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

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Abstract
The role of Abelson murine leukemia virus (A‐MuLV) in the accelerated development of murine plasmacytomas (PCs) (Potter et al., 1973: Science, 132, 592‐594) was studied in a new experimental system. Spleen cells from pristane‐treated or untreated BALB/c 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. Donor‐derived 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 41 pristane‐treated recipients that had received untreated donor‐derived spleen cells (latent periods: 65 and 120 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 D2/3. Four of these corresponded to a typical 12; 15 translocation, one was a variant 6; 15 translocation and the 6th may represent a previously unidentified translocation between chromosome 15 and the λ 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.