Decreased Nkx3.1 protein in Lo-MYC mice was also verified by western blotting of ventral prostate lysates (Figure 3J).
Transgenic adenocarcinoma of the mouse prostate.
We used animals designed to develop this disease, Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mice, to investigate the potential role of AHR signaling in prostate cancer development.
Primary prostate colonies from DsRED transgenic mouse prostate cells were trypsinized and dissociated into single cells.
Study of tumor development in mouse prostate cancer models can be instrumental in understanding human prostate cancer.
RNA from microdissected mouse prostate stroma and epithelium, and human prostate fibroblast (PSC27) were used as template for qRT-PCR.
Moreover, overexpression of Skp2 in mouse prostate leads to prostate intraepithelial neoplasia (PIN) [50].
TRAMP-C2 is a murine prostate cancer cell line derived from TRAMP mice (transgenic adenocarcinoma of mouse prostate) that spontaneously develop prostate cancer (Greenberg et al, 1995).
Similarly, CD73 deficiency also suppressed tumorigenesis in transgenic adenocarcinoma of mouse prostate (TRAMP) mice models [ 39].
These antigens include recombinant mouse prostate-acid phosphatase (PAP Fongng et al, 2001), human PAP (Small et al, 2000), PSA proteins or RNA (Heiser et al, 2002; Barrou et al, 2004), PSMA peptides (Tjoa et al, 1996), allogeneic tumour lysate (Pandha et al, 2004) and RNA amplified from autotumour cells (Heiser et al, 2001).
mPIN was not seen in WT mouse prostates.
