International Medical Conference Endometriosis 2025:
Endometriosis 2025: Your Mother Should Know, Your Doctor Should Know Better!
Discussion: Causes of Endometriosis Molecular Pathways to Explore
Okay, questions? Yes
The question is, can we distinguish progressive from regressive endometriosis at different times? At different times is a good thing At different times. Remember, endometriosis does not progress or regress in a linear fashion. It can come and go. It can get worse, it can get better. It can be like pimples. Sometimes they get worse, sometimes they get better, they disappear for years and then they come back again. Raring. Everything changes over time. So that what you have to be ready for is you'll not be able to answer the question and I can't answer the question. So what you have to do is be ready for what are we going to put into monitoring these patients over long courses? How many times a year do they need to be examined? Do we need to add to our examinations? Any sort of markers such as microRNAs, any sort of monitoring, do we need to add sonograms, particularly renal sonograms into that monitoring?
We need to over time to develop some sort of concept of what it takes to develop, do long-term care. In my practice, I just listened to 'em, examined them and hoped that they didn't get worse. All of the really bad ureteral endometriosis patients I saw did not come out of my population. They all came from patients who were referred. So it may be that those kind of cases where we're talking about worrying about asymptomatic regression are measured in the one in 10,000 rather than one in a thousand or one in a hundred. And when we start trying to do monitoring that's designed to look at something that's going to happen to one in 10,000 patients, it is very difficult. I see that Bruno looks like he's got an answer that he would like to
Well, thank you very much. First of all, I really enjoyed Frank's presentation. The only thing you miss one song, it was get back. So it's get back to birth TRO fields, let's maintain pre-industrial time. There was lots of a amenia in women reproductive life, but now it's replaced by, this is the slide I got from Sini. He sent me a slide about get back song and that was his message. I'm sure he is going to present that. Dan, I respectfully disagree with you. Endometriosis is not like pimples. I love you, but I totally disagree with you. When endometriosis format, this is the real challenge. Endometriosis disease of fibrosis. When fibrosis happens, the rest is somewhat fibrosis, take control in that fibrosis, we don't see much glands anymore. I'm sure Sanvey will touch that because he notifying me how they lose the perin and estrogen sensitivity as fibrosis takes away. This is the challenge we are meeting, the disease we are facing right now. The disease is not, is estrogen sensitive like pimples. You treat with antibiotic, it appears, but if there's scar tissue formed that pimples with those holes, permanent marks on the skin never disappears. So I hope I made my point.
Yes, yes. And Andrew Horn from Edinburg, first of all, thank you to all the speakers for a great session. My questions for Asgi wonderful work. I really enjoyed your talk. You show pretty convincing evidence that it's the endometrium that you think the eutopic endometrium that's driving the changes that you see in the lesions. Do you think there's any role for the adjacent peritoneal mesothelial cells and factors that are excreted into the peritoneal fluid given that it's bathing the areas where the lesions occur?
Yeah, I think the point I was trying to make there, Andrew, was really in terms of the origin of that tissue from the utopic endometrium. But no, without a doubt the peritoneal environment and the changes in the peritoneal environment are probably the most important in terms of driving that disease. So I mean, based on all of our non-human models that we've used, particularly with the non-human primate and the mouse models, any changes within the mesothelium is going to affect the way those lesions will attach invade. So I truly believe that the mesothelium plays a role. I think Tamara has shown, and Bruce Les, he has shown that there are micro changes within the mesothelium. That might be areas for attachment invasion. But I think changes in the mesothelium are really important and that's part of why we try to develop that matrix. It's not ideal. I know Linda hates that word and she'd rather we use something else. But for the LP nine cells, unfortunately that's about the best matrix that we have to work with. Do you want to write
David Wiseman from Dallas? Thank you very much. Wonderful speakers. A question for sort of follow on for the last question, Dr. Fa bass, two questions. Number one, did I understand correctly for some of the markers, not all of them, you're seeing changes in the uto endometrium end endometrium that correlate with what's going on the lesions. If so, could those be used diagnostically? Because obviously it's a lot easier to access those. That's question one number one. Question number two is when you are doing your transcriptomic analysis of the lesions, have you either done or plan to do any analysis of the surrounding tissue as to what changes is going on in the surrounding tissue that might drive or predict any further pathology? Thank
The rest of it was not clearly either of stromal origin, but didn't show much in terms of stromal characteristics. And that's why when we tried to do the analysis, we didn't see much change in the S stroma. Going back to your question with regards to the utopic and the ectopic, we've been really struggling with that because I mean, dogma has always said, well, there's something different about the eutopic endometrium of the patients with the endometriosis. And I think when it comes to menstrual tissue and maybe some of the changes during mensuration, there might be some very dramatic differences. But in a lot of the analysis we've done with both with our baboon model, and again, maybe this is because the horse has already left the barn, we are looking at endometrium way, way beyond the time from the early development of the lesions. We were very surprised that we didn't see a lot of differences between the eutopic endometrium and the ectopic endometrium.
And that just might be reflection of the time that we got the tissue. And maybe earlier on, and going back again to our early work with the baboon model where we induced the disease and follow the eutopic endometrium. Every three months paper we published several years ago showed that the early changes within the utopic endometrium happened within the first three months of disease induction. And as we moved beyond that point, and we looked at 12 and 15 months, the utopic endometrium really didn't show a lot of overall changes in transcriptomics. But if you selectively looked at markers that you would expect to see during the window of implantation, they were all changed. So individual genes are changed, but the overall transcriptomics seems to sort of settle back down.
