Background 

Endometriosis, defined as endometrial-like tissue outside the uterine cavity, affects approximately 10% of all women in the reproductive years. The disease is associated with certain malignancies such as ovarian cancer.  Endometriosis causes very painful periods, chronic pelvic pain, pain on intercourse, chronic fatigue and infertility.  The disease severely affects quality of life, resulting in days off work and decreased productivity.  The symptoms mimic those associated with other chronic pain disorders, e.g. irritable bowel syndrome and pelvic inflammatory disease.  It is widely believed that most endometriotic lesions develop from menstrual endometrium which entered the abdominal cavity via the Fallopian tubes and adhered to and invaded the peritoneal mesothelium.

Angiogenesis and angiogenesis inhibition in endometriosis

Although the pathogenesis of endometriosis remains uncertain, our group and others have shown that angiogenesis (the growth of new blood vessels from the existing vasculature) is essential for the establishment and growth of endometriotic lesions.  Proangiogenic cytokines such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) are elevated in the serum, peritoneal fluid, and endometrial tissue of affected women.  Thus, inhibition of angiogenesis has been suggested as a promising, novel therapeutic approach for endometriosis.

We are developing a non-invasive genetic model of endometriosis and ovarian cancer.  This project will enable us to learn more about the pathogenesis of the disease and allow the testing of novel therapeutic approaches.  This will reduce the numbers of necessary animals and refine current models as it will reduce the stress to animals.  We will be able to test various biological pathways at different stages of the disease, which should increase our knowledge of endometriosis significantly.