V‐ABL does not abolish IL‐6 requirement by murine plasmacytoma cells

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Abstract
Activation of c‐myc by juxtaposition to an immunoglobulin locus and introduction of the v‐ab/ oncogene act synergistically in generating a mouse plasmacytoma (PC). The question arose whether the effect of v‐ab/ could be attributed to a deregulation of interleukin‐6 (IL‐6) production or responsiveness, in view of the fact that IL‐6 exerts potent growth‐stimulatory activity on PC cells. We studied the effect of IL‐6 on the in vitro growth of primary PCs induced by pristane alone (TEPCs) or by pristane + A‐MuLV (ABPCs). Five of 13 TEPCs and 3 of 7 ABPCs responded to IL‐6. Macrophage supernatants prepared from both TEPCs and ABPCs had similar stimulatory effects on PC cells. From 30 primary PCs (including both TEPCs and ABPCs), we established 9 in vitro lines, 2 of which expressed v‐abJ. All were able to grow on macrophage feeder layers. Three types of behavior could be distinguished on the basis of growth in feeder‐free cultures in the presence and absence of IL‐6. Group I contained 4 IL‐6‐dependent lines. Group II contained 2 IL‐6‐independent lines (one v‐abl expressor) that grew faster In the presence of IL‐6. Group III consisted of 3 feeder‐dependent lines (one v‐ab/ expressor) that were not significantly stimulated by IL‐6. These findings indicate that v‐ab/ expression does not Influence IL‐6 dependence or responsiveness by itself. The supernatant of one line in group II was able to stimulate PC cells. All 6 lines of Groups I and II carried a typical (12; 15) translation, while all 3 lines in group III had a variant (6;15) or (15;16) translocation.

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