This week in techniques



Licensing status

Publication and contact information


Genomic rearrangements in the androgen receptor (AR) as an androgen-independent prostate cancer resistance mechanism

In vitro studies suggest genomic rearrangements in the AR gene driving androgen-independent prostate cancer growth could help predict drug response. In castration-resistant prostate cancer tissue samples, X-chromosomal rearrangements were identified that led to the exclusive production of truncated AR variants lacking the ligand-binding domain. In prostate cancer cells, genomic rearrangements introduced into the wild-type AR gene by transcription activator-like effector nuclease (TALEN)-based genome editing caused androgen-independent cell growth. Next steps include validating and qualifying the resistance mechanism as a biomarker.

SciBX 6(43); doi:10.1038/scibx.2013.1243
Published online Nov. 7, 2013

Patent applications filed covering the TALEN method and AR isoforms in prostate cancer; TALEN method licensed; additional methods, receptor isoforms and genome-edited prostate cancer cell lines available for licensing

Nyquist, M.D. et al. Proc. Natl. Acad. Sci. USA; published online Oct. 7, 2013;
Contact: Scott M. Dehm, University of Minnesota, Minneapolis, Minn.
Contact: Daniel F. Voytas, same affiliation as above