Thursday, October 3, 2013
Although numerous papers have detailed how
castration-resistant prostate cancers become refractory to Xtandi enzalutamide and
other second-generation androgen receptor
antagonists, comparatively little is known about how the disease eventually
evades CYP17 inhibitors such as Zytiga abiraterone.
Findings from a Cleveland Clinic team could change
that, as the group has detailed how some tumors engage an alternative synthesis
pathway for androgen.1
L. SciBX 6(38);
Published online Oct. 3, 2013
1. Chang, K.-H. et al.
Cell; published online Aug. 29, 2013; doi:10.1016/j.cell.2013.07.029
Contact: Nima Sharifi, Cleveland Clinic, Cleveland, Ohio
2. Attard, G. et al. J.
Clin. Endocrinol. Metab. 97, 507-516 (2012)
AND INSTITUTIONS MENTIONED
Aragon Pharmaceuticals Inc., San Diego, Calif.
Astellas Pharma Inc. (Tokyo:4503), Tokyo, Japan
Cleveland Clinic, Cleveland, Ohio
Fred Hutchinson Cancer Research Center, Seattle, Wash.
Johnson & Johnson (NYSE:JNJ), New Brunswick, N.J.
Medivation Inc. (NASDAQ:MDVN), San Francisco, Calif.
Progenics Pharmaceuticals Inc. (NASDAQ:PGNX), Tarrytown, N.Y.
Seragon Pharmaceuticals Inc., San Diego, Calif.
Tokai Pharmaceuticals Inc., Cambridge, Mass.
University of Michigan Medical School, Ann Arbor, Mich.
The University of Texas Southwest Medical Center, Dallas, Texas
University of Washington School of Medicine, Seattle, Wash.