So does this mean that theoretically a potential cure would work for PFS, PAS, and PSSD?
Maybe. Being that there is currently no standard diagnostic for any of these conditions, we can’t know with certainty they are the same. We only have the similarities in post-drug symptoms, the overlap in effects of the drugs, and a small body of biological research on PFS patients.
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Well, I’d be curious to see what the basis of those rumors is. There was a member of the board here who flew across the world to visit him and was told personally that he basically had no idea what PFS is. So, I think sitting and holding out hope for an outcome from Baylor is an extreme example of the Mark Twain or Ben Franklin or whoever it was definition of insanity.
What happened to the 23andme data? Did not enough people here contribute to it or what? Could that find what we need?
They didn’t get enough samples really to do anything I don’t believe…Moonchild said he thought he was clueless as well but said he told him he thought genes were “off”…I was told by others here genes were deregulated…point is that’s all we got and no other such study has or will be attempted as I know of…Nobody has the money to do anything…
The problem is simply that we haven’t provided enough incentive for scientists to investigate us. We haven’t given them anything. We’re just sitting here talking. Scientists have no incentive to help us until we provide it to them. We will sit here forever or until we get organized, get the survey filled out by thousands of people, get our condition publicized, and generally stop being useless. The way science works is that scientists can easily get millions of dollars from NIH and other funding agencies. They just need to have evidence to support a hypothesis in grant proposal. Right now they have nothing. If we get them some data then they can put that in grant proposal and in come the millions of dollars.
That’s why they are trying to get everyone to take the survey they think it will generate enough interest from scientists to open up that funding…
Myself Idk…It seems there is just not enough people who have the condition, symptoms are different for some and lots of those that do have it didn’t do the survey…Only hope left is melcangi who keeps going with it anyway…
That is what moonchild told me and he’s the only one I know who saw khera in person…Unless someone else did…Also he saw a geneticist there at Baylor also who told him it was impossible that finasteride could cause epigenetic changes but if genes were off he had no idea how they could be turned back on…And this is an expert in genetics…
Others here emailed khera and were patients of his and participated in the study and he always told them something to the effect…its coming it should be out next year etc…
Ya, we aren’t the experts so our opinions are irrelevant. Get as many people as you possibly can to fill out the survey. Especially people who have taken Accutane. By reaching out to those groups we multiply the people helped and multiply the seriousness with which our problem is taken. Throwing hands in the air, sitting, and hoping for the best consigns us to sad, lonely, purposeless, solitary lives devoid of love or people to care about. I wasn’t talking about moonman I was talking about someone else and it should be abundantly clear by this point that sitting and waiting for Baylor is one of the dumber things we’ve been doing over the last 10 years and would be the definition of insanity to continue.
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In conclusion, the CRISPR/Cas9 system was able to edit the expression of AR and restrain the growth of androgen-dependent prostate cancer cells in vitro , suggesting the potential of the CRISPR/Cas9 system in future cancer therapy.
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It’s safe to assume that more is happening than methylation of receptors. An example of an indirectly acting drug is isotretinoin, which has transcription factor activity. A two-tier mechanism is postulated for indirect effects in which acute exposure to a drug influences signaling pathways that may lead to an alteration of transcription factor activity at gene promoters. This stimulation results in the altered expression of receptors, signaling molecules, and other proteins necessary to alter genetic regulatory circuits. With more chronic exposure, cells adapt by an unknown hypothetical process that results in more permanent modifications to DNA methylation and chromatin structure, leading to enduring alteration of a given epigenetic network. Therefore, any epigenetic side-effect caused by a drug may persist after the drug is discontinued. It is further proposed that some iatrogenic diseases such as tardive dyskinesia and drug-induced SLE are epigenetic in nature.
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Hey Ryan do you have a source for this?
Kind of confused by this methylation of genes is an epigenetic mechanisms (ie they are the same thing). Most drugs have effects on singling pathways which in turn can alter transcription of genes through a variety of processes including reduction of transcription factor activity. It is unclear why permanent changes occur with certain stimuli/cellular conditions and not others.
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I’m beginning to think that there could be two potential causes to this disease one is Polymorphism of the androgen receptor and the other is Gene Amplification both are worth researching.
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Sorry to replay such an old post.
But they found a reverse correlation, meaning more AR meant less sexual symptoms.
Your text might be misinterpreted as that the symptoms increase with AR density.
Now if they would have had a third group of asymptomatic finsteride users OR would have been able to check amount of androgens in the tissue it would have been way easier to interpret how much of an impact overexpressed AR really has.
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Yes we really need this info ASAP. Differences between us and asymptomatic fin users may be crucial, it’s almost unbelievable there isn’t a single study like this yet!
The Harvard study was like that…They had 3 groups…But has you know it did not look at epigenetics…
Different hormones but potentially the same mechanisms effected?
We observe that loss of 3D chromatin interactions often occurs coincidently with hypermethylation and loss of ER binding. Alterations in active A and inactive B chromosomal compartments are also associated with decreased ER binding and atypical interactions and gene expression. Together, our results suggest that 3D epigenome remodelling is a key mechanism underlying endocrine resistance in ER+ breast cancer.
Maintenance of ER signalling is critical for the success of endocrine treatments and development of resistance is associated with loss of ER expression (https://www.nature.com/articles/s41467-019-14098-x#ref-CR36) or ER mutations (https://www.nature.com/articles/s41467-019-14098-x#ref-CR41). Upon development of tamoxifen resistance in MCF7 cells (TAMR cells), we observed a significant loss of ESR1 mRNA expression and reprogramming of ER binding sites across the genome. In fulvestrant-resistant cells (FASR), ESR1 gene becomes silenced, with almost complete loss of expression. In our previous work, we found that hypermethylation at ER-responsive enhancers is an important mechanism of endocrine resistance6. Here, we suggest that differential ER-bound enhancer−promoter interactions contribute to an underlying mechanism of endocrine resistance, where aberrant DNA methylation dynamically alters the ER-regulated enhancer−promoter interactions thus resulting in suppression of ER signalling pathways.
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