scholarly journals LINC00452 promotes ovarian carcinogenesis through increasing ROCK1 by sponging miR-501-3p and suppressing ubiquitin-mediated degradation

Aging ◽  
2020 ◽  
Vol 12 (21) ◽  
pp. 21129-21146
Author(s):  
Juan Yang ◽  
Wei-Gang Wang ◽  
Ke-Qiang Zhang
Keyword(s):  
Ovarian Carcinogenesis

scholarly journals BMI-1 Expression Heterogeneity in Endometriosis-Related and Non-Endometriotic Ovarian Carcinoma

2021 ◽  
Vol 22 (11) ◽  
pp. 6082
Author(s):  
Ludmila Lozneanu ◽  
Raluca Anca Balan ◽  
Ioana Păvăleanu ◽  
Simona Eliza Giuşcă ◽  
Irina-Draga Căruntu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Statistical Analysis ◽  
Ovarian Carcinoma ◽  
Clinicopathological Characteristics ◽  
Cell Phenotype ◽  
Epithelial Tumor ◽  
Normal Organ ◽  
Ovarian Carcinogenesis ◽  
Cellular Signaling Pathway ◽  
The Relationship

BMI-1 is a key component of stem cells, which are essential for normal organ development and cell phenotype maintenance. BMI-1 expression is deregulated in cancer, resulting in the alteration of chromatin and gene transcription repression. The cellular signaling pathway that governs BMI-1 action in the ovarian carcinogenesis sequences is incompletely deciphered. In this study, we set out to analyze the immunohistochemical (IHC) BMI-1 expression in two different groups: endometriosis-related ovarian carcinoma (EOC) and non-endometriotic ovarian carcinoma (NEOC), aiming to identify the differences in its tissue profile. Methods: BMI-1 IHC expression has been individually quantified in epithelial and in stromal components by using adapted scores systems. Statistical analysis was performed to analyze the relationship between BMI-1 epithelial and stromal profile in each group and between groups and its correlation with classical clinicopathological characteristics. Results: BMI-1 expression in epithelial tumor cells was mostly low or negative in the EOC group, and predominantly positive in the NEOC group. Moreover, the stromal BMI-1 expression was variable in the EOC group, whereas in the NEOC group, stromal BMI-1 expression was mainly strong. We noted statistically significant differences between the epithelial and stromal BMI-1 profiles in each group and between the two ovarian carcinoma (OC) groups. Conclusions: Our study provides solid evidence for a different BMI-1 expression in EOC and NEOC, corresponding to the differences in their etiopathogeny. The reported differences in the BMI-1 expression of EOC and NEOC need to be further validated in a larger and homogenous cohort of study.

Ovulatory Factor in Ovarian Carcinogenesis

2008 ◽  
pp. 119-128 ◽  
Author(s):  
William J. Murdoch
Keyword(s):  
Ovarian Carcinogenesis

Expression of Catechol O methyl transferase (COMT) with the contrasting effects of 17β estradiol (E2): Implications for the mechanism of estrogen-induced ovarian carcinogenesis.

2020 ◽  
Author(s):  
Nour Mohamed El-Etreby ◽  
Eman Medhat Osman ◽  
Nehal Abd El Latif El Badawy ◽  
Hoda Abd El Hamid Nour
Keyword(s):  
Ovarian Cancer ◽  
Epidemiological Data ◽  
Serum Levels ◽  
Ovarian Tumors ◽  
Tissue Homogenate ◽  
Ovarian Cancer Risk ◽  
Comt Inhibition ◽  
Methyl Transferase ◽  
Estrogen Exposure ◽  
Ovarian Carcinogenesis

Abstract Background Epidemiological data show that induction of ovarian cancer is related to estrogen exposure and metabolism. In addition catechol metabolites of estrogen also contribute to carcinogenesis. O methylation by Catechol O methyl transferase (COMT) is a phase II metabolic inactivation pathway for catechol estrogens. The goal of the present study was to investigate the role of COMT level in ovarian carcinogenesis with the contrasting effects of 17 β estradiol level. Subjects and methods Our study was conducted on 80 subjects divided into 30 patients with malignant ovarian tumors ,30 patients with benign ovarian tumors and 20 healthy controls. Tissue and serum levels of COMT and 17 17 β estradiol were determined using ELISA Results According to our results COMT inhibition in the malignant group was detected as high as 7.1 pmol/L E2 in serum and 15.6 pmol/L E2 in tissue homogenate. This inhibition was absent in the benign group as high as 7.53 pmol/L E2 in serum and as high as 14.9 pmol/L E2 in tissue homogenates. Conclusions Our results provide evidence for the protective effect of COMT in benign ovaries against neoplastic transformation. This supports the notion that targeting the metabolism of estrogen can be an another way to reduce ovarian cancer risk.

