Are low PSA's more aggressive?

My PSA was at 16 at dx, and though I am a Gleason 7, my cancer has acted aggressive at every stage of treatment. My surgery "failed" within 9 months, then I have Salvage Radiation, and it failed in less than 9 months. My current PSA in December had climbed quickly back to 14.

David in SC

I meant to say, welcome to HW, in the first post. Glad you found our community on the net.

Yes, I too was dx. at age 56 in August of 2008. My PSA in 2007 was 5.8 and rose to 16.3 in the year before my dx, so PSA velocity prior to dx. has been a big issue with my case. I had open RP in November of 2008. I had SRT from October through November of 2009. (I had lots of post-surgery and post-radiation issues, some severe, but that is another story).

I have been seeing a great oncologist that only sees patients with advanced prostate or breast cancer for nearly a year now. Despite my rapid rise in PSA since the failure of the SRT, he is of the school that doesn't believe in early HT in most cases.

My cancer has appeared to be an aggressive variety, despite my "stats". I see him in a week, for my first PSA test since December, and depending on where the number is, we will either continue to "wait and see", or he is considering in me by-passing HT altogether and at some point, going on Taxotere mysefl.

Due to all my extreme poor quality of life issues going on, because of the other problems I encountered, he is in no hurry to burden me with additional side effects, until he feels its at the right time. I am ok with this plan, as I have enough to deal with, being 100% disabled, dealing with severe chronic pain and fatigue, etc.

He does not believe there is any one number to draw the line for further treatment. He is watching over me in an overall sense. He feels with the aggresiveness of my cancer, that HT wouldn't work for long, and that at this point, it is unknown where the remaining cancer dwells, which makes it harder to treat. He tends to think that there may be several (or many) micro mets that together, are producing the quick rising level of PSA that I do have. At this point, no one of these clusters are large enough to show up on available scans.

David in SC

There are no simplistic rules in PCa, full of anomolies, inconsistencies and even exceptions. Hopefully a great onco-doc would know via blood panel testings and urine testings for bone break down, as to how aggressive it all is. Pathology by experts aka molecular pathology can help define some precise causes like over expressed AR (androgen receptor) and other genetic tests that can be done, let alone define does this patient have a variant type of PCa or even variant types happening (it can happen, just like having more than one Gleason scoring found, it may be rare but has happened). We in effect have imperfect pathology analysis as usually done right now, lousy scannings for the most part, and less than perfection in docs assessments (generally) and kind of rushed into many treatments and some patients assisted into not getting multiple opinions which might be in their best interests.

I would guess if you had a ploidy DNA analysis on the PCa, it is not diploid type anymore, those are more like normal cells and have dual even pairs of DNA chains. The weirded ones are aneuploid, and another I heard about call teteraploid (spelling?) Three classes used to define DNA, as it gets away from Diploid status, the DNA chain ends up with randomness, broken chains, non-paired strands, then into say chaotic mess. (this can be tested original in pathology and some have done so, why it is not standard practice seems dumb to me), the more that can be known up front the better. Your pathology slides can be reviewed, stained for various specialized testings, and even molecular analysis can be done by a very few select pathologists whom know how to do such. Hope this quicky gives you an idea on PCa issues.

Zimac- what kinds of drugs is he using to fight his PCa, and do you have more info as to when drug failed and psa changes???? Checkout www.yananow.net  (experiences to find 1000+ patients journies and histories and some have emails available, likely find similar patients)

Post Edited (zufus) : 4/4/2012 6:39:06 AM (GMT-6)

My husband was first started on Lupron immediately after surgery. He had bone mets at the time and they were watching something in his lung. After one year he tried an experimental drug, ARN-509. His PSA remained .05 for another year. His next drug was Abiraterone because the lung nodes were increasing in size. It did nothing for him so after three months he was taken off of the Abiraterone.
Currently, his bone scans remain quiet but his lung nodes continue to increase so it was suggested to start the Taxotere. His QOL is great. He remains active, works daily with bouts of fatigue. I'm hoping the Taxotere will have some effect on the lung nodes.
My husband is being treated in NYC at one of the top prostate cancer centers there. This disease seems like a crap shoot to me, trying a little bit of this and a little but of that.

Zimac- seeing the drugs you did, that in effect are now failed, you are no doubt dealing Hrpca so see their website www.hrpca.org     look for tab on proven treatments just to see what is going on. There still are some possible choices, even though your doc would likely not mention or use them, this happens often in PCa issues. Leukine might be effective, so might emcyt or combo drugs even with chemo ideas.

JFN- thanks for the support, I have been looking at alot of these optional drugs for years, and have tried a few more protocols or concepts myself, results trumps everything!

RandomPseudoNym,,

Do you know of any HW members (or elsewhere) that have that version of PC (There is an ugly subset of G8-9-10 tumors that produce very little PSA)?

It would be interesting to compare notes with them.  I certainly have the low PSA, high gleason, etc... thing going on, but generally controlled at the moment.

Thanks

Jerry

And my PSA after surgery/ adjuvant RT has been doubling at ~ 90 days. Currently 1.3.