Sixty per cent of BALB/cAnPt mice injected intraperitoneally (i.p.) wi
th tetramethylpentadecane (pristane) develop plasmacytomas (PCs), wher
eas less than 10% of BALB/cJ develop such tumours. Most other mouse st
rains are completely resistant. Resistance is dominant over susceptibi
lity in F1 hybrids between BALB/cAnPt and the resistant non-BALB/c str
ains, suggesting that susceptibility may be due to some genetic defect
. (BALB/cAnPtxBALB/cJ)F1 hybrids have a PC incidence of 36-42%. Previo
usly, BALB/cJ has been shown to harbour at least one resistance gene (
Potter et al., Genomics 1988, Vol. 2, pp. 257-262). On the assumption
that BALB/cJ may contain a segregating resistance gene, we crossed BAL
B/cJ females with pristane-pretreated BALB/cJ males that were found to
be carrying PC cells intraperitoneally 5-7 months after pristane trea
tment. After two selective crosses, 62% of the BALB/cJ subline BALB/cM
2/22 developed PC after pristane and 52% after pristane followed by Ab
elson virus, while unselected controls had an incidence of 11% and 0%,
respectively. Moreover, six spontaneous plasmacytomas developed in un
treated females of the selected colony. Five of these carried T(12; 15
)(F2; D2/3) translocations. The sixth had a T(1; 10)(G; C1) translocat
ion and an interstitial duplication of segment (C1/E3) on one chromoso
me 5. It may be concluded that pristane treatment is not a prerequisit
e for the induction of the PC associated Ig/myc translocations. (C) 19
97 Elsevier Science Ltd.