**5.1 Survivin gene expression**

In endometriotic lesions, although derived from normal endometrium, decreased expression of adhesion molecules and increased expression of proteolytic enzymes may contribute to establishment of endometrial glands and stroma at ectopic sites, likely as behaviour of cancer cells. Normal epithelial cells undergo apoptosis when they separate from their primary tissue. However, spontaneous apoptosis of ectopic endometrial tissue is impaired in women with endometriosis, and its decreased susceptibility to apoptosis might participate in the growth, survival, and invasion of endometriotic tissue. Although there have been some reports on the induction of apoptosis in endometriotic lesions, there is no consensus on the mechanism of escape from apoptosis in endometriosis, and little is known on the correlation between survival activity and invasive phenotype in endometriotic cells. Among the regulators of cell death, inhibitor of apoptosis (IAP) proteins has recently emerged as modulators of an evolutionarily conserved step in apoptosis, which may potentially involve the direct inhibition of terminal effector caspases 3 and 7.

Survivin is a novel inhibitor of apoptosis and is expressed during fetal development and in cancer tissues, but its expression has not been reported in normal adult tissues or benign diseases. Survivin gene and protein expression was detected in normal human endometrium and that survivin could play an important role in physiological homeostasis during the normal menstrual cycle (Konno et al., 2000). The survivin is also expressed in ectopic endometriotic tissue; however, there has been no report on the biological significance of survivin in endometriosis, an aggressive tumour-like benign disease.
