Gene expression data from the syngeneic mouse endometriosis model
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ABSTRACT:
PROVIDER: PRJNA786343 | ENA |
REPOSITORIES: ENA
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Project description:Retrograde menstruation is considered a major reason for the development of endometriosis. The syngeneic transplantation mouse model is an endometriosis animal model that is considered to mimic retrograde menstruation. However, it remains poorly understood which genetic signatures of endometriosis are reflected in this model. Here, we employed an in vivo syngeneic mouse endometriosis model and identified differentially expressed genes (DEGs) between the ectopic and eutopic tissues using microarray analysis.
2022-02-28 | GSE190209 | GEO
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Project description:The cell line-derived xenografts and patient derived xenografts have limited use in cancer immunotherapy evaluation because an immune compromised host is required for xenotransplantation. Syngeneic mouse models are derived by transplanting established mouse cell lines or tumor tissues to strain matched mouse hosts, which are better suited to study the interplay between immune and tumor cells. We investigated the differences as well as similarities of a panel of ten mouse syngeneic models to features of human tumors by proteomics, which will provide valuable information to assist experimental biologists in model selection.
2019-12-03 | PXD011885 | Pride
Project description:the cecal contents of CT26 syngeneic mouse model Raw sequence reads
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Project description:In this study, we performed transcriptomic analysis in ectopic lesions and eutopic endometrial tissues from both fertile and subfertile mice with endometriosis. We identified the positive correlation of the gene signatures between the mouse and human in ectopic lesions. Conserved gene networks were activated in all the ectopic lesions including estradiol, immune, fibrosis, and angiogenesis pathways. The interactions mediated through hormone, cytokine, and growth factor as well as their corresponding receptors were predicted between the ectopic and eutopic endometrium. EGF and WNT signaling were more suppressed in the eutopic endometrium from subfertile mice. Our results revealed that our mouse endometriosis model recapitulates the important transcriptomic changes of endometriosis progression in human ectopic lesions including the essential regulator network and intensive inter-communications between ectopic and eutopic endometrium. Our preclinical animal model for endometriosis will be invaluable to understand etiology and pathophysiology on endometriosis.
2024-05-29 | GSE240392 | GEO
Project description:Our understanding of molecular mechanisms contributing to the pathophysiology of endometriosis, and their upstream regulators, remains limited. Using a C57Bl/6 mouse model of endometriosis in which decidualized endometrial tissue fragments are transferred to subcutaneous sites in recipient mice to mimic endometriosis lesions, we have generated a comprehensive profile of gene expression in decidualized endometrial tissue (n=4), and endometriosis-like lesions at Day 7 (n=4) and Day 14 (n=4) of lesion formation. High throughput mRNA sequencing allowed identification of genes and pathways involved in the initiation and progression of endometriosis-like lesions. We found distinct patterns of gene expression with substantial differences between the lesions and the decidualized endometrium from which they arose, but no differentially expressed genes between the two lesion timepoints. The transcriptional changes at the outset of lesion formation indicated substantial upregulation of immune response-associated canonical pathways. Pathway enrichment analysis indicates multiple potential endogenous upstream regulators, and reveals multiple gene candidates not previously implicated in endometriosis lesion formation suggesting these mediators may have novel roles in disease progression. Collectively, the provided data will be a valuable resource to inform research on the molecular mechanisms contributing to endometriosis development.
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Project description:Syngeneic mouse model of YES-driven metastatic and proliferative hepatocellular carcinoma.
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Project description:The biologic basis for NSCLC metastasis is not well understood. Here we addressed this deficiency by transcriptionally profiling tumors from a genetic mouse model of human lung adenocarcinoma that develops metastatic disease owing to the expression of K-rasG12D and p53R172H. As a tool to investigate the biologic basis for metastasis in this model and to query the roles of specific genes in this signature, we isolated adenocarcinoma cell lines from these mice and used them to develop a syngeneic tumor model in wild-type littermates. Transcriptional profiling of the highly metastatic subcutaneous tumors revealed genes that regulate, among other processes, epithelial-to-mesenchymal transition and intra-tumoral inflammation and angiogenesis, whereas the non-metastatic tumors did not. Experiment Overall Design: Cell lines from p53R172Hâg/+ K-rasLA1/+ mice were derived from tumor tissues removed at autopsy from two different mice (#344 and #393). The tissues were minced, placed in culture, and passed serially in RPMI 1640 supplemented with 10% fetal bovine serum (FBS), which yielded mass populations of tumor cells derived from primary lung tumors (344P and 393P), mediastinal lymph nodes (344LN and 393LN), and a subcutaneous site (344SQ). Syngeneic tumors were isolated, carefully dissected to remove the adjacent tissue, snap-frozen in liquid nitrogen and stored at -80° until use. Part of each dissected tumor was histologically evaluated by a board-certified pathologist. Snap-frozen samples were processed and analyzed on Affymetrix Mouse Expression Array 430A 2.0 chips. Experiment Overall Design: Expression profiling performed on 344SQ, 393P, and 393LN
2009-11-28 | E-GEOD-14458 | biostudies-arrayexpress