Effect of medical treatment on malignant transformation to clear cell carcinoma in endometriosis patients: A comparative study on gene expression using next generation sequencing (NGS)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE283755 | GEO | 2025/12/03
REPOSITORIES: GEO
Similar Datasets
Project description:Endometriosis, a benign inflammatory disease whereby endometrial-like tissue grows outside the uterus, is a risk factor for endometriosis-associated ovarian cancers. In particular, ovarian endometriomas, cystic lesions of deeply invasive endometriosis, are considered the precursor lesion for ovarian clear-cell carcinoma (OCCC). To explore the transcriptomic landscape, OCCC from women with pathology-proven concurrent endometriosis (n = 4) were compared to benign endometriomas (n = 4) by bulk RNA and small-RNA sequencing.
2023-07-29 | GSE230956 | GEO
Project description:Ovarian clear cell carcinoma (OCCC) shows unique clinical features including an association with endometriosis and poor prognosis. We previously reported that the contents of endometriotic cysts, especially high concentrations of free iron, are a possible cause of OCCC carcinogenesis through iron-induced persistent oxidative stress. In this study, we conducted gene expression microarray analysis using 38 ovarian cancer cell lines and identified genes commonly expressed in both OCCC cell lines and clinical samples, which comprise an OCCC gene signature. The OCCC signature reproducibly predicts OCCC specimens in other microarray data sets, suggesting that this gene profile reflects the inherent biological characteristics of OCCC. The OCCC signature contains known markers of OCCC, such as hepatocyte nuclear factor-1b (HNF-1b) and versican (VCAN), and other genes that reflect oxidative stress. Expression of OCCC signature genes was induced by treatment of immortalized ovarian surface epithelial cells with the contents of endometriotic cysts, indicating that the OCCC signature is largely dependent on the tumor microenvironment. Induction of OCCC signature genes is at least in part epigenetically regulated, as we found hypomethylation of HNF-1b and VCAN in OCCC cell lines. This genomewide study indicates that the tumor microenvironment induces specific gene expression profiles that contribute to the development of distinct cancer subtypes. Affymetrix Human Genome U133A 2.0 Array was conducted for 38 ovarian cancer cell lines (13 OCCC cell lines and 25 non-OCCC cell lines). All specimens were arrayed in parallel and used for RMA normalization.
2011-05-16 | E-GEOD-29175 | biostudies-arrayexpress
Project description:Ovarian clear cell carcinoma (OCCC) shows unique clinical features including an association with endometriosis and poor prognosis. We previously reported that the contents of endometriotic cysts, especially high concentrations of free iron, are a possible cause of OCCC carcinogenesis through iron-induced persistent oxidative stress. In this study, we conducted gene expression microarray analysis using 38 ovarian cancer cell lines and identified genes commonly expressed in both OCCC cell lines and clinical samples, which comprise an OCCC gene signature. The OCCC signature reproducibly predicts OCCC specimens in other microarray data sets, suggesting that this gene profile reflects the inherent biological characteristics of OCCC. The OCCC signature contains known markers of OCCC, such as hepatocyte nuclear factor-1b (HNF-1b) and versican (VCAN), and other genes that reflect oxidative stress. Expression of OCCC signature genes was induced by treatment of immortalized ovarian surface epithelial cells with the contents of endometriotic cysts, indicating that the OCCC signature is largely dependent on the tumor microenvironment. Induction of OCCC signature genes is at least in part epigenetically regulated, as we found hypomethylation of HNF-1b and VCAN in OCCC cell lines. This genomewide study indicates that the tumor microenvironment induces specific gene expression profiles that contribute to the development of distinct cancer subtypes.
