The accelerating role of abelson murine leukemia virus in murine plasmacytoma development: in vitro infection of spleen cells generates donor-type tumors after transfer to pristane-treated BALB/c mice
✍ Scribed by Hiroyuki Sugiyama; Günther Weber; Santiago Silva; Magda Babonits; Francis Wiener; George Klein
- Publisher
- John Wiley and Sons
- Year
- 1989
- Tongue
- French
- Weight
- 863 KB
- Volume
- 44
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
The role of Abelson murine leukemia virus (A-MuLV) in the accelerated development of murine plasmacytomas (PCs) (Potter et a/., 1973: Science, 132, 592-594) was studied in a new experimental system. Spleen cells from pristane-treated or untreated BALBk mice carrying Robertsonian 6; I5 fusion chromosomes were infected in vitro with helper-free A-MuLV overnight and subsequently transplanted into the peritoneal cavity of pristane-treated or untreated BALB/c mice. Donorderived PCs developed in 4 out of 76 pristane-treated recipients [latent periods: 38-82 (mean 51) days] that had received spleen cells from pristane-treated donors, and also in 2 out of 4 I pristane-treated recipients that had received untreated donor-derived spleen cells (latent periods: 65 and I20 days). Three of the PCs in the former and both PCs in the latter group were tested for integration and expression of the v-abl gene, with positive results. This indicates that the spleen contains PC-precursor cells that can be activated by A-MuLV even before the impact of pristane. All 6 donor-origin PCs carried a translocation involving chromosone 15, band D213. Four of these corresponded to a typical 12;15 translocation, one was a variant 615 translocation and the 6th may represent a previously unidentified translocation between chromosome 15 and the A gene-carrying chromosome 16. No PCs developed among 29 pristane-untreated recipients that had received pristane-treated donor-derived spleen cells. In addition to PCs, monocytic tumors developed in 37 (26%) of all recipients. Their development was independent of pristane treatment of recipients but was particularly frequent in those who had received spleen cells from pristane-treated donors.