Tissue Factors Influencing Growth and Maintenance of Endometriosis^a

Abstract

The unpredictable response of endometriosis to steroids and its recurrence after therapy, led us to hypothesize a possible further control of this pathology by factors other than steroids. The presence of estrogen, progesterone and epidermal growth factor receptors (ER, PR, EGFr) was evaluated using immunohistochemistry before and after therapy with Danazol or a gonadotropin-releasing hormone analogue (GnRHa), Buserelin. EGFr, ER and PR were present in 100% of endometrial specimens, and in 71%, 29% and 49% of endometriotic implants, respectively. Danazol and GnRHa reduced immunohistochemical staining for EGFr antisera in the endometrial and endometriotic specimens. About 21% of endometriosis were EGFr positive and ER negative, suggesting a potential role of epidermal growth factor in growth and maintenance of endometrial ectopia.

Expression of interleukin-8 and monocyte chemotactic protein 1 in women with endometriosis

“…However, retrograde menstruation occurs in up to 80% of reproductive-age women; the discrepancy between the incidence of this phenomenon and the occurrence of pelvic endometriosis (10%-20%) might be explained by the presence of other permissive factors that promote the implantation and growth of endometrial cells (3). A growing body of evidence indicates that a combination of genetic, hormonal, immunologic, and environmental factors seem to be involved in the pathogenesis of this enigmatic disorder (4)(5)(6)(7)(8)(9).…”

Abnormal regulation of chemokine TECK and its receptor CCR9 in the endometriotic milieu is involved in pathogenesis of endometriosis by way of enhancing invasiveness of endometrial stromal cells

“…Retrograde menstruation occurs in up to 80% of women during their reproductive life; the discrepancy between the incidence of this phenomenon and the occurrence might be explained by the presence of further 'permissive' factors that promote the ectopic implantation and growth of endometrial cells. 2 The involvement of chemokines in endometriosis is becoming more evident as current research progresses. Chemokines have the ability to attract and activate inflammatory cells.…”

“…Dioxin (2,3,7, TCDD), an air pollutant, and estrogen also appear to be involved in endometriosis. Both endometrial stromal cells (ESCs) and the combination of 17b-estradiol and TCDD increase the secretion of TECK in the endometriosis-associated cells and promote the invasiveness of ESCs by increasing expression of matrix metalloproteinase (MMP)-2 and MMP-9.…”

Status of HER1 and HER2 in peritoneal, ovarian and colorectal endometriosis and ovarian endometrioid adenocarcinoma

“…Although molecular mechanisms remain to be defined, an increasing body of data suggests the possible transformation of endometriotic cells in endometrioid or clear cell carcinoma [14]. In addition, one EGFR gene polymorphism has been recently associated with susceptibility to endometriosis [15], and Melega et al reported that about 21% of endometriosis are EGFR positive and oestrogen receptor negative, suggesting a potential role of epidermal growth factor in the growth and maintenance of endometrial ectopia [16]. Finally, the development of new therapeutic agents targeting EGFR has attracted attention to treat various HER positive tumours.…”