Waiting

[Blair77]

We recently got a report back from a genomic study we had done on my husbands prostate. It listed several possible drugs to try once he failed ADT. I wrote them asking what he could use in the mean time to hopefully extend his response to ADT and deter his disease from coming “ castrate”. Their response was that there is no treatment he should just stay on ADT till it fails and then he can move to something else. I was disappointed that there was nothing to help him stay hormone sensitive.

[ctarleton]

I think in earlier posts you mentioned that he had already had some added docetaxel chemo, in addition to his ADT? That probably reduced the total number of disseminated metastatic prostate cancer cells that will eventually become hormone insensitive. If he has bone mets, the use of either Zometa or Xgeva (if he may not already be on one or the other of them) might have some effect in making those sites in bones less hospitable to increasing numbers of cancer cells that could mutate to become hormone insensitive.

Otherwise, a focus on some things other than trying to prevent "castrate resistance", per se, might be something to think about. All the usual good things to do to eat well and live in balance with lower levels of stress. Perhaps exploration of Immunotherapy approaches to treatment? Etc.

Just some thoughts.

As for anecdotal information about how long initial ADT "works" for particular individuals, I was diagnosed very metastatic with involvement of many bones and lymph nodes and a PSA of 5,006. On Lupron & Zometa my PSA dropped to below 3.0 within 4 months, and to a nadir of 1.0 within 13 months. It did not rise above 3.0 again until 19 months. When it rose to 4.2 at 20 months we tried a re-challenge with added Casodex, and got an extended response to 24 months before stopping the Casodex. At 25 months my PSA rose above 5.0, eventually reaching around 60 when I did some Provenge, and reaching 95.0 at 36 months, when I added Xtandi.

On added Xtandi, my PSA again dropped rapidly, from 95.0 to a nadir of 1.2 at 45 months from original diagnosis, and was most recently at 1.5 at 49 months since original diagnosis.

Anybody else's mileage may vary. We and the biology of our bodies and cancers are unique and a sample size of one. Sometimes we get lucky with biology and treatment responses, and sometimes we don't. We do as many rational things as we can in the meantime to help ourselves "heal" and live well in the present moment on a day-to-day basis, and to choose whatever treatment path is best for us among the informed available options, realizing that nobody can precisely predict the details of our futures. It is a learned art to be able to sometimes choose whether one's mind and actions are focused on purposefully and actively "living" this day, or feeling like we are just taking another step closer to "dying" this day. In my experience, this mental/emotional balancing is often easier to say than to do, particularly right after initial diagnosis, and during times of progressive disease indications, and transitions between treatment modalities.

Charles

[Blair77 in reply to ctarleton]

Charles you are correct he did 6 cycles of Docetaxel and he currently does Casodex daily, Lupron every 3 months and he does chevalier for bones. His PSA was 1000 and he had several bone mets. Your response has been awesome! I’m hopeful my husband will have the same good fortune. I’m even more hopeful that a cure is close for all.

[vandy69]

Good Morning Blair77,

I have been in this battle for 5 1/2 years (please see bio for treatment history).

Some genetic defects are actionable, as Lynparza (a PARP inhibitor) can be prescribed if your husband has BRAC 1 or 2 or ATM defect. Many genetic defects do not yet have any recognized treatments.

As for castrate resistance, Dr. Myers would vary my T suppressor from Lupron to Firmagon, as they have different properties. He kept me on Casodex and Avodart for years.

If your husband has lymph node mets, has he had either Zytiga or Xtandi? There are many paths to take to lengthen ADT effectiveness.

Best wishes. Never Give In.

Mark, Atlanta

[Blair77 in reply to vandy69]

Thanks Mark. The genetic test only identified PTEN, HER 2 and TM something. No BRCA or ATM. I will ask about the rotating of the medicines. Who do you see now that Dr. Meyers has retired?

[vandy69 in reply to Blair77]

Dr. Myers referred me to Dr. Oliver Sartor of the Tulane Cancer Center in New Orleans.

Dr. Sartor has now closed his practice to new patients until 2019. My chemo was managed locally by Dr. Vasily Assikis in Atlanta.

Best wishes. Never Give In.

Mark, Atlanta

[pjoshea13]

I'll give my standard response.

If he is on ADT monotherapy (e.g. Lupron), there are a few things that may forestall resistance.

1] As Dr Myers has said, ADT is about denying PCa dihydrotestosterone [DHT] rather than testosterone [T]. Usually, zero T = zero DHT, but PCa can create DHT via a pathway that does not include T. Therefore, Avodart, which inhibits DHT creation, is used by some as insurance.

2] Androgens can be made within PCa cells from cholesterol. Therefore, a statin, such as Simvastatin, is useful for reducing access.

3] PCa cells can even make cholesterol when they can't get what they want. Again, a statin prevents the generation of cholesterol within the cell. The effect is dose-dependent.

4] Ultimately, if androgen is being somehow obtained, an androgen receptor [AR] antagonist can inhibit AR activation & cell division. Casodex (or Xtandi).

5] Zytiga inhibits the generation of androgen from pregnenolone & progesterone.

Any & all of the above will strengthen ADT monotherapy IMO.

...

And I would add Metformin at 2,000 mg/day.

-Patrick

[Blair77 in reply to pjoshea13]

So how do we get our doctor do give him this? Our doctor definently thinks he knows everything🙄🙄🙄

[softwaremom00 in reply to Blair77]

I have fought this battle.. not an easy one. Wish I had an easy solution.