CRPC (Castrate Resistant Prostate Cancer)
I had surgery 9 years ago, PSA 31, Gleason 7, negative margins, local spread. PSA jumped after surgery, went on Casodex, the Lupron which I am still on. PSA non-detectable for 7 years. Then it slowly started doing up every three month check-up and Lupron shot: .2, .3, .4, .5, etc. until it reach .9 last month. I've discussed this but my oncologist (a prominent researcher) doesn't seem too concerned. I get the impression that unless it jumps suddenly or I become symptomatic, I need not worry. He's never mentioned RT although I've noticed other postings where doctors recommend it when PSA hits .2--.5. Should I be concerned?
Will
Comments
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Thresholds and AAWR
Will
Welcome to the board.
I think that your doctor is in the “good track”. He seems not to worry but the info you shared regarding the increasing PSA does not indicate yet that you are CRPC (hormone refractory). Probably he is waiting for “that” threshold he considers a patient in such a status.
The first thing to do is to check the effectiveness of the therapy with a testosterone test. Usually refractory occurs when one is in castration levels (T= less than 30 ng/dL) but with a rising PSA.
If the present HT protocol is not working effectively, then you may increase the dose of the antiandrogen (50 to 150 mg) or change to other medication of the same type (Lupron to Eligard or Firmagon; Casodex to Cyproterone, etc.). If such still does not lower the PSA, then you may try drugs of 2nd-line HT (such as Zytiga, Ketoconazole, etc.) which will address the intratumoral effects of the cancer cells.
All of the above drugs relate to hormonal manipulations.There is another way to ascertain of CRPC by withdrawing the antiandrogen (such as Casodex). If the PSA decreases once one stops taking the antiandrogen then such is indicative that the cancer is “feeding” on the drug reflecting hormone refractory. You can read about this condition on the net here;
http://www.ncbi.nlm.nih.gov/pubmed/18383517
http://prostate-cancer.org/aawr-the-anti-androgen-withdrawal-response/Better to discuss with your oncologist about details on the above and request for his reason for “doing nothing”. What is his threshold to judge refractory?
Hope for the best.
Best wishes for 2014
VGama
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Post Therapy PSAVascodaGama said:Thresholds and AAWR
Will
Welcome to the board.
I think that your doctor is in the “good track”. He seems not to worry but the info you shared regarding the increasing PSA does not indicate yet that you are CRPC (hormone refractory). Probably he is waiting for “that” threshold he considers a patient in such a status.
The first thing to do is to check the effectiveness of the therapy with a testosterone test. Usually refractory occurs when one is in castration levels (T= less than 30 ng/dL) but with a rising PSA.
If the present HT protocol is not working effectively, then you may increase the dose of the antiandrogen (50 to 150 mg) or change to other medication of the same type (Lupron to Eligard or Firmagon; Casodex to Cyproterone, etc.). If such still does not lower the PSA, then you may try drugs of 2nd-line HT (such as Zytiga, Ketoconazole, etc.) which will address the intratumoral effects of the cancer cells.
All of the above drugs relate to hormonal manipulations.There is another way to ascertain of CRPC by withdrawing the antiandrogen (such as Casodex). If the PSA decreases once one stops taking the antiandrogen then such is indicative that the cancer is “feeding” on the drug reflecting hormone refractory. You can read about this condition on the net here;
http://www.ncbi.nlm.nih.gov/pubmed/18383517
http://prostate-cancer.org/aawr-the-anti-androgen-withdrawal-response/Better to discuss with your oncologist about details on the above and request for his reason for “doing nothing”. What is his threshold to judge refractory?
Hope for the best.
Best wishes for 2014
VGama
I have been on this merry-go-round for a year now and have no more idea where I stand than I did when I started. After 10 years of rising PSA (60) and negative biopsies, my (new) urologist performed a turp biopsy and found a small G7 tumor. After 8 weeks of RT and 8 months of Lupron, my PSA is <.1. So what does this all mean? Should I continue on HT and fret about my PSA forever? My dad's PSA was in the teens for decades, and he died at 88 from non PC causes. Is diagnosis anything more than reference to a probability table?
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"Probability Table"
Dear Woodie
It seems that you got the answer in your question. Diagnosis in PCa is more than a probability; it is the reality of being positive to cancer. The PSA is just a marker (probably the best in present times) indicating risks and prognosis in a case of PCa. Your dad most probably had no PCa case but a high level of the PSA serum produced by prostatic cells. Only a biopsy could in fact diagnose him for cancer, which it seems that he never had "any".
I recall your previous thread (http://csn.cancer.org/node/257218) discussing about the combo treatment of HT plus RT. It seems that it did well in your case as per the constant remission levels in PSA. In any case, the portion that killed the bandit was the radiation and such success can only be ascertained once you lose the effects in your body from the HT portion. This can be achieved two to six month pos the end of the HT treatment.
In other words, if the PSA is maintained at low levels after given up with the HT, you got into the “probability table” as a cured status or with cancer but in a indolent status. Only time will judge your case. Until then you may as well die of other causes.Please remember that you still got a gland in place producing serum PSA from benign prostatic cells. Those may increase the PSA level above <0.1 (ng/ml) but with no meaning of a risk of recurrence.
You have not shared your treatment protocol.
What Is the length of the period in adjuvant HT?
Can you tell what are the HT drugs used?Best wishes for a continuing remission.
VGama
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Thanks VG
I started four-month Lupron shots last April (at age 65) and 8 weeks of IMRT in June. My frustration stems from having undergone 10 years of procedures and still not knowing whether any of it was necessary. Is there any definitive test between PSA (probability) and metastisis (diagnosis)? It seems that many of the "5 year survivial" studies are largely retroactive confirmations of whether the participants had fast-growing or slow-growing PC in the first place. I feel as if I am undergoing rabies treatment as a precaution after getting bitten by a squirrel.
As always, I appreciate your knowledge and insight.
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