Genetics of Susceptibility to Plasmacytoma Induction. I. BALB/cAnN (C), C57BL/6N (B6), C57BL/Ka (BK), (C × B6)F 1 , (C × BK) F 1 , and C × B Recombinant-Inbred Strains

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Abstract
Plasmacytomas were found in 58% of 373 BALB/cAnN (C) mice given three 0.5-ml doses of minerai oil (Bayol F or light mineral oil) or 2,6,10,14-tetramethylpentadecane (pristane) ip. The incidence of plasmacytomas in C57BL/6N (B6), C57BL/Ka (BK), (C × B6)F1 and (C × BK)F1 was 6.4, 0, 11.5, and 16.5%, respectively. The plasmacytomas occurred in old B6 mice, in contrast to their early appearance in strain C mice. The incidence of plasmacytomas in mineral oil-treated or pristane-treated C × B recombinant-inbred (RI) strain mice was 28.3% in C × BD, 17.5% in C × BE, 36.5% in C × BG, 0% in C × BH, 2.9% in C × BI, 48% in C × BJ, and 4.3% in C × BK. C × BD, C × BG, and C × BJ strains were considered susceptible to plasmacytoma induction by mineral oil or pristane; C × BE had a low susceptibility, and C × BH, C × BI, and C × BK were resistant. The results suggested that there were only a few gene differences between C and B6 or BK that determined susceptibility or resistance to plasmacytoma induction, and that B6 and BK have at least one dominant resistance gene. The distribution pattern of susceptibility and resistance in the C × B RI strains suggested the presence of a resistance gene on chromosome 9, linkage group II.

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