Estrogen, again?

[tarhoosier]

Michael Glodé (Glo-day) has a depth of knowledge in our disease unmatched. His blog post mentions it as he gives an update to the estrogen treatment option for Prostate cancer. Worth subscribing for a monthly or so message:

prost8blog.com/2021/02/28/r...

[pjoshea13]

I enjoy his blog.

He mentions "DES, an oral form of estrogen" . DES is-diethylstilbestrol, a synthetic estrogen. "Orchiectomy or DES or both were the standard initial treatment for symptomatic advanced prostate cancer for over 40 years"[1]. It began to be phased out when Lupron was FDA-approved in 1985, although I can't imagine that many without insurance made the switch. When I began joining PCa groups in 2004 I met many men who were using Honvan (diethylstilbestrol diphosphate), if not DES itself.

I don't know when the PATCH study began, but the first paper came out in 2003 [2]:

"Transdermal estradiol therapy for advanced prostate cancer--forward to the past?"

Our very own Richard Wassersug was an early adopter & seems to be doing splendidly on E2 patches. & I know that others here use E2 too.

But: The efficacy of E in treating the prostate cancer in these patients will be reported in 2023 and 2024" & we are forever being warned to wait for the definitive study before trying something new. LOL

-Patrick

[1] en.wikipedia.org/wiki/Dieth...

[2] pubmed.ncbi.nlm.nih.gov/126...

[noahware in reply to pjoshea13]

Yes, it is a bit LOL funny to consider that a variation on the oldest form of ADT (aside from castration itself) that has been used without apparent problem for decades is considered "something new."

Now let's suppose tE2 gets glowing reviews in those 2023 and 2024 reports... how long after THAT will it be before it is considered an appropriate and acceptable SOC in mainstream US medical practices? Another decade? Two decades? NEVER?

[My money is on door number three.]

[MateoBeach in reply to pjoshea13]

Not waiting, like many others. E2 takes T to castrate levels and by the same mechanism: inhibiting hypothalamic pituitary axis blocking release of LHRH. So it “works”.

The caution is in very advanced disease with heavy mutations burden of AR to where estrogens can be a substitute ligand for androgen signaling. This would appear similar to the situation with bicalutamide resistance and would be recognized by rising PSA or progression and must be stopped. ER a and b activities are very complicated. But living must go on now!