Proliferative activity and genetic alterations in TP53 in endometriosis

In the secretory phase of the menstrual cycle, proliferative activity and expression levels of cell cycle-regulatory molecules are higher in endometriotic lesions than in the corresponding eutopic endometrium. In some endometriotic lesions, proliferative activity remains high in the postmenopausal period. By immunostaining, one can recognize TP53 overexpression in epithelial cells in a considerable number of endometriotic lesions. In those endometriotic lesions that show TP53 overexpression, neither TP53 point mutations (exons 5 to 8) nor microsatellite alterations (microsatellite instability or loss of heterozygosity) has been detected. Thus, the TP53 overexpression demonstrated in endometriotic epithelia seems to result from an overproduction of wild-type TP53 protein. The biological role of TP53 in endometriotic lesions is still unclear.