Plasmacytomas are readily induced in all sublines of Balb/c mice except Balb/c J following intraperitoneal injections of 2, 6, 10, 14 Tetramethylpentadecane (Pristane) (Potter et al, this volume). The molecular basis for resistance and susceptibility to plasmacytoma induction is not known but chromosomal aberrations (Ohno et al 1980 and 1984), viral ocogenes (Potter et al 1984) and growth promoting influences of granulomatous inflammation (Potter and MacCardle 1964) all appear to be associated with pathogenesis. Although the initial mutagenic event remains ellusive, generation of clastogenic oxidants and/or prostaglandin metabolites within oil-induced granulomatous inflammation may contribute to plasma cell tumor induction. This is further supported by the observation that the antiinflammatory drug indomethacin prevented development of plasmacytomas in susceptible strains (Potter et al, to be published). The present study examines cellular and microenvironmental features of oil-induced lesions in Balb/c sublines which differ with regard to susceptibility to Pristane-induced plasmacytomagenesis.