In plasmacytomas samples we found methylation of p16 in 55%, p15 in 22%, MGMT in 67% and DAPK in 44%. hMLH1 was unmethylated in all cases of MGUS and plasmacytomas.
When tested with wild-type (DBA/2) p16, both A134C and G232A BALB/c-specific variants of p16 were inefficient in their ability to inhibit the activity of cyclin D2/CDK4 in kinase assays with retinoblastoma protein, suggesting this defective, inherited allele plays an important role in the genetic susceptibility of BALB/c mice for plasmacytoma induction and that p16(INK4a) is a strong candidate for the Pctr1 locus.