| First Author | Wiener F | Year | 1990 |
| Journal | Genes Chromosomes Cancer | Volume | 2 |
| Issue | 1 | Pages | 36-43 |
| PubMed ID | 2126192 | Mgi Jnum | J:38378 |
| Mgi Id | MGI:85749 | Doi | 10.1002/gcc.2870020107 |
| Citation | Wiener F, et al. (1990) The missing mouse plasmacytoma (MPC) associated translocation T(15;16) occurs repeatedly in new MPC induction systems [published erratum appears in Genes Chromosom Cancer 1990 Nov;2(4):345-6]. Genes Chromosomes Cancer 2(1):36-43 |
| abstractText | A reciprocal translocation between chromosomes 15 and 16 has been detected in seven murine plasmacytomas induced by a combination of pristane and Abelson virus. Six of the tumors were induced in a new, unconventional experimental system based on transfer of uninfected or Abelson virus infected bone marrow and spleen cells, respectively, into pristane treated mice. All six tumors were of donor type. The seventh tumor appeared in a conventional pristane + Abelson virus treated mouse. This tumor was unusual in carrying both the 15;16 variant translocation and the typical 12;15 translocation, in the same tumor cells. In the new 15;16 variant, the breakpoint of chromosome 15 was at the interphase of the D2/3 sub-bands, as in mouse plasmacytomas with the previously well-known typical 12;15 and variant 6;15 translocations. The breakpoint on chromosome 16 was mapped to band 16B1, corresponding to the presumed cytogenetic site of the Ig-lambda gene. In three of the seven tumors with the 15;16 translocation, the derivative chromosome 15 had undergone a duplication, a feature that has not been previously encountered in the MPC-associated 12;15 and 6;15 translocation carriers. The reciprocal derivative chromosome 16 was lost from one of the seven tumors. We postulate that the 15;16 translocation results in juxtaposition of the myc gene to lambda sequences, probably in a similar orientation as previously described for the variant 6;15 translocation. |
