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

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

PROVIDER: PRJNA812889 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18220727_1.fastq.gz	Fastqsanger.gz
	SRR18220727_2.fastq.gz	Fastqsanger.gz
	SRR18220728_1.fastq.gz	Fastqsanger.gz
	SRR18220728_2.fastq.gz	Fastqsanger.gz
	SRR18220729_1.fastq.gz	Fastqsanger.gz

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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 identify 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.

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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.

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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 nCounterÂ® 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.

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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.

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