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Transcriptome and DNA methylation analyses highlight the role of menstrual cycle phase in tumorigenesis of endometriosis-related ovarian carcinoma histotypes.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE226872 | GEO | 2023/10/13

REPOSITORIES: GEO

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Transcriptome and DNA methylation analyses highlight the role of menstrual cycle phase in tumorigenesis of endometriosis-related ovarian carcinoma histotypes [methylation]

Project description:Epithelial ovarian cancer, or ovarian carcinoma (OC), is a diverse disease. Two of the rarer subtypes, clear cell OC (CCOC) and endometrioid OC (ENOC), both arise from ovarian endometriotic cysts, particularly atypical endometriosis. CCOC and ENOC have similar mutation profiles and share a common cell of origin, but their cellular phenotypes and clinical outcomes are distinct; in particular, CCOC has poor clinical survival. The most well-known difference between the histotypes is the universal overexpression of HNF1B (Hepatocyte nuclear factor-1β) in clear cell tumors and overexpression of ESR1 in ENOC. It is not well understood how these discrete histotypes arise from the same cell of origin. Via transcriptional (n=57) and DNA methylation analysis (N=127) of these rare tumors, we show that CCOC closely resembles secretory endometrium in transcriptional profile; whereas ENOC transcriptomes resemble proliferative endometrium.

2023-10-13 | GSE226823 | GEO

Transcriptome and DNA methylation analyses highlight the role of menstrual cycle phase in tumorigenesis of endometriosis-related ovarian carcinoma histotypes [RNA-Seq]

2023-10-13 | GSE226870 | GEO

Transcriptome and DNA methylation analyses highlight the role of menstrual cycle phase in tumorigenesis of endometriosis-related ovarian carcinoma histotypes.

Project description:Transcriptome and DNA methylation analyses highlight the role of menstrual cycle phase in tumorigenesis of endometriosis-related ovarian carcinoma histotypes.

| PRJNA941909 | ENA

Transcriptome and DNA methylation analyses highlight the role of menstrual cycle phase in tumorigenesis of endometriosis-related ovarian carcinoma histotypes [methylation]

Project description:Transcriptome and DNA methylation analyses highlight the role of menstrual cycle phase in tumorigenesis of endometriosis-related ovarian carcinoma histotypes [methylation]

| PRJNA941842 | ENA

Transcriptome and DNA methylation analyses highlight the role of menstrual cycle phase in tumorigenesis of endometriosis-related ovarian carcinoma histotypes [RNA-Seq]

Project description:Transcriptome and DNA methylation analyses highlight the role of menstrual cycle phase in tumorigenesis of endometriosis-related ovarian carcinoma histotypes [RNA-Seq]

| PRJNA941916 | ENA

Cell State of Origin Impacts Development of Distinct Endometriosis-Related Ovarian Carcinoma Histotypes.

Project description:Clear cell ovarian carcinoma (CCOC) and endometrioid ovarian carcinoma (ENOC) are ovarian carcinoma histotypes, which are both thought to arise from ectopic endometrial (or endometrial-like) cells through an endometriosis intermediate. How the same cell type of origin gives rise to two morphologically and biologically different histotypes has been perplexing, particularly given that recurrent genetic mutations are common to both and present in nonmalignant precursors. We used RNA transcription analysis to show that the expression profiles of CCOC and ENOC resemble those of normal endometrium at secretory and proliferative phases of the menstrual cycle, respectively. DNA methylation at the promoter of the estrogen receptor (ER) gene (ESR1) was enriched in CCOC, which could potentially lock the cells in the secretory state. Compared with normal secretory-type endometrium, CCOC was further defined by increased expression of cysteine and glutathione synthesis pathway genes and downregulation of the iron antiporter, suggesting iron addiction and highlighting ferroptosis as a potential therapeutic target. Overall, these findings suggest that while CCOC and ENOC arise from the same cell type, these histotypes likely originate from different cell states. This "cell state of origin" model may help to explain the presence of histologic and molecular cancer subtypes arising in other organs.SignificanceTwo cancer histotypes diverge from a common cell of origin epigenetically locked in different cell states, highlighting the importance of considering cell state to better understand the cell of origin of cancer.

| S-EPMC10758692 | biostudies-literature

Menstrual cycle phase modulates reward-related neural function in women.

