Price quote for a personal Androgen Receptor Silencing assay

About 9 months ago I was searching around for a lab would had the capabilities to investigate whether our androgen receptors were silenced and if so, if it was an epigenetic modification such as mehtylation, etc.

I found one, but the price was slightly hefty, $3,400. A couple of PFSers I know were willing to crowdfund it, but we just had to find a subject and a control (a non-PFS male) who was willing to get a biopsy off his penis.

Ultimately we decided to scrap this, because we expected that the Foundations studies would be published soon. Now that is has been 9 months I am wondering if we should consider trying this assay again.

Its $3,400. It would tell us whether or not our AR is silenced. And if it is, it would tell us by which epigenetic modification it is silenced.

What do you guys think? Any discussion is welcome.

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This sounds very interesting and I don’t see anything bad coming from investigating it.

I’m not opposed entirely but you need to flesh out a bit more what you are looking for and hoping to achieve. Haven’t we already found an overexpression of androgen receptors based on genital skin samples? Isn’t the problem more to do with gene expression further up the chain (as discussed in this thread viewtopic.php?f=27&t=2216&start=20)?

What instruments would be used to carry out the test? How would they ascertain whether or not there has been an epigenetic modification and of what type? Who would be analysing the data on our behalf, a lab technician or an actual specialist in the field?

It sounded good when I first read it there then these questions pop up. I know it isn’t massively expensive (by PFS standards lol) but the PFS Foundation itself is currently desperate for funds.

In fact, given that shamefully there’s been no mention of their latest appeal I’ll paste it on here:

"[b]Dear Friends:

Looking ahead to 2016 and the expected publication of the first round of PFS Foundation-funded clinical studies, we need to ensure that as many medical professionals as possible will be aware of that research, its implications, and how to build upon it.

But properly stepping up such efforts—worldwide, no less—means additional expenses.

So as we enter the holiday season, I’m asking you to consider making a contribution to the foundation to help us reach our target goal of $25,000[/b]."

Again, I’m not averse to extra testing if it sheds some more light on this, and appreciate the initiative you’ve shown, but we need to be careful that scarce funds are being directed to the most important projects.

Hello everyone,

I’m a PFS Victum from Germany, i suffer from Post Finasterid Syndrom since i quit Propecia in 2011. This drug destroyed my life and my Health i’m in a very bad condidion. six Months ago i was by a specialist for PFS here in Germany his Name is Prof.Zitzmann in Muenster and he made a lot of tests also a molekular Genetic test of the AR Receptor in Exon1 and he found a partial androgen insensitivity wich i defently don’t had before i took Propecia. In my case that’s the proof that Propecia is the reason why i have the partial androgen insensitivity now and all the problems that comes with. I’m sorry for my very bad English :wink:

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Can you give us more details on what exactly this test was and what it found?

It wasnt just CAG repeats was it?

Michael.Zitzmann@ukmuenster.de

His contact info

Very interesting

would be interested to know more details onhow they would test for AR silencing? I was looking around for this but ended up thinking it wasnt possible to do. I even emailed a few companies.

What about that professor, how did he test you?

I try to answer the Questions but like i sad it’s not easy for me with my bad English:(
For all the tests that has been made in Muenster i don’t have to pay anything for it because it’s get paid by the health insurence wich everyone here in Germany has. They are tested for AR silencing with a sperm sample.
The result of the sizing of CAG triplet region of exon 1 of androgen receptor are that i have 25 tripple repeats wich means a partial androgen insensitivity. Prof.Zitzmann and the other Doctors in Muenster knows a lot of PFS and they treat 2-3 patients per month and i think that they have patients from all over Europe and specially the Prof.Zitzmann travels a lot to the USA and Italy to help by the research of PFS.
I also found something about Prof.Zitzmann here in the Forum.

viewtopic.php?f=3&t=6512&start=60

on page 4

This IS very interesting.

A. M. Traish, J. Hassani, A. T. Guay, M. Zitzmann, and M. L. Hansen, “Adverse Side Effects of 5α‐Reductase Inhibitors Therapy: Persistent Diminished Libido and Erectile Dysfunction and Depression in a Subset of Patients,” The Journal of Sexual Medicine, vol. 8, no. 3, pp. 872–884, Mar. 2011.

http://onlinelibrary.wiley.com/doi/10.1111/j.1743-6109.2010.02157.x/full

The same M. Zitzmann is listed as doing the research in affiliation with the university of Muenster.
But why wouldn’t he be collaborating with the PFS foundation regarding a potential test for PFS?
Almost sounds too good to be true, but I hope it is.

Interesting find


How can our genes be damaged?

So many people quit fin and recovered for months then one day woke up fucked. Alot crashed on the drug. And alot crashed when they were sick or on antibiotics.

