Ovarian Surface Epithelium and Human Ovarian Cancer

Dietl, Johannes; Marzusch, K.

doi:10.1159/000292682

Cited by 33 publications

(11 citation statements)

References 47 publications

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“…The carcinogenic effects of estrogens on the surface epithelium of the ovary has been extensively documented [25,26], but the mechanisms by which these steroids promote tumorigenesis remain unresolved. Our studies demonstrate the existence of a direct relationship between E2 and E-cad m R N A levels.…”

Section: Discussionmentioning

confidence: 99%

“…Although hormonal contraceptives have been shown to be effective in reducing the risk of developing ovarian carcinoma, the mechanisms by which these agents act have not been elucidated [26]. High levels of estrogens and progestins are known to be capable of down-regulating the estrogen receptor [38][39][40].…”

Section: Discussionmentioning

confidence: 99%

“…Although the levels of endogenous steroids are low in immature mice [20], steroid receptors have been shown to be present in the ovaries of these animals [21]. The growth and differentiation of the surface epithelium is known to be dependent on steroids [22][23][24][25][26]. Furthermore, the chronic administration of steroids (in particular, estrogens) has been shown to result in the formation of ovarian carcinomas from the surface epithelium [25,26].…”

Section: Introductionmentioning

confidence: 99%

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Estradiol regulates E-cadherin mRNA levels in the surface epithelium of the mouse ovary

1994

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E-cadherin is a calcium-dependent cell adhesion molecule which is present in the surface epithelium of the mouse ovary. This cell adhesion molecule has been implicated as a suppressor of tumorigenesis. The regulators of E-cadherin mRNA levels in the ovary have not been identified. We have examined the ability of steroids to influence ovarian E-cadherin mRNA levels in vivo. Immature mice were injected with either progesterone, testosterone, dihydrotestosterone, 17-beta estradiol or 17-alpha estradiol. Only 17-beta estradiol caused a rapid and significant increase in the ovarian E-cadherin mRNA levels. We speculate that this steroid is a key regulator of E-cadherin-mediated epithelial cell interactions in vivo. We also discuss the possibility that the carcinogenic effects of estrogens on the ovary may be related to their ability to regulate E-cadherin levels in this tissue.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Estradiol regulates E-cadherin mRNA levels in the surface epithelium of the mouse ovary

1994

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“…19 A number of more recent molecular, genetic, and immunohistochemical studies have provided evidence that many or most pelvic and extrauterine high-grade serous carcinomas likely originate in the fallopian tubes. 1–11 The current study, an examination of a series of low-stage ovarian carcinomas including low-stage HGSCs, supports the idea that many HGSCs do not arise within the ovary; as compared to the other major ovarian carcinoma subtypes, low-stage HGSCs are significantly more often distributed bilaterally and multifocally with ovarian surface involvement of relatively small ovaries, patterns which, with the exception of SC, are almost always equated with metastasis to the ovaries.…”

