UroToday.com published a dual-center study today that confirms that carboplatin and paclitaxel (a taxane product) has an active effect on PSA when used in the treatment of men with castrate resistant prostate cancer (CRPC) after docetaxel (chemotherapy for prostate cancer).
The study reported that even though the majority (88%) of the subject men were docetaxel refractory, 76% still experienced a decline in their PSA score, with 19 of 25 having a PSA decline >30% (Figure 1). However, remember that a decrease in PSA may not mean that there will be either slower disease progression of a survival advantage.
They reported that the carboplatin and paclitaxel regimen was well tolerated (with no grade 3-4 non-hematologic toxicities), even in the men who were up to age 80 years. Although retrospective in nature and only including 25 men, this is the first study to report clinical outcome using this regimen.
Previous phase II trials of carboplatin, paclitaxel, and estrumustine showed similar response rates but they also showed significantly higher toxicity, this study supports the use of carboplatin and paclitaxel with the omission of the estramustine.
The recent approval of cabazitaxel (Jevtana) by the U.S. FDA because it demonstrated a survival benefit for cabazitaxel over mitoxantrone demonstrated that men can still respond with an additional survival advantage to another taxane (docetaxel is a taxane) after progressing on docetaxel.
Not all of the men in this study (nor in the TROPIC trial which demonstrated the survival advantage for cabazitaxel) ) were docetaxel-refractory, but the results are clear. Men can derive a clinical advantage from a second taxane treatment Further study is warranted exploring issues of taxane resistance and secondary taxane use.
Original article written by:
Himisha Beltran, David M. Nanus, and Scott T. Tagawa as part of Beyond the Abstract on UroToday.com.
Joel T Nowak, M.A., M.S.W.
After many years of edcating myself on this disease, I still do notunderstand how disease progresses while psa declines. My husband was dx at a psa of 112,1.65 nadir on Lupron, is now resistant and failed 2nd & 3rd line HT and is on 5th cycle of Taxotere, PSA was 34 at 1st cycle, up to 44 at 2nd, 34 at 3rd and now 19 , HOWEVER pain is increasing again in back and hip, already had radiation to spine in Jan and things seem to be progresing despite drop in PSA, Can anyone explain this?
Around 10% of all prostate cancer does not generate significant PSA. This is one reason that PSA is not accepted by the FDA as a surrogate bio-marker. This is the reason that clinical trials must wait for the actual deaths of our brothers.
Joel