**3. Endometrial markers**

The adhesion of endometrial cells to the extracellular matrix (ECM) would be expected to play a central role in the pathogenesis of endometriosis. Various cell adhesion molecules (CAMs) have been investigated for their expression in endometriotic endometrium. Each cell type expresses a distinct pattern of integrins and other CAMs, including the cadherins, selectins and members of the immunoglobulin family that determines cell shape, maintains cell position and polarity and affects hormonal responsiveness. In addition, apoptosis might be mediated through loss of appropriate signals from the ECM through alternations in the integrin expression. Based on cell adhesion and the genes involving in adhesion and invasion aspects, cell adhesion molecules (CaMs) and proteolytic enzymes were investigated for their mechanisms in association with the progression of endometriosis.

Current Insights and Future Advances in Endometriosis Diagnostics 429

could explain the high proliferative activity of endometriotic tissue in this phase. Conversely, a decrease in ER and PR expression in ectopic implants during the secretory phase might lead to diminished proliferation. The expression of oestrogen and progesterone receptors may be regarded as an index of differentiation of the endometriotic implant. Consequently, ER and PR receptors may be used as markers of the activity of all subtypes of

Several genetic abnormalities or mutations have been suggested that might be related to endometriosis. Many technological approaches can help identify possible genetic markers of endometriosis. A number of technologies have emerged to facilitate progress in this direction (Taylor et al., 2002). Gene based technologies includes subtractive cDNA

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

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

Genomic alterations may represent important events in the development of endometriosis. Tumour suppressor genes play a role in the regulation of cell growth and prevention of carcinogenesis. The altered tumour suppressor genes might be related with the development of endometriosis. p53, a representative tumour suppressor, is involved in cell

significance of survivin in endometriosis, an aggressive tumour-like benign disease.

proliferation and progression of various tumour types (Akahane et al., 2007).

endometriotic lesions.

**5. Genetic markers** 

**5.1 Survivin gene expression** 

caspases 3 and 7.

**5.2 p53 mutations** 

hybridization and cDNA microarray techniques.
