Do False-Stable results exist? My latest tests

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,

VG  

Gene,

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;

https://csn.cancer.org/comment/1574637#comment-1574637

Best wishes.

VG