Section: Discussionmentioning

confidence: 99%

Low-Stage High-Grade Serous Ovarian Carcinomas

Morency

Leitao

Soslow

2016

International Journal of Gynecological Pathology

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Summary Many adnexal high-grade serous carcinomas (HGSCs) may derive from microscopic precursors in the fallopian tube. By studying a series of low-stage ovarian carcinomas, we anticipated that HGSCs would be distributed in a pattern suggesting secondary involvement, helping to indirectly validate the fallopian tube origin theory, and that most ovarian carcinomas other than SCs would demonstrate features consistent with derivation from precursors located in or transplanted to the ovary. Seventy-six patients with low-stage (FIGO I/II) sporadic ovarian carcinoma who underwent primary surgical management at Memorial Sloan Kettering Cancer Center from 1980 to 2000 were included in the study. Histologic type was assigned using Gilks’ criteria.13 Similar to the approach taken when distinguishing primary and metastatic mucinous or endometrioid carcinoma involving ovary, cases interpreted as showing a “primary” pattern of ovarian involvement had 3 or more of the following features: unilateral tumor, size greater than 12 cm, no surface involvement, no multinodularity, no destructive stromal invasion. All other cases were considered to show a “metastatic” pattern of ovarian involvement. Cases were evaluated for p53 and WT-1 expression, using standard techniques on a tissue microarray. TP53 gene sequencing was also performed. Cases comprised HGSC (n=22), endometrioid carcinoma (n=30), clear cell carcinoma (n=13) and mucinous carcinoma (n=11). HGSCs displayed substantially more “metastatic features” than the non-HGSC group and a mean overall size that was smaller (8.85 cm vs 14.1 cm). Statistically significant differences were found for bilaterality (63% vs 7.3%), p = 0.0001; multinodularity (55% vs 7.3%), p = 0.0001; tumor size, p = 0.003; and surface involvement (50% vs 13%), p = 0.002. Five of 22 (23%) of HGSCs showed a “primary pattern” of ovarian involvement. There were no significant differences between these cases and “metastatic pattern” HGSCs when comparing morphology, immunophenotype, TP53 mutational status, and clinical outcomes. Most low-stage HGSCs demonstrate patterns of ovarian involvement that suggest metastasis from another source, such as the fallopian tube. Both metastatic pattern HGSCs and unilateral, low-stage HGSCs can behave aggressively.

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“…The exactly initiating cell population for epithelial ovarian carcinoma (EOC) remains to be defined. Different evidences have suggested that EOC originate from the ovarian surface epithelium, inclusion cysts lined [4-7] or alternatively, the fallopian tube epithelium [8] or components of the secondary Müllerian system, including the epithelial cells of the rete ovarii, paraovarian/ paratubal cysts, endosalpingiosis, endometriosis or endomucinosis [9-13]. …”

Section: Backgroundsmentioning

confidence: 99%

Enhanced efficacy and specificity of epithelial ovarian carcinogenesis by embedding a DMBA-coated cloth strip in the ovary of rat

et al. 2012

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BackgroundOvarian cancer is predominant of epithelial cell origin and often present at an advanced stage with poor prognosis. Most animal models of ovarian carcinoma yield thecal/granulose cell tumors, rather than adenocarcinomas. The best reported induction rate of adenocarcinoma in rats is 10-45% by an ovarian implantation of 7, 12-dimethylbenz[a]anthracene (DMBA) coated silk suture. We provided an improved procedure to construct the model by the ovarian implantation of DMBA-coated cloth strip.MethodsA sterile suture (as S group) or a piece of cloth strip (as CS group) was soaked in DMBA before ovarian implantation in Wistar rats. Tumor size, incidence rate and pathological type were analyzed.ResultsOvarian tumors in rats of CS group were first noted at 16 wk post implantation and reached a cumulative incidence of 75% (96/128) at 32 wk, while the tumor incidence rate in S group at 32 wk was only 46.25% (37/80). The tumor size in CS group (3.63 ± 0.89 cm) was larger than that of S group (2.44 ± 1.89 cm) (P < 0.05). In CS group, there were only two types of tumor formed: adenocarcinoma (90/96) and sarcoma (6/96). While in S group, there were different types, including adenocarcinoma (21/37), squamous carcinoma (3/37), granulosa cell tumor (3/37), sarcoma (4/37), undifferentiated carcinoma with no adeno character (2/37), benign ovarian tumor (2/37), and malignant teratoma (1/37).ConclusionThe model in our study yields much higher incidence and specificity of epithelial derived tumors and showed histological similarities to human ovarian cancers, which would be more suitable for therapeutic research.

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Ovarian Surface Epithelium and Human Ovarian Cancer

Cited by 33 publications

References 47 publications

Estradiol regulates E-cadherin mRNA levels in the surface epithelium of the mouse ovary

Estradiol regulates E-cadherin mRNA levels in the surface epithelium of the mouse ovary

Low-Stage High-Grade Serous Ovarian Carcinomas

Enhanced efficacy and specificity of epithelial ovarian carcinogenesis by embedding a DMBA-coated cloth strip in the ovary of rat

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