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Something’s got to give

by Guest Author on 6 Nov 2012

Vicky Young (Copyright: Vicky Young)

Vicky Young (Copyright: Vicky Young)

In her shortlisted article for the Max Perutz Science Writing Award 2012, Vicky Young explains her research into endometriosis and why a protein that seems to make organ linings ‘stickier’ could be the key to treating this painful and debilitating condition, treatments for which have changed little since the days of Marilyn Monroe.

“What good is it being Marilyn Monroe? Why can’t I just be an ordinary woman? A woman who can have a family … I’d settle for just one baby. My own baby.”

As the quintessential sex symbol of modern time, Marilyn Monroe oozed femininity and appeared to be the ideal women, but behind closed doors she spent most of her life in chronic pain, became addicted to pain-killers, and suffered from difficulties in conceiving and at least two miscarriages.

Marilyn Monroe suffered from a disease called endometriosis, a condition where the cells that line the womb, known as the endometrium, are found on the surface of other organs within the pelvis. These endometrial cells still act like endometrium and each month they thicken and bleed, but unlike in the womb the cells can’t leave the body at the end of each cycle so they just keep growing. In time these cells grow to form lesions on the organs and can interfere with organ functions and irritate nerve endings, causing chronic pelvic pain. What’s more if the disease is not treated then the lesions can affect fertility and even fuse organs together.

Endometriosis is more common than you might think with up to one in 10 women suffering from the disease. Right now the only way to diagnose endometriosis is to perform pelvic keyhole surgery under general anaesthetic to look for endometriotic lesions. However this can be really traumatic for the woman and costs the NHS millions of pounds each year. Although there is no cure, the lesions can be removed during the surgery, which can help with pain, and symptoms can also be managed with pain medication and hormone treatments. But the lesions return in most women after one or two years, meaning that they need regular surgeries throughout their lives.

My research focuses on how endometriosis originates within the pelvis. If I can find out how endometriosis develops then it could help us identify and develop a drug that can stop it. Right now most of the scientific research in endometriosis has focused on how the endometrial cells are different in women with and without the condition but what has been ignored is the pelvic lining that the endometrial cells grow on. Lining the whole of the pelvis, including the surface of all the organs inside it, is the ‘peritoneal membrane’. This is a very thin layer of specialised cells that protect the organs and stop them sticking together. These are the cells that the endometrial cells stick to and grow on. My research is looking at changes within the peritoneal membrane that might make it easier for endometrial cells to stick to it and grow.

In particular I am researching a protein called transforming growth factor beta or TGF-β. This protein is important in cancer where it causes cells to multiply quickly and in the development of scars where it makes cells stickier and produces scar tissue or ‘collagen’. I am trying to prove that TGF-β protein is increased in endometriosis and acts on the peritoneal membrane to make it stickier so that endometrial cells are more likely to attach to it. Once stuck the TGF-β might also cause the cells to multiply quickly and produce excess collagen creating the endometriosis lesion.

So far I have shown that TGF-β protein is increased in the peritoneal membrane where endometriosis lesions are usually found. This means that TGF-β might be responsible for endometriosis developing, at least in part. I have also shown that peritoneal membrane cells become stickier when exposed to TGF-β in the lab explaining why endometrial cells stick to the peritoneal membrane. Although more research needs to be done here, it looks like TGF-β is central to this disease.

So why is my research important? If I can prove that TGF-β is responsible for the development of endometriosis then we can develop drugs that target TGF-β to stop endometriosis lesions forming. These types of drugs are already being developed for the treatment of other conditions and are already showing clinical promise.

Unlike Marilyn Monroe who had to endure major pelvic surgery to treat her endometriosis, women today undergo minor keyhole surgery but that’s where the differences end. The contraceptive pill and painkillers that Marilyn Monroe would have been prescribed are the same form of treatment prescribed today. The development of a new drug to treat women who suffer from endometriosis is vital to improve their quality of life and avoid the suffering that so many women experience from this disease.

Vicky Young

Vicky is a PhD student at the MRC Centre for Reproductive Health. She has blogged for us previously about her outreach activity, the Egg and Sperm Race.


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