Results
| PMID | 22926846 |
| Gene Name | CADM1 |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 75 |
| Population details | 75 (55 women undergoing endometrial biopsy or surgery for endometriosis (20 proliferative endometrium from women with endometriosis, proliferative endometrium from women without endometriosis, 20 peritoneal endometriosis, 20 ovarian endometriosis, 20 colo |
| Sex | Female |
| Associated genes | Nectin-1, -3, -4 and Necl-2 |
| Other associated phenotypes |
Endometriosis |
|
Hum Reprod. 2012 Nov;27(11):3179-86. doi: 10.1093/humrep/des304. Epub 2012 Aug Ballester, Marcos| Gonin, Julie| Rodenas, Anita| Bernaudin, Jean-Francois| Rouzier, Roman| Coutant, Charles| Darai, Emile ER2 UPMC, Universite Pierre et Marie Curie, Paris 6, France. marcos.ballester@tnn.aphp.fr STUDY QUESTION: How is the expression of nectins and nectin-like molecules (Necls) detected by immunostaining altered by endometriosis? SUMMARY ANSWER: Our results suggest that Nectin-1, -3, -4 and Necl-2 may contribute to the pathogenesis of endometriosis. Immunostaining of nectins and Necls varies according to the anatomical location of endometriosis. WHAT IS KNOWN AND WHAT THIS PAPER ADDS: Nectin and Necl molecules are immunoglobulin-like cell adhesion molecules involved in apoptosis, cell proliferation and in metastases. Previous studies have demonstrated the involvement of adhesion molecules in the development of endometriotic lesions but no data exist on immunostaining of nectins and Necls molecules in endometriosis. DESIGN, PARTICIPANTS AND SETTING: This retrospective study was conducted in a tertiary-care hospital (Tenon Hospital, Paris, France). Samples were collected from 55 women undergoing endometrial biopsy or surgery for endometriosis and 20 controls having hysterectomy or endometrial biopsy for other reasons; multiple samples were collected from 15 women. We studied the immunostaining of Nectin-1, -3, -4 and Necl-2 in secretory and proliferative endometrium from women with (n = 20) or without endometriosis (i.e. control group, n = 20), and in peritoneal (n = 20), ovarian (n = 20) and colorectal endometriosis (n = 20). MAIN RESULTS: Semi-quantitative immunostaining demonstrated that (1) Necl-2 staining was stronger in all types of endometriotic lesions than in the eutopic endometrium from patients with endometriosis (P < 0.0125) and in ovarian endometriotic cysts compared with other locations (P < 0.001); (2) Nectin-3 staining was stronger in the eutopic endometrium of patients with endometriosis compared with controls (P = 0.03) and in all endometriotic lesions compared with the eutopic endometrium from patients with endometriosis (P < 0.0125); (3) Nectin-4, staining was stronger in the eutopic endometrium of patients with endometriosis compared with controls (P = 0.04) and (4) Nectin-1 staining was significantly increased in colorectal endometriosis compared with other locations (P = 0.004). BIAS, CONFOUNDING AND OTHER REASONS FOR CAUTION: We did not assess the pattern of expression in endometriosis of all nectins and Necl molecules. Indeed, Necl-5 is implicated in many pathophysiological processes such as cell movement and proliferation with potential relevance to endometriosis. GENERALISABILITY TO OTHER POPULATIONS: At present, few data on implication of nectins and Necl molecules in endometriosis exist. Hence, our results should be confirmed by further quantitative studies at protein or RNA levels. STUDY FUNDING/COMPETING INTEREST(S): No funding source. All the authors declare no conflict of interest. Mesh Terms: Adult| Cell Adhesion Molecules/genetics/*metabolism| Colonic Diseases/metabolism/pathology/surgery| Digestive System Diseases/*metabolism/pathology/surgery| Endometriosis/*metabolism/pathology/surgery| Endometrium/*metabolism/pathology/surgery| Fema |
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