**31. Pathogenesis of malignant transformation of endometriosis**

The molecular pathology studies of both atypical and malignant glandular epithelium of endometriosis have shown aneuploid DNA, in contrast to adjacent benign epithelium which is diploid, and a loss of heterozygosity on the arm of chromosome 12 or X-chromosome inactivation, consistent with a common lineage. Aneuploidy of chromosome 17, implicated in the genesis of ovarian cancer, was discovered in about 65% of the endometrioid cells (Jiang et al, 1998). There is evidence that malignant transformation of endometriosis is a multistep pathway involving somatic genetic changes and changes in hormone receptor status (Hompes & Mijatovitc, 2007).

In conclusion, endometriosis is a chronic gynecological disease that results in severe morbidity, including chronic pain and infertility. The pathogenesis of the condition is multifactorial and various factors, genetic, immunological, environmental are implicated Recent data provide evidence that there is an endometrial stem/progenitor cell capable of establishing endometriotic implants .The functions of this stem cell may represent the primary defect in the endometriosis pathway. Current research uses the endometrial stemcell system as a model to study the molecular biology regulating endometriosis (Sasson & Taylor, 2007).
