title: Evasion of targeted cancer therapy through stem-cell-like reprogramming.
abstract: Prostate cancer variants expressing alternative lineage markers appear at relapse from antiandrogen therapy. We show that loss of the retinoblastoma (RB1) and tumor protein 53 (TP53) genes drives expression of stem cell reprogramming factors, lineage plasticity, and antiandrogen resistance. Epigenetic manipulation restores antiandrogen sensitivity-suggesting an approach for treating lethal prostate cancers.
authors.affiliation: Department of Pharmacology & Therapeutics, Roswell Park Cancer Institute , Buffalo, NY, USA.
authors.forename: Kristine M
authors.initials: KM
authors.lastname: Wadosky
authors.affiliation: Department of Oncologic Pathology, Harvard Medical School, Brigham and Women's Hospital, Dana-Farber Cancer Institute , Boston, MA, USA.
authors.forename: Leigh
authors.initials: L
authors.lastname: Ellis
authors.affiliation: Department of Pharmacology & Therapeutics, Roswell Park Cancer Institute , Buffalo, NY, USA.
authors.forename: David W
authors.initials: DW
authors.lastname: Goodrich
keywords: Epigenetic reprogramming; mouse models; prostate cancer; therapeutic resistance; tumor suppressor genes