2011-05-16 | GSE29175 | GEO
Project description:Endometriosis -associated ovarian carcinoma (EAOC) is mostly malignant transformation from endometriomas. However, the endometriosis cancerogenesis remains to be established. Using spatial transcriptomic of human specimens of normal, endometriomas and EAOC, activation of Interleukin-17C (IL-17C) signaling is identified, with higher IL-17 receptor E (IL-17RE) expression in endometriotic cells, to be associated with cancerogenesis and which has no previous association with EAOC. Elevated IL-17C concentration is found in peritoneal fluid in women with ovarian cancer and IL-17RE-overexpressed endometriosis mice. In particular, IL-17C knockout reduces peritoneal fluid IL-17C concentration and inhibits ectopic lesion growth in endometriosis mice. Besides, the role of IL-17C in the endometriosis cancerogenesis was investigated by blocking the IL-17C/IL-17RE, modulating IL-17RE and neutralizing IL-17C in endometriotic cells, endometrial organoids and endometriosis mice. These data defined peritoneal fluid-mediated endometriosis cancerogenesis through IL-17C regulation and suggests that IL-17C/IL-17RE can thus potentially serve as novel targets for with high IL-17C.
2025-04-30 | GSE291389 | GEO
Project description:Endometriosis is a common disease seen by gynecologists. Clinical features involve pelvic pain and unexplained infertility. Although endometriosis is pathologically characterized by endometrial tissue outside the normal uterine location, endometriosis is otherwise not easily explained. Endometriomas, endometriotic cysts of the ovary, typically cause pain and distortion of pelvic anatomy. To begin to understand the pathogenesis of endometriomas, we carried out transcriptome:microRNAome analysis of endometriomas and eutopic endometrium, using gene expression arrays and next generation small RNA sequencing technology. Keywords: two group comparison
2011-05-09 | GSE23339 | GEO
Project description:Endometriosis is a common disease seen by gynecologists. Clinical features involve pelvic pain and unexplained infertility. Although endometriosis is pathologically characterized by endometrial tissue outside the normal uterine location, endometriosis is otherwise not easily explained. Endometriomas, endometriotic cysts of the ovary, typically cause pain and distortion of pelvic anatomy. To begin to understand the pathogenesis of endometriomas, we carried out transcriptome:microRNAome analysis of endometriomas and eutopic endometrium, using gene expression arrays and next generation small RNA sequencing technology. Keywords: two group comparison Patients undergoing surgery for endometriomas, suspected endometriosis, pelvic pain, abnormal uterine bleeding, pelvic organ prolapse, or uterine leiomyomas were approached for participation. After informed consent, the patients underwent scheduled surgical procedure. Tissues were collected either as cyst wall of endometrioma or endometrial curettage of hysterectomy specimen and placed directly into RNALater (Ambion, Austin, TX) and eventually frozen at -80?C. Samples were designated as endometriomas or non-endometriosis control endometrium based on surgical pathology reports. Total RNA was isolated from frozen tissue. High quality RNA was subjected to Illumina’s Human WG-6 version 2.0 BeadChips (Illumina). . *** This Series represents the transcriptome component of the study. ***
2011-05-09 | E-GEOD-23339 | biostudies-arrayexpress
Project description:Endometriosis is an estrogen-dependent inflammatory disease. A pivotal contributor to endometriosis is the estrogen receptor beta (ERβ), which drives the condition by impeding cell death through interferon (IFN) signaling. One noteworthy component of this cascade is the N-myc and STAT Interactor (NMI), an interferon alpha (IFNα) target gene whose expression is repressed in endometriotic lesions compared to normal endometrium. This repression is particularly pronounced in stromal cells, mediated by ERβ. The results of Western blot analyses, comparing IFNα-treated and untreated cells, demonstrate that IFNα treatment triggers cell death signaling, including apoptosis and necroptosis, in endometrial stromal cells. Intriguingly, NMI knockdown (KD) obstructed IFNα-induced cell death signaling in human endometrial stromal cells. Moreover, NMI KD amplified non-canonical IFNα pathways, such as β-Catenin/GSK3β and PI3K/AKT signaling, in endometrial stromal cells following IFNα treatment. RNA sequencing analyses unveiled that NMI KD augmented the expression of genes responsible for cell-cell adhesion and extracellular structural organization in IFNα-independent manners. These findings suggest that NMI KD plays an indispensable role in enhancing the adhesion and invasion of endometriotic cells during endometriosis progression. In summary, NMI functions as an endometriosis suppressor gene in endometriotic stromal cells, curbing the advancement of endometriosis. This intricate interplay of ERβ, IFNα signaling, and NMI offers novel insights into the mechanisms governing endometriosis development.