Diethylstilbestrol regulates expression of avian apolipoprotein D during regression and recrudescence of the oviduct and epithelial-derived ovarian carcinogenesis

2015 ◽  
Vol 52 ◽  
pp. 82-89 ◽  
Author(s):  
J. Jeong ◽  
H. Bae ◽  
W. Lim ◽  
F.W. Bazer ◽  
G. Song
Keyword(s):  
Ovarian Carcinogenesis ◽  
Apolipoprotein D

Dual modality imaging of a novel rat model of ovarian carcinogenesis

2006 ◽  
Vol 11 (4) ◽  
pp. 041123 ◽  
Author(s):  
Elizabeth M. Kanter ◽  
Ross M. Walker ◽  
Samuel L. Marion ◽  
Molly Brewer ◽  
Patricia B. Hoyer ◽  
...  
Keyword(s):  
Rat Model ◽  
Dual Modality ◽  
Ovarian Carcinogenesis ◽  
Dual Modality Imaging

Nutrition and ovarian carcinogenesis: A critical review

2005 ◽  
Vol 5 (2) ◽  
pp. 81-94
Author(s):  
Karen Gil ◽  
Vivian von Gruenigen
Keyword(s):  
Critical Review ◽  
Ovarian Carcinogenesis

The fallopian tube: a change in the paradigm of the ovarian carcinogenesis

2018 ◽  
Vol 1 ◽  
pp. 1-1
Author(s):  
Gautier Chene ◽  
Emanuele Cerruto
Keyword(s):  
Fallopian Tube ◽  
Ovarian Carcinogenesis

scholarly journals Onset of Telomere Dysfunction and Fusions in Human Ovarian Carcinoma

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 414 ◽  
Author(s):  
Nazmul Huda ◽  
Yan Xu ◽  
Alison M. Bates ◽  
Deborah A. Rankin ◽  
Nagarajan Kannan ◽  
...  
Keyword(s):  
Genomic Instability ◽  
Critical Role ◽  
Telomerase Activity ◽  
Diagnostic Tools ◽  
Early Event ◽  
Molecular Heterogeneity ◽  
Telomere Dysfunction ◽  
Ovarian Carcinogenesis ◽  
Tumor Tissues ◽  
Human Solid Tumors

Telomere dysfunction has been strongly implicated in the initiation of genomic instability and is suspected to be an early event in the carcinogenesis of human solid tumors. Recent findings have established the presence of telomere fusions in human breast and prostate malignancies; however, the onset of this genomic instability mechanism during progression of other solid cancers is not well understood. Herein, we explored telomere dynamics in patient-derived epithelial ovarian cancers (OC), a malignancy characterized by multiple distinct subtypes, extensive molecular heterogeneity, and widespread genomic instability. We discovered a high frequency of telomere fusions in ovarian tumor tissues; however, limited telomere fusions were detected in normal adjacent tissues or benign ovarian samples. In addition, we found relatively high levels of both telomerase activity and hTERT expression, along with anaphase bridges in tumor tissues, which were notably absent in adjacent normal ovarian tissues and benign lesions. These results suggest that telomere dysfunction may occur early in ovarian carcinogenesis and, importantly, that it may play a critical role in the initiation and progression of the disease. Recognizing telomere dysfunction as a pervasive feature of this heterogeneous malignancy may facilitate the future development of novel diagnostic tools and improved methods of disease monitoring and treatment.

scholarly journals A Mechanistic Study of Ovarian Carcinogenesis Induced by Nitrofurazone Using rasH2 Mice

2000 ◽  
Vol 28 (5) ◽  
pp. 649-655 ◽  
Author(s):  
Kiyoshi Takegawa ◽  
Kunitoshi Mitsumori ◽  
Kazuo Yasuhara ◽  
Matsuko Moriyasu ◽  
Masamitsu Sakamori ◽  
...  
Keyword(s):  
Mechanistic Study ◽  
Ovarian Carcinogenesis ◽  
Rash2 Mice
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