Endometriosis is characterized by the growth of endometrial tissue (normal uterine lining) outside of the uterus. It affects more than 8.5 million women and teens in North America alone, with 176 million more worldwide. The disease can only be diagnosed definitively through invasive surgery, and there is no absolute cure. Similar to cancer, endometriosis lesions require establishment of blood supply for survival and growth. This has led to the idea that suppression of blood vessel growth (anti-angiogenic therapy) may be a successful approach. One of the key components of new blood vessel formation is recruitment of specialized blood vessel growth promoting cells called endothelial and hematopoietic progenitor cells from bone marrow. These cells are recruited by stromal-cell derived factor-1 protein. We confirmed abnormally high expression of stromal-cell derived factor-1 protein and corresponding increase in the progenitor cells in the lesions from endometriosis patients. The goal of this study is to test the hypothesis that endothelial and hematopoietic progenitor cells are recruited at the lesion sites by stromal-cell derived factor-1 and that blocking of this protein in combination with anti-angiogenic drug, ABT-898 prevent new blood vessel development and ultimately survival of endometriosis lesions. We will test this hypothesis using a combination of molecular biology approaches, patient-based studies and animal models. These innovative and clinically relevant research studies will allow us to gain a greater understanding of endometriosis progression and identify new treatment for this disease.