A BRIEF COMMUNICATION

2005 ◽  
Vol 230 (6) ◽  
pp. 429-433 ◽  
Author(s):  
William J. Murdoch ◽  
Edward A. Van Kirk ◽  
Brenda M. Alexander
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Cells ◽  
Laying Hens ◽  
Ovarian Surface Epithelium ◽  
Egg Laying ◽  
High Rate ◽  
Surface Epithelium ◽  
Ovarian Surface ◽  
Guanine Adducts ◽  
Ovarian Surface Epithelial

A cause-effect relationship between ovulation and common (surface) epithelial ovarian cancer has been suspected for many years. The ovarian surface epithelium apparently becomes exposed to genotoxins that are generated during the ovulatory process. Intensive egg-laying hens readily develop ovarian carcinomatosis. Indeed, elevated levels of potentially mutagenic 8-oxo-guanine adducts were detected in avian ovarian epithelial cells isolated from the apical surfaces and perimeters of pre-and postovulatory follicles, respectively. Internucleosomal DNA fragmentation indicative of apoptosis was evident in ovarian surface epithelial cells associated with the formative site of ovulation (stigma line) and regressive ruptured follicles. It is conceivable that a genetically altered progenitor cell with unrepaired DNA but not committed to death (i.e., a unifocal “escape”) could give rise to a transformed phenotype. Hence, the high rate of ovarian cancer in egg-laying hens could be the consequence of genomic damages to the ovarian surface epithelium associated with incessant ovulations, thereby increasing the likelihood of mutation and clonal expansion.

333 GENERATION OF OOCYTE-LIKE STRUCTURE FROM OVARIAN SURFACE EPITHELIAL STEM CELLS OF GOAT

2015 ◽  
Vol 27 (1) ◽  
pp. 255 ◽  
Author(s):  
S. Fatima ◽  
V. Sharma ◽  
S. Saini ◽  
S. Saugandhika ◽  
H. N. Malik ◽  
...  
Keyword(s):  
Stem Cells ◽  
Endangered Species ◽  
Epithelial Cells ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Epithelial Stem Cells ◽  
Rt Pcr ◽  
Ovarian Surface ◽  
Ovarian Surface Epithelial

Stem cells have potential for therapeutic application. Continuous repair of ovarian surface epithelium following folliculogenesis and ovarian carcinoma suggests the presence of stem cells in ovarian epithelial cells. In vitro gametogenesis in livestock will result in large numbers of oocytes production from a single ovary, resulting in faster multiplication of superior germplasm of livestock species, treatment of infertile animals, and conservation of endangered species. The present study was conducted with the objective of in vitro differentiation of putative ovarian surface epithelial stem cells into oocyte-like structures in goat model. Ovary samples of 1- to 2-year-old goats were collected from slaughterhouse. The surface of the ovary was gently scraped using sterile blunt scraper to isolate ovarian surface epithelial stem cells. These scraped cells were cultured in DMEM/F12 supplemented with 20% FBS for 3 weeks in 5% CO2 at 37°C with maximum humidity. The cultured stem cells were characterised for stemness by RT-PCR and immunostaining for Oct4, Sox2, and Nanog genes after 3 weeks. These putative stem cells were in vitro differentiated spontaneously to oocyte-like structures in DMEM/F12 medium and characterised for premeiotic markers by RT-PCR and immunostaining for VASA, DAZL, and STELLA genes. Results of this study provide evidence for the presence of putative stem cells with pluripotent characteristics in the ovarian surface epithelium. The cultured cells were found to be round in shape, with a high nucleus to cytoplasm ratio under inverted microscope, and found positive for stem cell markers of Oct4, Sox2, and Nanog genes. A total of 66 oocyte-like structures were produced from 12 ovaries. These oocyte-like structures were nearly similar to oocytes produced in vivo, both morphologically and in molecular gene expression. The oocyte-like structures were also found positive for premeiotic markers of VASA, DAZL, and STELLA genes by RT-PCR and immunostaining. From this study, we concluded that the ovarian surface epithelial cells have putative stem cells which can be in vitro differentiated into oocyte-like structures in goat. These oocyte-like structures need further characterisation of their surface membrane, more molecular markers, and following their developmental potential. These oocytes can help for multiplication of elite germplasm, curing infertile animals, and saving endangered species.

scholarly journals Loss of GATA6 Leads to Nuclear Deformation and Aneuploidy in Ovarian Cancer

