Abelson murine leukemia virus transforms preneoplastic Eμ‐myc transgene‐carrying cells of the B‐lymphocyte lineage into plasmablastic tumors

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Abstract
Eμ‐myc transgenic mice were back‐crossed to BALB/c mice up to back‐cross generation 3. The offspring that included transgene‐carrying and ‐negative mice in approximately equal proportions were randondy divided into 2 groups. Thirty‐four mice (group I) were treated with pristane, fol‐lowed by A‐MuLV, and 40 (groulp II) were injected with AMuLV alone. Altogether, 16 lymphoid tumors developed in group I and 17 in group II. Nine oJ the tumors in group I and 4 in group II appeared as ascitic tumors. The ascites contained lymphoblasts and 10 to 45% plasrriacytoid cells. These tumors were designated as plasmablastic lymphomas (PLs). All tumors except one were transgene‐positive and did not carry translocations. An exceptional tunnor in group I carried a variant 6; 15 translocation but not the transgene. It obviously corresponds to the regular Abelson + pristane‐induced plasmacytoma. Among II tested PLs, 10 had a single retroviral insertion site, while one tumor showed 3. Among 18 untreated transgenic descendants (group III), chosen randomly during serial back‐crosses, 15 (83%) developed lymphomas, with no sign of plasmacytoid differentiation. The incidence was comparable in all 3 groups, assuming 50% of the mice in groups I and II to be transgenic. The time distribution of tumor development was also similar. Spleen cells from transgene‐carrying mice with no clinical sign of lymphoma were infected in vitro with A‐MuLV and transplanted i. p. into BALB/c recipients. PLs developed in 26 of 31 pristane‐treated recipients, but in only one of 18 untreated recipients. One of 6 PLs tested was monoclonal, whereas the remainiing 5 were oligoclonal. They all expressed v‐abl. These results show that some of the preneoplastic B‐cells that expressed constitutively active rnyc transgene turned into plasmablasts after infection with AMuLV. Full development of their neoplastic potential was facilitated by the presence of pristane‐granuloma.