Do False-Stable results exist? My latest tests
Speaking as one of the New Kids On The Block, I have been reading the archives, now back to 2012, and I want to express gratitude to the long timers for continuing to post all these years so new guys to this experience can find solace and much needed information for just about every jot and tittle there is to know about PC. Why watch fakey tv medical shows when there is stark and honest reality, sometimes sad, sometimes encouraging, sometimes tragic, sometimes finding light in the darkest places.
We do need more humor though. You guys need to step it up in the comedy dept. How come there's no comedians in this forum? Is there a correlation between wisecracking and PC resistance? If so, maybe we should break out a few one liners about prostates. Jokes about BPH and my prostate... it's the next big thing.0
VascodaGama Member Posts: 3,595 MemberAlso Serious about Comedy
Thanks for the kind words. I would like to hear from guys at the comedy dept too. I think that those reading but later decide not to participate for the seriousness we imply in our posts. We from time to time share little bits of funny conversations but not that often.
A note to desperate for hope's inquire; My initial Gleason score was (2+3) 6. That was confirmed 17 years ago at my surgery, however, I do not know which Gleason rate is the bandit made of today. It could still be the rate 3 but it could be a different one that may have existed but was not reported at the biopsy. Your link regards a scare case of metastasis. I am aware of that possibility too. I hope the PET exam provides a clue about the bandit's hideaways. Nevertheless, the capability of choline PET scans seem to be low for the detection of small metastases, in particular in a case of micrometastases (I was diagnosed with such well back in 2001 and never got a positive image along these years).
Thanks to all,
Is that Right? You're not getting Lupron Shots or other HT?
VG, Did I read that right? It's been over five years since your last Lupron Injection or other form of initial HT and your PSAs have held steady under 2.00? And you have not been using any other form of PCa treatment except regular blood draws for PSA checking? That's a really interesting strategy because I thought the standard treatment was to continue getting injections until they were no longer effective and then switching to another line of defense. This certainly would extend the clock for the effectiveness of initial HT. Any ideas on why more Medical Oncologists don't do this? In a separate post of yours, I read an exchange with an old friend who was in his 80s and had been using this very same strategy since his RP in his mid-50s. I wanted to copy that to discuss with my Oncologist on my next visit but can't seem to find it. I can certainly see the benefits to trying this. So far, I've had two Lupron Injections and they've worked perfectly - my PSAs are in the undetectable range and my testosterone levels are way down too. I know that the PCa will eventually mutate and figure out a way to work around the Lupron (start making it's own testosterone) but if there's a way to extend that timeline, I certainly want to explore it. I'm delighted to see that things are going well for you. Best/Gene0
VascodaGama Member Posts: 3,595 Memberedited July 2017 #65Intermittent vz continuous
You are reading it correctly. I am enjoying a long period away from the drugs, free of their risks and side effects, and giving an opportunity for my androgens dependent systems to recuperate to their normalcy. In short words, it is like giving me a chance to become healthier but at the same time I am also providing the bandit to get its testo-cocktails parties. This is the principle and purposes of the intermittent modality: a temporary return to normalcy while faking the cancer into believing that its survival is not threatened. Surely refractory (mutations of cancer biostructure) can be expected to occur much latter. This extension in living with quality also provide systemic patients with precious time that may bring to them the benefits from newer researches (on the drawing boards) on systemic treatments for PCa.
Xofigo and Zytiga are two examples of drugs that become effective members in the protocol of PCa therapies worldwide when I just started my IADT (intermittent androgen deprivation therapy) back in 2010. Today I got better modalities for imaging, more precision ways for identifying aggressive forms of the bandit (genetic testing) and an understanding on possible failure of certain prescribed drugs to my case (individual tailored treatment), and, most importantly, the so called radiopharmaceuticals therapies (the evolution into future ways for treating cancer) already effectively on course in certain places. Nothing of these was readily available at the time I started to discuss with my doctor after failed salvage RT of 2006.
Intermittent ways for treatment may not work in all cases. There have been trials trying to verify the benefits of intermittent vz continuous, which reports saw intermittent not better than continuous. However, I believe that the data from those trials were corrupted because the standards use to regulate the periods (on and off) drugs were fixed equally to a number of months to all patients, independently from the status each one were once this cohort stop taking the drugs. Many guys never got to castration levels and many never got to periods of remission. Nevertheless, the researchers use the PSA to identify failure and comment on the trial's final conclusions. Surely a guy taking a drug but that never got into castration should expect no influence on his PSA. Also guys that got into castration but saw their PSA fast increasing should understand that refractory was occurring and that the modality of therapy was never influencing his result in the trial. Testosterone tests were not used to verify the above in the trial. PSA remission levels were also not used to limit the use of the drugs.
My intermittent modality follow the standards used by several famous oncologists like Myers, Scholz, Strum, Bob, Lam, etc, with strictly regulated on/off periods in the intermittent. You can read my posts explaining details, however, the on-period requires one year into PSA remission of less than 0.05 ng/ml (Myers prefer levels of <0.01 ng/ml) while the castration is lower than T<20 ng/dL. The off-period starts when a patient gets the above status and ends when the PSA gets to a certain level determined by the oncologist that can be different in each case. Mine (a micrometastases case with failed RP and RT) was set for a PSA=2.5 ng/ml. Some guys Gleason 7 and 9 with failed RT got a trigger threshold at PSA=5.0 ng/ml and guys without radical treatments got still higher triggers at PSA=10.0 ng/ml but they use tactics for further control to try extending the off-period (ex; taking drugs to avoid Angiogenesis). All of these follow the principle of one year on remission. The restart of the HT treatment also may involve different drugs and one may get additional blockades (move from IADT1 to IADT 2 or 3 +α).
Thanks for the curiosity. I have deeply researched into this therapy since 2001. The post you commented may refer to Henryb's story (another IADT patient) in this link;
Vasco, This is a remarkable report on your success with Intermittent ADT (IADT) and a blueprint for how I want to modify my treatment. Right now my PSAs reveal that my PCa is undetectable and that my T score is well below castrate level. I don't see any reason why I can't give this a try. So far, I've had two Lupron Injections, in February and May of this year, and they've worked perfectly. I have two more injections scheduled for this year, in August and November, and will discuss with my medical oncologist that we start intermittent ADT in January of next year. Before I start, I want a new round of tests, PET Scan and whole body CT, to compare with my January 2017 Tests. That's my plan going into my next meeting with my Oncologist and I have you to thank for helping me navigate to this point. How did you arrive at identifying a PSA of 2.5 as the trigger for restarting ADT? Did you base that off your research of the clinical trials or was this your personal comfort level with the risk? I don't know how everyone else see's this, but I think it took a lot of guts, on your part, to do this and possibly show the rest of us a better set of tactics . BTW, I view Henryb's report as the Holy Grail of IADT and have already sent it, along with your report, to my Oncologist. I hope everyone in the initial stages of PCa is following along on this.0
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