It’s that time again, that time when the best and brightest in the field of endometriosis gather together in one place to share their collective experience and figure out where the future of endometriosis research and treatment is going; all whilst enjoying a caipirinha on the sunny beaches of Sao Paulo (us science types know how to multitask). Although I managed to go to the previous WCE in France, unfortunately I couldn’t make it this year, so instead of enjoying the glorious heat of the Brazilian south I was enjoying the drizzly rain of the English northwest, oh well. However, thanks to a friend, I did manage to get the book of abstracts (which is basically a summary of all the talks, presentations and posters at the conference) so I can give you a rundown of what’s been going on in the field of endometriosis research now and in the future.
Before I continue I must mention that the information I’ll be presenting here is taken only from the abstracts, which as basic summaries of the research and not in depth discussions and may or may not be taken from completed or peer-reviewed research. Also because these are conference papers I can’t provide links to source material as I normally would.
To start with, just looking at the book is encouraging, over 400 pages of research into all the many and varied aspects of endometriosis, which is broken down into different subject matters, so I’ll start with genetics and endometriosis.
Genetics is an important factor in endometriosis, mainly because we don’t really fully understand how genetic changes contribute to endometriosis risk. A team from Sweden aimed to examine indirectly the role genetics play, by looking at the rate of endometriosis in twins. There are two different types of twins: monozygotic (where both twins come from the same egg and are essentially genetically identical) and dizygotic twins (where each embryo comes from a different egg and can so each twin can be very different from the other). Of all the female twins this research looked at they found that there was a much higher risk of endometriosis if your monozygotic twin also had endometriosis. That certainly seems to suggest that genetics plays a role in the origin of the disease. Of course there are other factors at play too in determining endometriosis risk. This team, after doing some calculations, found that in the women they studied, genetics accounted for around half of the risk associated with endometriosis and environmental factors accounted for the other half. Finding out what the specific genetic and environmental factors are and how they increase or decrease the risk of endometriosis, is an ongoing challenge for the future.
Several other studies presented at the conference aimed to find out what these genetic factors are. Our genetic material (our DNA) is a funny thing, it can change in many different ways, some bits can swap, duplicate or be deleted all together and sometimes specific changes can be associated with specific diseases. Other research identified some of these specific changes associated with endometriosis which may, in the future, might allow us to identify women at risk of the disease with greater ease and hopefully give us to better understand the way in which the disease works.
Of course there are problems to consider, for example, are the genetic changes we see the same across all women? One of the presentations from an international team found that the genetic changes we know of so far are very similar between women of European and Japanese ancestry, but we still have no information on women of African, Chinese, Indian etc ancestry to compare them to. These types of studies though require a great deal of time and money invested in them, so it may be a while before we see a complete picture of the genetic risk associated with endometriosis for women across the world.
Another point to consider is the difference between types of endometriosis. One piece of research from a Danish team found genetic alterations specific to deeply infiltrating endometriosis. Therefore it could be that peritoneal, deeply infiltrating and ovarian endo all have different genetic alterations (and different genetic risks) associated with them. It’s good to know though there are people actually looking into this and one day, maybe soon, we’ll have that complete picture.
More to follow soon.