Project description:There is considerable evidence from animal studies that the mesolimbic and mesocortical dopamine systems are sensitive to circulating gonadal steroid hormones. Less is known about the influence of estrogen and progesterone on the human reward system. To investigate this directly, we used functional MRI and an event-related monetary reward paradigm to study women with a repeated-measures, counterbalanced design across the menstrual cycle. Here we show that during the midfollicular phase (days 4-8 after onset of menses) women anticipating uncertain rewards activated the orbitofrontal cortex and amygdala more than during the luteal phase (6-10 days after luteinizing hormone surge). At the time of reward delivery, women in the follicular phase activated the midbrain, striatum, and left fronto-polar cortex more than during the luteal phase. These data demonstrate augmented reactivity of the reward system in women during the midfollicular phase when estrogen is unopposed by progesterone. Moreover, investigation of between-sex differences revealed that men activated ventral putamen more than women during anticipation of uncertain rewards, whereas women more strongly activated the anterior medial prefrontal cortex at the time of reward delivery. Correlation between brain activity and gonadal steroid levels also revealed that the amygdalo-hippocampal complex was positively correlated with estradiol level, regardless of menstrual cycle phase. Together, our findings provide evidence of neurofunctional modulation of the reward system by gonadal steroid hormones in humans and establish a neurobiological foundation for understanding their impact on vulnerability to drug abuse, neuropsychiatric diseases with differential expression across males and females, and hormonally mediated mood disorders.

| S-EPMC1892961 | biostudies-literature

A multi-level investigation of the genetic relationship between endometriosis and ovarian cancer histotypes.

Project description:Endometriosis is associated with increased risk of epithelial ovarian cancers (EOCs). Using data from large endometriosis and EOC genome-wide association meta-analyses, we estimate the genetic correlation and evaluate the causal relationship between genetic liability to endometriosis and EOC histotypes, and identify shared susceptibility loci. We estimate a significant genetic correlation (rg) between endometriosis and clear cell (rg = 0.71), endometrioid (rg = 0.48), and high-grade serous (rg = 0.19) ovarian cancer, associations supported by Mendelian randomization analyses. Bivariate meta-analysis identified 28 loci associated with both endometriosis and EOC, including 19 with evidence for a shared underlying association signal. Differences in the shared risk suggest different underlying pathways may contribute to the relationship between endometriosis and the different histotypes. Functional annotation using transcriptomic and epigenomic profiles of relevant tissues/cells highlights several target genes. This comprehensive analysis reveals profound genetic overlap between endometriosis and EOC histotypes with valuable genomic targets for understanding the biological mechanisms linking the diseases.

| S-EPMC9040176 | biostudies-literature

The influence of menstrual cycle and endometriosis on endometrial methylome.

Project description:BackgroundAlterations in endometrial DNA methylation profile have been proposed as one potential mechanism initiating the development of endometriosis. However, the normal endometrial methylome is influenced by the cyclic hormonal changes, and the menstrual cycle phase-dependent epigenetic signature should be considered when studying endometrial disorders. So far, no studies have been performed to evaluate the menstrual cycle influences and endometriosis-specific endometrial methylation pattern at the same time.ResultsInfinium HumanMethylation 450K BeadChip arrays were used to explore DNA methylation profiles of endometrial tissues from various menstrual cycle phases from 31 patients with endometriosis and 24 healthy women. The DNA methylation profile of patients and controls was highly similar and only 28 differentially methylated regions (DMRs) between patients and controls were found. However, the overall magnitude of the methylation differences between patients and controls was rather small (?? ranging from -0.01 to -0.16 and from 0.01 to 0.08, respectively, for hypo- and hypermethylated CpGs). Unsupervised hierarchical clustering of the methylation data divided endometrial samples based on the menstrual cycle phase rather than diseased/non-diseased status. Further analysis revealed a number of menstrual cycle phase-specific epigenetic changes with largest changes occurring during the late-secretory and menstrual phases when substantial rearrangements of endometrial tissue take place. Comparison of cycle phase- and endometriosis-specific methylation profile changes revealed that 13 out of 28 endometriosis-specific DMRs were present in both datasets.ConclusionsThe results of our study accentuate the importance of considering normal cyclic epigenetic changes in studies investigating endometrium-related disease-specific methylation patterns.

| S-EPMC4710036 | biostudies-literature

The influence of menstrual cycle and endometriosis on endometrial methylome

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-02-15 | E-GEOD-73950 | biostudies-arrayexpress