2009 ◽  
Vol 29 (17) ◽  
pp. 4766-4777 ◽  
Author(s):  
Callinice D. Capo-chichi ◽  
Kathy Q. Cai ◽  
Joseph R. Testa ◽  
Andrew K. Godwin ◽  
Xiang-Xi Xu
Keyword(s):  
Ovarian Cancer ◽  
Nuclear Envelope ◽  
Cancer Cells ◽  
Human Cancer ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Ovarian Cancer Cells ◽  
Ovarian Surface ◽  
Ovarian Surface Epithelial ◽  
Ovarian Tumorigenesis

ABSTRACT A prominent hallmark of most human cancer is aneuploidy, which is a result of the chromosomal instability of cancer cells and is thought to contribute to the initiation and progression of most carcinomas. The developmentally regulated GATA6 transcription factor is commonly lost in ovarian cancer, and the loss of its expression is closely associated with neoplastic transformation of the ovarian surface epithelium. In the present study, we found that reduction of GATA6 expression with small interfering RNA (siRNA) in human ovarian surface epithelial cells resulted in deformation of the nuclear envelope, failure of cytokinesis, and formation of polyploid and aneuploid cells. We further discovered that loss of the nuclear envelope protein emerin may mediate the consequences of GATA6 suppression. The nuclear phenotypes were reproduced by direct suppression of emerin with siRNA. Thus, we conclude that diminished expression of GATA6 leads to a compromised nuclear envelope that is causal for polyploidy and aneuploidy in ovarian tumorigenesis. The loss of emerin may be the basis of nuclear morphological deformation and subsequently the cause of aneuploidy in ovarian cancer cells.

Spontaneous transformation of the ovarian surface epithelium and the biology of ovarian cancer

1995 ◽  
pp. 145-156 ◽  
Author(s):  
H. Salazar ◽  
A. K. Godwin ◽  
L. A. Getts ◽  
J. R. Testa ◽  
M. Daly ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Spontaneous Transformation ◽  
Ovarian Surface

scholarly journals Ovarian Surface Epithelium: Biology, Endocrinology, and Pathology*

2001 ◽  
Vol 22 (2) ◽  
pp. 255-288 ◽  
Author(s):  
Nelly Auersperg ◽  
Alice S. T. Wong ◽  
Kyung-Chul Choi ◽  
Sung Keun Kang ◽  
Peter C. K. Leung
Keyword(s):  
Ovarian Cancer ◽  
Molecular Mechanisms ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Neoplastic Progression ◽  
Ovarian Carcinomas ◽  
Genetic Changes ◽  
Ovarian Surface ◽  
Histological Characteristics ◽  
Epithelial Ovarian Carcinomas

Abstract The epithelial ovarian carcinomas, which make up more than 85% of human ovarian cancer, arise in the ovarian surface epithelium (OSE). The etiology and early events in the progression of these carcinomas are among the least understood of all major human malignancies because there are no appropriate animal models, and because methods to culture OSE have become available only recently. The objective of this article is to review the cellular and molecular mechanisms that underlie the control of normal and neoplastic OSE cell growth, differentiation, and expression of indicators of neoplastic progression. We begin with a brief discussion of the development of OSE, from embryonic to the adult. The pathological and genetic changes of OSE during neoplastic progression are next summarized. The histological characteristics of OSE cells in culture are also described. Finally, the potential involvement of hormones, growth factors, and cytokines is discussed in terms of their contribution to our understanding of the physiology of normal OSE and ovarian cancer development.

scholarly journals Inactivation of TRP53, PTEN, RB1, and/or CDH1 in the ovarian surface epithelium induces ovarian cancer transformation and metastasis

2020 ◽  
Vol 102 (5) ◽  
pp. 1055-1064 ◽  
Author(s):  
Mingxin Shi ◽  
Allison E Whorton ◽  
Nikola Sekulovski ◽  
Marilène Paquet ◽  
James A MacLean ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Surface Epithelium ◽  
Genetically Engineered ◽  
Surface Epithelium ◽  
Low Grade ◽  
Type I ◽  
Epithelial Hyperplasia ◽  
Genetically Engineered Mouse Models ◽  
Ovarian Surface ◽  
Tumor Dissemination

