Department of Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York, NY 10461, USA

Correspondence to: Nicole Schreiber-Agus, Department of Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York, NY 10461, USA

The pathogenetic basis of prostate cancer remains highly elusive; its clarification could be facilitated greatly by laboratory and clinical models of the disease. Although the genetically manipulated mouse has been invaluable for the modeling of other human cancer types, it has fared less well with respect to prostate cancer. Nevertheless, several highly valuable transgenic models exist and are highlighted in this review. Emerging reagents and strategies may allow us to use the mouse more effectively to define the molecular, cellular and physiological events that lead to prostate cancer initiation and progression.

mouse model; prostate cancer; transgenic

BPH, benign prostatic hyperplasia; CGH, comparative genomic hybridization; FISH, fluorescence in situ hybridization; MAR, matrix association region; MMTV-LTR, mouse mammary tumor virus long terminal repeat; MPR, mouse prostate reconstitution; PIN, prostatic intraepithelial neoplasia; PSA, prostate specific antigen; PSBP, prostatic steroid binding protein; SCID, severe combined immunodeficient; TRAMP, transgenic adenocarcinoma mouse prostate