The C3(1)/TAg transgene has the 5' flanking region of the rat prostatic steroid binding protein gene [C3(1)] directing expression of the early region of simian virus 40 large tumor antigen (TAg) to prostate and mammary gland tissues. The original C3(1)/TAg founder line C contained ~six transgene copies at a single locus in the telomeric portion of chromosome 6 (which contains the Ki-ras proto-oncogene) - resulting in multistage oncogenesis in prostate and mammary gland (see Stock No. 013591).
From that original line, the C3(1)/TAg-REAR subline (Stock No. 030386) was identified with transgene rearrangement/deletion to only one copy (or a partial copy) in the original chromosome 6 locus. As a result, C3(1)/TAg-REAR mice exhibit no spontaneous cancer phenotype and retain immunological tolerance to cells expressing TAg (including tumors from the C3(1)/TAg and TRAMP models). C3(1)/TAg-REAR have a normally functioning immune system - as evidenced by a normal complement of subclasses of immune cells and the rejection of both human tumor cells and murine tumors derived from a non-FVB/N background. Additionally, induction of an anti-tumor immune response can be elicited in C3(1)/TAg-REAR mice (e.g., irradiated C3(1)/TAg tumor cell vaccination significantly inhibits growth of injected C3(1)/TAg-derived mammary fat pad tumors). Furthermore, C3(1)/TAg tumors or cell lines can be implanted synchronously into the mammary fat pads of large cohorts of immunocompetent C3(1)/TAg-REAR mice - this bypasses the need to wait for tumors to develop spontaneously in multiple transgenic mice over a variable time course and allows therapeutic interventions to be performed in a relatively short timeframe.
Mice hemizygous or homozygous for the C3(1)/TAg-REAR transgene are viable and fertile with normal breeding, and no spontaneous overt phenotype.