I sure hope its not gene damage. Only thing i can see it as being autoimmune like CFS is. People with CFS wake up one day fucked and stay like that for decades.

I feel like the neurosteroid obsession is a wild goose chase. The neurosteroids are fucked because androgens are not working correctly.

I think we need some hormome and enzyme antibody tests to rule out things, then again there could be 1000 things that regulate DHT that could have an antibiody.

Its a mystery. Whats even more of a mystery is arimidex did the same thing. Now estrogen cream doesn’t give me any estrogenic effects just like dht cream.(estrogen not working has left me disabled so i advice stay away from arimidex )

Seems like a repeatable mechanism across multiple hormomes that’s induced by potent anti-hormome compounds that requires perfect genetic and biochemical predispositions.

A mystery indeed.

There is evidence that fin isnt mutagenic.
This guy must have had this all along in form of MAIS but either it was not expressed or he didnt have any symptoms from it


On the other hand the teratogenic effect seems really related to androgen receptor insensitivities because if a pregnant woman touches fin her baby may be born with genitalia issues, namely undifferentiated genitalia, which is somethjng typical of PAIS.

Dont know what to think of this. I hope he comes back to write more.

-“Exon 1” might refer to the actual gene, or the corresponding RNA transcript.

-Exon 1 of the AR gene contains DNA/RNA coding for a ligand binding domain and a region responsible for dimerization of 2 recptors after nuclear localization. For whatever reason, AR splice variants that are transcriptionally active, but missing exon 1 have been found in abundance in androgen insensitive prostate cancer cells. and have been found to be produced in abundance after androgen deprivation therapy has been initiated. Not sure how the receptors could be functional without a ligand binding domain, but apparently they are.

-RT-PCR (a method that produces DNA from RNA) could have been used to produce “diagnostics purposes only” DNA with exon 1 missing from the mRNA in that case.

Anyways, many questions to be answered.

Has anyone contacted this researcher who MXrider spoke of?

This guy is also on The german pfs Forum , he just said that he has a partial androgenic resistance I highly doubt that dr. Zitzmann said anything except proposals’ for potential therapies because explaining to a laymen anything about receptors or genes is a very time consuming task. But if he explained anything more than the stuff you mentioned please feel free to share it to this community. By the way Germany still denies PFS , I visited a urologist last month to get a prescription for generic Viagra (sildenafil) . I told him my story and I think he thought that I am nuts . He said " it is impossible when you only got 1 mg of finasteride daily" I asked whether he recognized that it is controversially discussed all over the world and especially in the USA and that even Harvard is researching . His answer was “so what” 
what an ignorant asshole. Well at least I got my prescription .

Its not that they dont have ligand binding domain, its that there is a mutation that makes it less sensitive to that ligand. The same ligand is not activating it like before.
So this guy probably doesnt understand very well the test made to him, fin isnt mutagenic according to what we know. The professor must have used tgat reverse transcription pcr to simulate the result of his epigenétics.
So there is some degree of silencing of the gene.

Androgeb receotirs form heterodimers ewith GC and Progesterone receptirs right?

Btw, my comment about this being linked to teratogenecity is obviously wrong BĂ©cause in that case the drug would be actively inhibuting 5ar ofc.

I can’t have had a partital androgen resistance bevor i took fin because i had absolutly no symptoms that comes with a born androgen resistance . I have a lot of body hair strong growth of beard a deep voice my genitals are well developed and my sperm sample was also OK and bevor i took fin i had absolutly no gynokomastia.
It is possible to have no symptoms with a mild androgen resistence (MAIS) but not with a partitial androgen resistance(PAIS) or a complete androgen resistance(CAIS)
But i know that it comes a lot of answers who you guys say that this is not tru bla bla bla because everyone here knows it better. That’s the reason why this is my last comment in this forum.
I don’t unterstand why you guys asking for a “Price quote for a personal Androgen Receptor Silencing assay” when everyone here is absolutly sure that fin is not affected AR receptor.
It’s like most of the answers here in this forum

hairlosstalk.com/interact/sh 
 -Receptors

it’s not possible bla bla bla

Its too bad that nobody with a bachelors or so in biology who has PFS has of yet taken it upon themselves to dedicate their life to solving this thing to the extent that they go back to college to work on a PhD in molecular biology with a focus on PFS. They could literally do their dissertation on the study of PFS than they could receive university backing and research resources to conduct the study.

Without sounding like a smart ass but I think it is more likely to understand when you study biochemistry or have a degree in biochemistry.I think It is hard enough to study this subject without having PFS but studying it with this condition is probably almost impossible. But you’re right we need somebody who dedicate their life to research this condition instead of voluntarily doing it in their free time.

Dubya does this invalidate what you said or is it still valid?

hindawi.com/journals/au/2012/781459/