2025-08-31 | GSE241751 | GEO
Project description:Accumulating evidences suggest that various epigenetic aberrations play definite roles in the pathogenesis of endometriosis. The aim of this study is to identify 1) the panel of aberrantly expressed genes that are epigenetically suppressed by histone acetylation in endometriosis; 2) the roles of CCAAT/enhancer-binding protein (C/EBP) alpha, one of the candidate molecules whose expression was epigenetically repressed in endometriotic cyst stromal cells (ECSCs), in the pathogenesis of endometriosis; and 3) the efficacy of the histone deacetylase inhibitors for the treatment of endometriosis. Subconfluent ECSCs cultured in 10-cm dish were further incubated for 72 h with or without VPA (8 mM) and/or 5aza. Total RNA from untreated ECSCs (n=4), VPA-treated ECSCs (n=4), 5aza-treated ECSCs (n=4), and VPA- and 5aza-treated ECSCs (n=4) was extracted and subjected to gene expression microarray analysis.
2013-10-21 | E-GEOD-44207 | biostudies-arrayexpress
Project description:Mechanisms of immune dysregulation against established tumors are relatively well understood. Much less is known about the role of immune effectors against cancer precursor lesions. Endometrioid and clear cell ovarian tumors may partly derive from endometriosis, a commonly diagnosed chronic inflammatory disease. We performed here the most comprehensive immune gene expression analysis of pelvic inflammation in endometriosis and endometriosis-associated ovarian cancer (EAOC). RNA was extracted from 120 paraffin tissue blocks comprising of normal endometrium (n=32), benign endometriosis (n=30), atypical endometriosis (n=15) and EAOC (n=43). Serous tumors (n=15) were included as non-endometriosis associated controls. The immune microenvironment was profiled using Nanostring and the nCounter® GX Human Immunology Kit, comprising probes for a total of 511 immune genes. Please note that 3 normal endometrium samples did not pass the array quality filtering and therefore excluded in the data analyses.
2015-01-07 | E-GEOD-57545 | biostudies-arrayexpress
Project description:The pathophysiology of endometriotic lesion development remains unclear but involves a complex interaction between ectopic endometrium and host peritoneal tissues. We hypothesised that disruption of this interaction was likely to suppress endometriotic lesion formation. We hoped to delineate the molecular and cellular dialogue between ectopic human endometrium and peritoneal tissues in nude mice, as a first step towards testing this hypothesis. Human endometrium was xenografted into nude mice and the resulting lesions were analysed using microarrays. A novel technique was developed that unambiguously determined whether RNA transcripts identified by the microarray analyses originated from human cells (endometrium) or mouse cells (stroma). Four key pathways (ubiquitin/proteosome, inflammation, tissue remodelling/repair and ras-mediated oncogenesis) were revealed, that demonstrated communication between host stromal cells and ectopic endometrium. Morphometric analysis of nude mouse lesions confirmed that necrosis, inflammation, healing and repair and cell proliferation occurred during xenograft development. These processes were entirely consistent with the molecular networks revealed by the microarray data. The transcripts detected in the xenografts overlapped with transcripts differentially expressed in a comparison between paired eutopic and ectopic endometrium from human endometriotic patients. For the first time components of the interaction between ectopic endometrium and peritoneal stromal tissues have been revealed in ectopic endometrial lesions. Targeted disruption of this dialogue is likely to disrupt endometriotic tissue formation and may prove to be an effective therapeutic strategy for endometriosis. Experiment Overall Design: Xenografts of human endometrium in nude mice hybridised to both human and mouse specific genechips. 2 biological replicates, at 3 time points. Control human endometrium and mouse pertioneum were hybridised to both human and mouse genechips
2009-01-02 | E-GEOD-11768 | biostudies-arrayexpress