D-type cyclins regulate androgen receptor function in prostate cancer cells. A) Cyclin D1 is induced following androgen stimulation, and acts through discrete mechanisms to both promote cell cycle progression and attenuate androgen receptor (AR) activity (left panel). These control mechanisms are hypothesized to modulate the strength and duration of the androgen response (right panel). B) The cyclin D1b variant harbors enhanced oncogenic function as compared to cyclin D1, and interrogation of cell cycle function suggests that cyclin D1b may impinge on additional factors to promote proliferation. In the context of prostate cancer, compromised ability of cyclin D1b to modulate AR function may disrupt modulation of the androgen response, and yield an enhanced proliferative response.