Abstract Ovarian cancer (OvCa) remains the most common cause of death from gynecological malignancies. Genetically engineered mouse models have been used to study initiation, origin, progression, and/or mechanisms of OvCa. Based on the clinical features of OvCa, we examined a quadruple combination of pathway perturbations including PTEN, TRP53, RB1, and/or CDH1. To characterize the cancer-promoting events in the ovarian surface epithelium (OSE), Amhr2cre/+ mice were used to ablate floxed alleles of Pten, Trp53, and Cdh1, which were crossed with TgK19GT121 mice to inactivate RB1 in KRT19-expressing cells. Inactivation of PTEN, TRP53, and RB1 with or without CDH1 led to the development of type I low-grade OvCa with enlarged serous papillary carcinomas and some high-grade serous carcinomas (HGSCs) in older mice. Initiation of epithelial hyperplasia and micropapillary carcinoma started earlier at 1 month in the triple mutations of Trp53, Pten, and Rb1 mice as compared to 2 months in quadruple mutations of Trp53, Pten, Rb1, and Cdh1 mice, whereas both genotypes eventually developed enlarged proliferating tumors that invaded into the ovary at 3–4 months. Mice with triple and quadruple mutations developed HGSC and/or metastatic tumors, which disseminated into the peritoneal cavity at 4–6 months. In summary, inactivation of PTEN, TRP53, and RB1 initiates OvCa from the OSE. Additional ablation of CDH1 further increased persistence of tumor dissemination and ascites fluid accumulation enhancing peritoneal metastasis.

scholarly journals Loss of LKB1 and PTEN tumor suppressor genes in the ovarian surface epithelium induces papillary serous ovarian cancer

2013 ◽  
Vol 35 (3) ◽  
pp. 546-553 ◽  
Author(s):  
Pradeep S. Tanwar ◽  
Gayatry Mohapatra ◽  
Sarah Chiang ◽  
David A. Engler ◽  
LiHua Zhang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Serous Ovarian Cancer ◽  
Suppressor Genes ◽  
Ovarian Surface

scholarly journals Role of Gonadotropin-Releasing Hormone as an Autocrine Growth Factor in Human Ovarian Surface Epithelium1

Endocrinology ◽  
2000 ◽  
Vol 141 (1) ◽  
pp. 72-80 ◽  
Author(s):  
Sung Keun Kang ◽  
Kyung-Chul Choi ◽  
Kwai Wa Cheng ◽  
Parimal S. Nathwani ◽  
Nelly Auersperg ◽  
...  
Keyword(s):  
Gnrh Agonist ◽  
Messenger Rna ◽  
Ovarian Surface Epithelium ◽  
Inhibitory Effect ◽  
Surface Epithelium ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Rt Pcr ◽  
Ovarian Surface ◽  
Ovarian Surface Epithelial

Abstract Epithelial ovarian cancer, which accounts for 80–90% of all ovarian cancers, is the most common cause of death from gynecological malignancies and is believed to originate from the ovarian surface epithelium. In the present study we investigated the expression of GnRH and its receptor in human ovarian surface epithelial (hOSE) cells and provided novel evidence that GnRH may have antiproliferative effects in this tissue. Using RT-PCR and Southern blot analysis, we cloned the GnRH and GnRH receptor (GnRHR) in hOSE cells. Sequence analysis revealed that GnRH and its receptor have sequences identical to those found in the hypothalamus and pituitary, respectively. To address whether GnRH regulates its own and receptor messenger RNA (mRNA), the cells were treated with different concentrations of the GnRH agonist (d-Ala6)-GnRH. Expression levels of GnRH and its receptor were investigated using quantitative and competitive RT-PCR, respectively. Interestingly, a biphasic effect was observed for the GnRH and GnRHR mRNA levels. High concentrations of the GnRH agonist (10−7 and 10−9m) decreased GnRH and GnRHR mRNA levels, whereas a low concentration (10−11m) resulted in up-regulation of GnRH and receptor mRNA levels. Treatment with the GnRH antagonist, antide, prevented the biphasic effects of the GnRH agonist in hOSE cells, confirming the specificity of the response. Furthermore, to investigate the physiological significance, we studied receptor-mediated growth regulatory effects of GnRH in human ovarian surface epithelial cells. The cells were treated with GnRH analogs, and the proliferative index of cells was measured using a [3H]thymidine incorporation assay. (d-Ala6)-GnRH had a direct inhibitory effect on the growth of hOSE cells in a time- and dose-dependent manner. This antiproliferative effect of the GnRH agonist was receptor mediated, as cotreatment of hOSE cells with antide abolished the growth inhibitory effects of the GnRH agonist. The results strongly suggest that GnRH can act as an autocrine/paracrine regulator in hOSE cells.

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