Ovarian epithelial dysplasia after ovulation induction: time and dose effects

Chêne, Geneviève; Penault‐Llorca, Frédérique; Bouëdec, G. Le; Mishellany, Florence; Dauplat, Marie-Mélanie; Jaffeux, P.; Aublet-Cuvelier, Bruno; Pouly, Jean-Luc; Déchelotte, P.; Dauplat, J.

doi:10.1093/humrep/den358

Cited by 34 publications

(30 citation statements)

References 27 publications

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“…27,32 The process is further facilitated by close spatial anatomic relationship between the tubal fimbria and the ovarian surface and their synergistic role of ovulation and egg capture and subsequent transportation. 26,29 Furthermore, ovulation induced wound formation on the ovarian surface, [37][38][39] pelvic inflammation, [40][41][42] inflammation induced ovarian surface adhesion 43,44 and ovarian stromal proliferation under the influence of gonadotropins 39,[45][46][47] provide all necessary conditions for those tubal epithelia to enter the ovarian cortex. Actually, this common process from morphologic perspective has long been described as 'endosalpingiosis'.…”

Section: Discussionmentioning

confidence: 99%

Tubal origin of ovarian endometriosis

Zeng

Wang

et al. 2014

Modern Pathology

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Endometriosis is a puzzling and debilitating disease that affects millions of women around the world. Ovary is the most common organ site involved by endometriosis. Despite various hypotheses about its cell of origin, uncertainty remains. On the basis of our clinicopathologic observations, we hypothesize that fallopian tube may contribute the histogenesis of ovarian endometriosis. To examine if the hypothesis, tubal origin of ovarian endometriosis, has scientific supporting evidence, we identified a set of novel genes, which are either highly expressed in the normal fallopian tube or in the endometrium through a gene differential array study. Among many differentially expressed genes, FMO3 and DMBT1 were selected as the initial biomarkers to test the hypothesis. These biomarkers were then validated in ovarian sections with foci of endometriosis by comparing their expression levels in the fallopian tube and the endometrium within the same patients with real-time PCR, western blot and immunohistochemistry analysis. FMO3 was highly expressed in the tubal epithelia while low in the paired endometrium. In contrast, DMBT1 was high in the endometrium but low in the fallopian tube. In 32 ovarian endometriosis cases analyzed by real-time PCR, 18 (56%) showed a high level of FMO3 and a low level of DMBT1 expression. However, 14 (44%) endometriosis cases showed a reversed expression pattern with these two markers. Results were similarly seen in the methods of western blot and immunohistochemistry. The findings suggest that approximately 60% of the ovarian endometriosis we studied may be derived from the fallopian tube, whereas about 40% of the cases may be of endometrial origin. The fallopian tube epithelia may represent one of the tissue sources contributing to ovarian endometriosis. Such novel findings, which require confirmation, may have a significant clinical impact in searching for alternative ways of prevention and treatment of endometriosis.

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Section: Discussionmentioning

confidence: 99%

Tubal origin of ovarian endometriosis

Zeng

Wang

et al. 2014

Modern Pathology

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“…The data reported from France revealed a higher ovarian dysplasia score in the ovulation induction group than in the control group, although the number of cases in this study is low. They also found a relationship between the number of ovulation-induced cycles and the severity of ovarian dysplasia (dose-effect) and a relationship between time after the end of ovulation induction (over 7 years) and the severity of ovarian dysplasia (time-effect) [48].…”

Section: Fertility Medicationmentioning

confidence: 91%

Current Understanding of Risk Factors for Ovarian Cancer

Sueblinvong¹,

Carney²

2009

Curr. Treat. Options in Oncol.

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Ovarian cancer is the deadliest gynecologic cancer. Unlike many cancers such as breast, cervical and colon cancers, there is no easily clinically identifiable pre-malignant phase of this malignancy making early identification difficult. Similarly, unlike lung, head and neck, and skin cancers, there is not easily identifiable risk factor making prevention short of oophorectomy difficult. Even so, theories as to the causative factors of ovarian cancer continue to evolve making our understanding of the genesis of ovarian cancer more clear. Genetics, parity, environment, hormonal factors, and inflammation all play an important and pivotal role in the development of ovarian cancer. The most current understanding of these elements and their respective contribution to the development of this cancer are presented in this chapter.

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“…Afin que la méthodologie soit reproductible, nous avons retenu 11 critères histopathologiques évalués lors de précé-dentes études, à la fois sur les ovaires à risque génétique et les ovaires stimulés [12,13] :…”

Section: Critères Histopathologiquesunclassified

“…Nieto et al [11] ont, les premiers, retrouvé des anomalies significatives au niveau d'ovaires stimulés par rapport à une population témoin et à une population de patientes nullipares. Une de nos précédentes études a confirmé ces données en montrant en plus l'existence probable d'un effet-temps et d'un effet-dose [12] : les anomalies histopathologiques seraient d'autant plus sévères et nombreuses qu'il y a de cycles de stimulation (> 3) et après un délai suffisamment long (plus de sept années). Il semble cependant que le profil de dysplasie des ovaires stimulés soit différent de celui des ovaires à risque génétique, ce qui irait dans le sens d'une évolution différente : le cancer pour les ovaires à risque génétique (mutation BRCA 1 ou 2), et probablement les tumeurs borderlines pour les ovaires stimulés (protocoles de stimulation en Assistance médicale à la procréation) si l'on en croit les dernières séries épidémiologiques de suivi de patientes infertiles [18][19][20].…”

Section: Sous L'influence Hormonale Stromale Et Sous L'effet De Celluunclassified

“…Pourtant, ce score ne tient pas compte des kystes d'inclusion, invaginations épithéliales profondes et hyperplasie stromale, alors que ces critères apparaissent pourtant fondamentaux dans la physiopathologie de la dysplasie. Par ailleurs, aucun seuil de dysplasie n'est défini ; • le score de Clermont-Ferrand : notre score reprend l'ensemble des items décrits dans les études précédentes [12,13] afin d'obtenir un score exhaustif (11 critères histopathologiques) et reproductible ( Tableau 3). Il offre à la fois une description cytologique et architecturale de la dysplasie (analyse qualitative) et permet aussi une éva-luation quantitative grâce à deux niveaux de sévérité des anomalies.…”

Section: Sous L'influence Hormonale Stromale Et Sous L'effet De Celluunclassified

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