how many are on Zytiga and Prednisone ONLY ?

[Scout4answers]

I know some of you have said that you are on Zytiga (Abiriterone) only .

Since it is intended to block the AR pathway (Androgen Receptors) it seems like it is a good candidate to prevent becoming hormone resistant.

it has been shown that nearly all prostate cancer cells depend on androgens and AR signaling for growth. Early in carcinogenesis, prostate cancer cells switch from AR-guided cytodifferentiation of luminal epithelial cells to the AR driving the uncontrolled proliferation of these cells. This switch is a critical event in carcinogenesis, as the AR becomes the primary driver of neoplastic growth in malignant cells.

[Magnus1964]

I was on abiratorone and prednisone only for 3 1/2 years until it failed.

[CAMPSOUPS in reply to Magnus1964]

However you had a orichtomy correct? If so that would be similar to Lupron plus abi.

[Magnus1964 in reply to CAMPSOUPS]

maybe, my orchiectomy was done back in -90's. I don't know if that would have any bearing on this situation.

[Jeremiad53 in reply to Magnus1964]

I was on the Abiraterone and prednisone for 4 months. It worked at lowering what it was supposed to, it raised my liver enzymes to the point I was taken off for 3 weeks, enzymes went down, then on it for a month and retested. Now I am in limbo waiting for the next move.

[Tall_Allen]

Zytiga without Lupron is experimental. I have no idea why you think it delays castrate resistance. If it works, it works only because it also prevents testosterone production in the testicles in addition to the adrenals.

[Scout4answers in reply to Tall_Allen]

I do not know that it does, I am asking the question.As you probably have figured out Allen, I question every thing and want to know how it works.

By the time I figure out how to not become castrate resistance. I hope to understand PCa as well as you do.

it has been shown that nearly all prostate cancer cells depend on androgens and AR signaling for growth. Early in carcinogenesis, prostate cancer cells switch from AR-guided cytodifferentiation of luminal epithelial cells to the AR driving the uncontrolled proliferation of these cells. This switch is a critical event in carcinogenesis, as the AR becomes the primary driver of neoplastic growth in malignant cells.

The switch they are referring is what I think we call castrate resistance, NO ?

[Tall_Allen in reply to Scout4answers]

No, they are talking about EMT and the process of metastasis.

[AlanMeyer in reply to Scout4answers]

Hello Scout,

I admire your dedication to knowledge.

You wrote: "By the time I figure out how to not become castrate resistance. ..."

There's a lot of very smart people working on that problem. If you figure it out, please let us know the answer ;>). I used to think that rocket science was the epitome of complicated science until I read my first books on biochemistry and molecular biology. Having studied philosophy, history, and literature back in school in the 1960s and 70s, I was not well prepared for the new materials. I had to start with pretty basic books.

Good luck.

Alan

[Scout4answers in reply to AlanMeyer]

Hi AlanMI know the problem, I only spoke the language of money and love before my DX of PCa.

I am very optimistic that someone will find a way to at least put our nemesis into permanent remission in the very near future.

[AlanMeyer in reply to Scout4answers]

I think your optimism is justified. If the future is like the past what we'll find is that the remissions last longer and longer, and apply to more and more patients over time. Given the heterogeneous nature of prostate cancer and many other cancers too, it may take a long time before we have every variety of PCa nailed down, but I think it will eventually happen.

[depotdoug]

I am confused. I too am only on Abiraterone and 5mg Pred. Stopped Lupron June 2021…

[maley2711 in reply to depotdoug]

Did you ask the Doc for reasoning?

[depotdoug in reply to maley2711]

Yes I did. We MO did agree to a “break” from Lupron Depot last June ‘21 because with semi-mutual agreement my Cardiac issues were priority One!Ok that is exactly what happened last Fridays’ phone call. That MO’s RN called me personally said Dr Albany can no longer take care of me with my many cardiac arrythmia issues.

Should I be rejected or positive?

Got transferred to a local great Med Onc appt next Thursday.

Hope this helps.

[maley2711 in reply to depotdoug]

Thanks...interesting.....admitting his knowledge was insufficient?

[depotdoug in reply to maley2711]

Yeh and Dr Albany, dont care if I mention his name, had his pre med residency in Cardiology schooling. Yes, he was trained schooled in cardiology first, then moved on to GU medical oncology… Interesting.I still al inclined to message him, his office and try to get a more appropriate “can’t handle me” reasoning.

To do or not to do?

Doug

[maley2711 in reply to depotdoug]

why not?

[leo2634]

4 years next week the only treatment other than Provenge 2nd year into treatment. PSA 0.1 since first month.

[GeorgeGlass in reply to leo2634]

Your profile says you take several other drugs

[leo2634 in reply to GeorgeGlass]

No it doesn't Eligard is Lupron and Xgeva is for bone strengthening. The Xgeva was stopped after the first year due to Jawbone problems. I've never had anything but Zytiga, Eligard.

[CAMPSOUPS in reply to leo2634]

The provenge 2 years ago might have made a big difference.I kind of wish it were offered to me but I am stable so it wouldn't change anything.

What led to you being offered/treated with Provenge?

[leo2634 in reply to CAMPSOUPS]

My Doctor said Provenge administered at low PSA was the best time receive its benefits.

[GeorgeGlass in reply to leo2634]

Is that low psa with and without ADT usage?

[leo2634 in reply to GeorgeGlass]

Low PSA was after ADT treatment. PSA was 17 before.

[FCoffey]

I'm on intermittent abiraterone acetate (Zytiga) and dexamethasone. My quality of life is far higher than it was on Lupron, which brought with it "multiple grade 3 toxicities." (Oncologist's words)