PCS, a Gene Related to the Immunoglobulin Super Family of Axonal Glycoproteins is Expressed in Murine Plasma Cell Tumors

Abstract

Intraperitoneal plasma cell tumors (PCTs) are induced by pristane (tetramethylpentadecane), a branched-chain alkane paraffin oil, in BALB/cAn and other susceptible mouse strains with minimal to mean latencies of 120 to 210 days respectively (Potter, 1972). PCTs harbor one of two reciprocal chromosome translocations always involving band D2/3 on chromosome 15 and either the Immunoglobulin heavy chain (IgH) locus on 12 or the kappa light chain locus (IgK) on 6 (Ohno et al., 1979). Band D2/3 was subsequently found to be the c-myc gene locus and the activation of this proto-oncogene by such chromosomal rearrangements has been shown to be a contributing factor for plasmacytomagenesis (reviewed by Mushinski, 1988; Marcu et al., 1992). Plasmacytomagenesis was rapidly accelerated (50–120 day mean latencies) upon injection of oncogene-containing retroviruses (v-abl, myc and raf or myc and ras) along with pristane (Potter et al., 1973; Ohno et al., 1984; Potter et al., 1987; Clynes et al., 1988; Troppmair et al., 1989) and viruses-containing an activated myc oncogene induced PCTs without c-myc associated chromosome translocations (Potter et al., 1987; Clynes et al., 1988; Troppmair et al., 1989). Recently, a retrovirus harboring v-abl and c-myc was found to be the most potent oncogene combination inducing PCTs in 100% of adult BALB/c mice with or without a wild type Moloney helper virus and also in the absence of pristane (Weissinger et al., 1991). These observations would collectively argue that multiple genetic events in addition to c-myc activation are required for malignant plasma cell tumor formation. Indeed, at least three recessive genetic loci are believed to confer resistance to PCT formation in non-sensitive mouse strains but the identities of these genes and other dominant acting ones in addition to myc remain unknown.