Bipolar androgen therapy (BAT) has intrigued me since 2015 when I first wrote about it. But the nagging question has always been, and still is, what are the biomarkers that determine if BAT helps, hurts, or does nothing other than provides a nice vacation from ADT? A small trial suggests that there may be genomic predictors. They found that some mCRPC patients got a better PSA response from BAT if they had germline (inherited) or somatic (tumor biopsy) genomic mutations of the tp53 gene and one of either RBI gene or PTEN gene loss. It did not guarantee success - in fact 7 of the 17 men with tp53+PTEN loss had increases in PSA on BAT, and in 3 of the 7 men with increases, PSA more than doubled, indicating that BAT may have made them much worse off.
They also pointed out that in the recent trial of cabazitaxel+carboplatin at MD Anderson, the same genomic predictors of success were found. They propose a comparative trial of the 2 therapies in men who have mutations in tp53 and one of the two (either rb1 or pten).