I was diagnosed with hormone sensitive PC in Spring 2019 (PSA 119) and then diagnosed with CRPC in summer 2020 (PSA .252). My PSA stayed relatively low from Summer 2020 through Summer 2021 (PSA .252 to 2.154) and at the same time my scans showed some progression in my bones but also spread to a few lymph nodes. My MO suspected that I may have progressed to neuroendocrine cancer. I had a lymph node biopsy in summer 2021 and it showed NEPC.
But a few days ago I had a PSA test and it was 15! My MO did not expect it since she thought had progressed to NE cancer. Has anybody seen this before? Thanks!
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Danielgreer
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Well, you certainly do not have all NEPC with a PSA of 15. But often it is a component along with acinar adenocarcinoma. That's why the first choice often is a combination of docetaxel and carboplatin. Any actionable info from IHC or genomics?
Thanks Tall for the quick response. I did two cycles of Etoposide and Carboplatin which didn’t show much of an impact in the scans so I’m switching to Docetaxel and Carboplatin tomorrow. I’m not sure why my MO started with Etoposide and Carboplatin? Any ideas? Regarding genomics, I haven’t had my biopsy tested yet but did find that I inherited ATM through germline.
There are varying degrees of neuro-endocrine differentiation since it's a mixture. My understanding is that Etoposide and Carboplatin (also used for de novo small cell PCa and SCLc) is more beneficial for prostate cancers that have a higher level of neuro-endocrine differentiation and Docetaxel/Carboplatin for those that have a lower level of NEPC cells.
This does not address your main question but I believe patients should be more aware of their PSA DOUBLING TIME. This (calculated) metric is more meaningful than the absolute PSA value. There is a neat online tool for calculating your PSA doubling value on MSK’s website (just enter dates and PSA lab results). In my opinion, MO’s don’t always pay sufficient attention to PSA doubling times (otherwise, they should rarely be “surprised” by a PSA reading). When I was taken off Zytiga, my PSA doubling time increased from 3 weeks to 3 months. My MO hasn’t even noticed or commented on the significance of this (that is not to say that a 3 month doubling time is all that wonderful either! ) 😀
That was my experience too. I read a paper (I wish I could find it again!) which suggested Zytiga can sometimes speed up cancer growth rates in soft tissues (ie not bone). If this is true, I imagine it will be suppressed/no commercial sponsorship will be devoted to confirming it. Did your MO determine Zytiga was no longer working for you?
One thing that seems fairly consistent about prostate cancer is it is a polyclonal cancer. So you may have one clone that responds well to therapy and if it is the dominant clone all looks good for an indeterminant and unpredictable period until another clone takes over (simple view but supported in literature). With regard to neuroendocrine prostate cancer you may want to look into trials by AMGEN for one of their BITEimmune-oncology therapies. The following link may help ascopubs.org/doi/abs/10.120...
I believe City of Hope may also be involved now via Tanya Dorff, MD.
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