, 2, 36-43]. Chromosome 16 harbors the lambda light-chain gene. To explore whether the 15; 16 translocation represents the lambda/myc juxtaposition, we have mapped the breakpoints on chromosomes 15 and 16 by pulsed-field gel electrophoresis (PFGE). The pvt-1 region was mapped to approximately 220 kb 3' of c-myc. The breakpoint on chromosome 15 in ABPC-Ch-163-10, one of the six 15; 16 translocation-carrying MPCs, was situated approximately 80 kb 3' of c-myc and 140 kb 5' of pvt-1b, the major breakpoint cluster region of the previously analysed 6; 15 variant MPCs. The breakpoint on chromosome 16 was found to cut between the V1 and C3 regions of the lambda locus. Co-migration experiments showed that the C3 and the myc gene were juxtaposed head to tail on the 15; 16 translocation chromosome. On the reciprocal product V1 was juxtaposed to pvt-1.
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2.
  • Axelson, H, et al. (författare)
  • Three exceptional IgH/myc-translocation-carrying rat immunocytomas have breakpoints 50 to 80 kb 5' of c-myc
  • 1994
  • Ingår i: International Journal of Cancer. - : John Wiley & Sons Inc.. - 0020-7136. ; 56:3, s. 21-418
  • Tidskriftsartikel (refereegranskat)abstract
    • The spontaneously arising immunocytoma of the Louvain rat (RIC) carries a consistent chromosomal translocation between chromosomes 6 and 7. This translocation juxtaposes immunoglobulin heavy chain and c-myc sequences. In an earlier study on 14 RIC tumors, we found that the translocation breakpoint is located within 1.5 kb immediately upstream of c-myc in 10 of the tumors. Here we describe 3 exceptional tumors that had no rearrangement within 20 kb 5' of c-myc. Using pulsed-field gel electrophoresis we show that the translocation breakpoints in these tumors are located 50-80 kb 5' of c-myc and that c-myc rearranges to the 3' end of the IgH cluster.
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3.
  • Imreh, S, et al. (författare)
  • Hypersomy of chromosome 15 with retrovirally rearranged c-myc, loss of germline c-myc and IgK/c-myc juxtaposition in a macrophage-monocytic tumour line
  • 1994
  • Ingår i: European Journal of Cancer. - : Elsevier. - 0959-8049. ; 30A:7, s. 994-1002
  • Tidskriftsartikel (refereegranskat)abstract
    • From a lymphoid tumour induced by 7,12-dimethylbenz-[a]-anthracene (DMBA) + methyl-N-nitrose-N-urea (MNU) in an [AKR Rb(6.15) x CBAT6T6]F1 mouse, a macrophage- monocyte line (KT-10) was isolated. Following ethyl methanesulfonate (EMS) treatment, a bromodeoxyuridine (BUdR) resistant subline was selected. Serial propagation of this line in vitro in the presence of BUdR (28 months) with periodic cytogenetic and molecular examinations, has led to the definition of four successive stages. During stage I, the cells were trisomic for chromosome 15. They contained Rb(6.15) and Rb(del6.15) of AKR and T(14;15) of CBA origin. Southern blotting showed the presence of both germline (G) and rearranged (R) c-myc. At stage II, Rb(del6.15) has duplicated. Both Rb(6.15) and T(14;15) persisted together with G-myc and R-myc. In stage III, the CBA-derived T(14;15) was lost, in parallel with G-myc. At this stage, a Dic.In(6.15) was detected. One of its arms was cytogenetically identical with the long arm of In(6.15) in the variant IgK/myc translocations. This chromosome carried R-myc and IgK in juxtaposition, as indicated by comigration on pulsed field electrophoresis (PFGE). At stage IV, the R-myc carrying AKR-derived chromosome 15s were present in six copies. Possible relationships between the increasing R/G myc ratio and changed growth characteristics in vivo and in vitro are discussed.
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4.
  • Wang, Y, et al. (författare)
  • Functional homology between N-myc and c-myc in murine plasmacytomagenesis : plasmacytoma development in N-myc transgenic mice
  • 1992
  • Ingår i: Oncogene. - : Nature Publishing Group. - 0950-9232. ; 7:6, s. 7-1241
  • Tidskriftsartikel (refereegranskat)abstract
    • Mouse plasmacytomas induced by pristane oil alone, or in combination with Abelson murine leukemia virus (A-MuLV), regularly carry one of three alternative chromosomal translocations that juxtapose c-myc to immunoglobulin heavy- or light-chain loci. E mu-c-myc transgenic mice develop translocation-free plasmacytomas after induction by pristane oil and/or A-MuLV [Sugiyama, H., Silva, S., Wang, Y., Weber, G., Babonits, M., Rosen, A., Wiener, F. & Klein, G. (1990). Int. J. Cancer, 46, 845-852]. In order to test whether another member of the myc family, N-myc, could play a similar role as c-myc, we treated E mu-N-myc transgenic mice with pristane and helper-free A-MuLV. Of 20 mice that received a single pristane injection followed by A-MuLV, 17 developed plasmacytomas with a mean latency period of 54 +/- 20 days. In a corresponding group that only received a single pristane injection, five out of six transgenic mice developed plasmacytomas with a mean latency period of 142 +/- 32 days. However, after three monthly injections of pristane, all 15 transgenic mice developed plasmacytomas with a mean latency period of 128 +/- 20 days. All plasmacytomas expressed the N-myc transgene, while none of them expressed either c-myc or endogenous N-myc. None of the tumors carried the usual plasmacytoma-associated translocations.
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  • Resultat 1-4 av 4
Typ av publikation
tidskriftsartikel (4)
Typ av innehåll
refereegranskat (4)
Författare/redaktör
Klein, G (4)
Axelson, H. (4)
Panda, C K (4)
Wiener, F (3)
Wang, Y. (2)
Silva, S (2)
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Sugiyama, H (2)
Babonits, M (2)
Imreh, S (1)
Szeles, A (1)
Sumegi, J (1)
Ma, A (1)
Alt, F. W. (1)
Steinberg, J M (1)
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Lärosäte
Lunds universitet (4)
Språk
Engelska (4)

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