Undetectable PSA results from Olaparib; now starting to rise.

[HopingForTheBest1]

BRCA2+. After experiencing recent rise in my PSA , from undetectable for over a year to 0.02 to 0.05 to 0.14 in less than 3 months, I am searching for possible next steps. Have been on Olaparib for 18 months, in addition to ADT (Eligard).

While my PSA# is still small, I am concerned about the level of acceleration and possibility that Olaparib has run its' course.

Less exercise due to COVID for the past several months may be a contributing detrimental factor.

My next oncologist's appointment is coming up, and I want to come prepared with viable ideas to discuss, including possible PSMA scan. But, due to my current low PSA #, I expect I am probably limited as to what scans may be useful at this point.

I can easily drive to the NIH in Bethesda MD where they are conducting a PSMA clinical trial (NCT03173924) . Spoke to the nurse coordinator yesterday (8/6/20), and due to COVID they have not been accepting very many if any new participants.

[Ahk1]

I did the one at NIH last year. The people there are great. Unfortunately , my psa doubled since then. Tough choices.

[HopingForTheBest1 in reply to Ahk1]

Did your PSMA scan find cancer cells that other scans didn't? Did you also have theranostic treatment?

[Ahk1 in reply to HopingForTheBest1]

I did it at .6 psa and it didn’t find anything. I have not had any other treatments aside from the RP and SRT.

[Tall_Allen]

1) When PARP inhibitors work, carboplatin usually works too when used in sequence. But wait to see radiological progression.

2) Low PSA may not preclude detection by a PSMA scan, when there is a rapid PSADT or a type of PC that expresses little PSA. Always a good idea to get an FDG PET the next day.

3) A biopsy of a metastasis (histology and IHC) may tell you if your cancer is PSMA-avid even without a PSMA-PET/CT (If you can't get to or afford a PSMA PET/CT at UCLA). That may tell you if you're a good candidate for any of the PSMA-targeted therapies now in clinical trials.

[HopingForTheBest1 in reply to Tall_Allen]

Thank you Allen. I always value your input.

[Hidden in reply to Tall_Allen]

My doctor said the same thing about Carboplatin at my last appointment. He said he would treat a patient with a BRCA mutation first with a PARP inhibitor, then Carboplatin.

[Moespy]

Had the PSMA Scan at NIH 2 years ago at 0.5 PSA. This was my 2nd recurrence after RP in 2011. Had IMRT to Prostate Bed after 1st recurrence. PSMA Scan lit up a Pelvic Lymph node, I then requested and had a biopsy of the node at NIH. It came back positive for PCa. I immediately started Lupron and then had IMRT to the entire Pelvic Region with a higher dose to node area.

That was 18 months ago and I remain undetectable. I will have my last 6 month Lupron shot early next month and then cross my fingers going forward.

The PSMA Scan at NIH changed my treatment plan and gave myself and my RadOnc confidence to move forward with radiation to the Pelvic Area.

[HopingForTheBest1 in reply to Moespy]

Thanks for your encouraging reply.

[Pleroma]

I am about a year behind you - also BRCA-2+

Starting Olaparib next month. I just had a PET scan with PSA of 0.6 after being undetectable for few months. 8 new bone mets seen.

Clearly a more aggressive cancer in my case.

I talked with my doc about future treatments after Olaparib fails. He believes we still have options - LU-177 (if feasible), taxotere or jevtana with CarboPlatin with an Xtandi thrown in somewhere.

We with BRCA-2 seem to be at a disadvantage in the PC game.

Good luck and keep us posted.

[HopingForTheBest1 in reply to Pleroma]

Thanks for your response. BRCA2+ definitely predisposes us to aggressive PC. My Gleason score is 10.

[p3d1]

Ask if you can try Rucaparib, another Parpi but women with ovarian cancer are getting a benefit from challenging with a different parp.

They are two different compounds so what is escaping the first may not be able to bypass the second. Also check your mutations, some guys on Rucaparib with BRIP, FANCA and others did very well.

[HopingForTheBest1 in reply to p3d1]

Thanks for responding. My Oncologist had told me that PARPs work the same way, and using another one would not be effective. My genetic test did not reflect BRIP nor FANCA.

Any resources I can follow-up on, especially to challenge my doctor, would be appreciated.

[p3d1]

Look up - Facebook - Parp Inhibitors - Drugs and Trials. It is run for anyone using a PARPi but mostly it was Ovarian cancer as that was the first approval. These women have been on these Parp treatments for years. It is indicated for repeat use in OC and also as a maintenance drug. You need to join the Facebook group but the application only takes a couple of days in my experience. I remember reading of some women getting benefit from the second and third Parpi, not everyone but some did and have been doing well.