The scan report reveals that there is a modest improvement visible in the liver and that the liver has shrunk a little but that there is still extensive illness. The radiologist gave one example where the mets have shrunk from 28 mm to 24 mm. The CT scan report also shows that there are no new mets anywhere.
AST and ALT are still improving.
The PSA is 253. We asked the doctor again if he had any explanation for this and he said that the only explanation he could think of was that perhaps the Chemotherapy was the reason and that the prostate cancer cells that get killed by the Chemotherapy were going around in Paul's bloodstream. Hm, that sounds like a strange explanation to me, what do you think?
So we had the fourth Carbo infusion today and will have two more after that. Then they will repeat the scan.
Still Paul has no other side-effect apart from fatigue.
Best wishes to all
Mel.
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MelaniePaul
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My understanding is the kind of cancer cells that typically go after the liver and respond well to Carboplatin don't express the PSA. I think at this point its more important to look at the imaging and symptoms than the PSA. You are doing the best treatment you can right now and it's working. That's really what matters most.
I have heard that theory on why psa increases, because they are dead but still in blood stream Many Times in the past. It is good that the scans show decrease , and that the liver looks better. The scans are a more reliable indicator at this point than PSA, as Gregg said. It is also remarkable that he is doing docetaxol with carbo, and only real SE is fatigue, He is tough! We can always sleep more. I wish you both the best , and please keep us posted.
I am happy for you that it is shrinking and not growing. I have heard about labs or markers increasing when there is tumor die off. Hopefully that is the case. Keep up the good work. Hugs to you!
Like Paul, my PCa has metastasized to my liver and I have already used all available drugs. My chemo combo is Docetaxel and Carboplatin and have completed 3 cycles.
My understanding is that Docetaxel is used against "normal" PCa and its mets, but PCa in liver is best attacked by Carboplatin (and PCa in liver does not express PSA so progress is measured by scans, primarily an MRI).
My concern for Paul would be where, besides his liver, is the PCa that is seemingly untouched by Carboplatin? Has he had a recent full body Axumin PET/CT?
What else is Paul taking for his prostate cancer? Was he not able to take both Docetaxel and Carboplatin together? What was his PSA at beginning of chemo?
Sorry for all the questions, but his doctor's explanation does not make sense to me, especially with PCa in Paul's liver.
I agree with you in saying that it all doesn't make much sense. And, while we are celebrating the good news that the mets in the liver are shrinking, we are still wondering what is going on.
PSA doubled from 129 to 253 within two months. The latest CT scan shows that there are no new mets in bones, that the organs are clear and that in the liver, which is the only organ with mets, the mets are slowly but steadily shrinking. So, like yourself, I am wondering: Where is the growth? Can it maybe not be picked up by a scan? Or is it true that it is PSA from cells dying? And that would only make sense if prostate cancer in the liver would express PSA, which it doesn't do.
Paul wasn't able to combine both therapies because of his general health, they felt it would be too toxic for him and too much for the body to handle. I would think so too. But don't know... I think they should have tried it...
Paul's Alkaline Phosphatase level? Where would I find that out? Is it one of the blood markers and what is the abreviation? I can certainly have a look. I will get back to you on that.
Paul is only on ProStop (3-monthly) and on Prednisolone and on the Chemotherapy. But he was for years on the hormone treatments and for three years on Zytiga, finished in July of this year.
It seems to me that he still has some of the prostate cancer cells that express the PSA. At some point the PSA value is really not very useful any more. The main focus should be on looking at the scans for mets and also how he feels. There is a chance that his prostate cancer will regain some hormone sensitivity and those androgen-based treatments will have some effect again. Of course he would have to be able to tolerate them. Just a thought. Just out of curiosity, is Enzalutamide available for him?
Well, Paul is very sleepy all the time, something which could be due to the Chemo itself as well as to the cancer, hard to know. But it is really extreme; so much so that he can't sit down and listen to a podcast without falling asleep, he would nap all day if he didn't feel that at some point he wants to get up and do things.
But other than the fatigue he doesn't have any problems, no aches or pains, no nausea, no weight loss.
Is Enzalutamide Xtandi? Yes, that is available to us here, but his oncologist was of the opinion that we shouldn't try it. That was back in July when he discovered the spread to the liver. He said it was so serious that we really had to do Chemo now and not try any other hormone treatments.
Mel.
Mel, from the time that I did my six-month Chemo Trial in 2004, it took 12 months from the end to the first <0.1 PSA reading. In other words, the cancers cells floating around in the vascular and lymphatic systems took a year to completely die off.
Well, I am asking myself: If the dead cancer cells floating around in Paul's system show PSA, then shouldn't the PSA be exactly the same as before because the cells are still the same, the only difference is that the cells are dead now? And the scan showed that there are no new mets, so with cells dying but no cancer growing the PSA should get lower?
So, I am not a biologist or biochemist or any other expert, but it doesn't seem to be true... The explanation doesn't make sense...
As I understand it, an increase in PSA after any new treatment can be do to what is know as the PSA Flare Effect. As the cancer cells die, they decompose and give up their PSA. This causes the temporary increase in PSA.
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