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Molecular characterization of PRM associated endometrial changes, PAEC, following mifepristone treatment.

ABSTRACT: The molecules significantly altered in endometrium displaying PAEC after three months of mifepristone exposure are mainly involved in the structural architecture of tissue, which may explain the morphological features of PAEC Our study has generated new knowledge on the molecular profile of endometrium displaying PAEC after 3 months of mifepristone treatment due to symptomatic leiomyoma. This knowledge is of great importance as the application of progesterone receptor modulators (PRMs) for the medical management of benign gynecological conditions is increasing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110232 | GEO | 2018/12/01

REPOSITORIES: GEO

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Molecular characterization of PRM associated endometrial changes, PAEC, following mifepristone treatment.

Project description:Molecular characterization of PRM associated endometrial changes, PAEC, following mifepristone treatment.

| PRJNA433220 | ENA

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Project description:Illumina sequencing was used to assay the effect of mifepristone treatment on gene expression in adult Drosophila, including males, virgin females and mated females.

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Effect of mifepristone on gene expression in Drosophila

Project description:Illumina sequencing was used to assay the effect of mifepristone treatment on gene expression in adult Drosophila, including males, virgin females and mated females. Males of strain w[1118]; p53B[6] were crossed to virgins of w[1118]; rtTA(3)E2 and progeny males and virgins were collected over 48 hours. One half of the virgins were mated to w[1118] males at ratio of 1:1 virgins to males for 4 days. Mated females were then separated from the w[1118] males. The mated females, males and virgins females were then maintained at approximately 20 flies per vial, on food with and without supplementation with 160ug/ml mifepristone for 12 days. Total fly RNA was isolated from 20 animals per sample. Three replicate samples were generated for each type of flies: males, mated females and virgin females.

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Transcriptome analysis for uterine leiomyosarcoma and myoma

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Gene expression profile associated with a cytostatic does of mifepristone in ovarian cancer cells by microarray analysis

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Mifepristone-induced tumor regression in C4-HD tumors

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Beneficial effects of mifepristone treatment in breast cancer patients selected by the progesterone receptor isoform ratio: Results from the MIPRA trial

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Project description:Circulating progesterone (P4) levels decline before the onset of parturition in most animals, but not in humans. This has led to the suggestion that there is functional withdrawal of P4 action at the myometrial level prior to labor onset. However, to date, no evidence of a loss of P4 function has been provided. Mifepristone is a mixed progesterone and glucocorticoid receptor antagonist that is frequently used to induce human labor. However, its effect on the myometrial tissue transcriptome hs not been determined. In this study, we aimed to identify the effects of mifepristone treatment on the pregnant myometrium at term in order to better understand the possible mechanisms underlying the loss of P4 function in human labor.

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Effects of high concentrations of progesterone and Mifepristone: a gene expression study of endometrial cancer cells

Project description:Patients with endometrial hyperplasia representing preliminary stages of endometrial cancer have shown to respond to therapy in 100% of the cases when treated with levonorgestrel -impregnated intrauterine device. Antiproliferative effect has also been reported after application of an anti-progestin impregnated intrauterine device which showed to induce endometrial atrophy. The intention of the present study was to obtain more information of novel therapeutic targets for hormonal treatment in endometrial hyperplasia and endometrial cancers. Gene expression of signaling pathways after stimulation of Ishikawa cells with high doses of progesterone (10 Î¼M) or Mifepristone (10 Î¼M) was performed. After using an oligo microarrays representing 24,650 human genes and 37,580 gene transcripts, 6,154 genes remained after pre-processing and filtering. This resulted in a total of 993 up-regulated genes with 189 genes for progesterone and 255 genes for Mifepristone. The 550 down regulated genes were distributed with 256 genes for progesterone, 127 genes for RU 486. The results showed that genes presenting the epidermal growth factor (EGF)/MAP-kinase pathway were significantly over-represented by progesterone treatment, whereas, by Mifepristone treatment genes involved in the p53 pathway were also up-regulated (data not shown). These genes may be interesting as potential new therapeutic targets in endometrial hyperplasia and endometrial cancer, as candidate genes for therapy response or as candidate markers for tumor progression. 20 samples, 4 different condition groups with 5 replicates for each group, linear factorial experimental design. Short time (4hrs) dose response to progesterone and Mifepristone in combination and alone. Only 18 samples are represented in this Series.

2010-05-06 | E-GEOD-14713 | biostudies-arrayexpress

Mifepristone-induced tumor regression in C4-HD tumors

Project description:Comparison of gene expression data between control and MFP-treated C4-HD tumors. The role of active antitumor immunity in hormone receptor positive (HR+) breast cancer has been historically underlooked. The aim of this study was to determine the contribution of the immune system to antiprogestin-induced tumor growth inhibition using a hormone-dependent breast cancer model. BALB/c-GFP+ bone marrow (BM) cells were transplanted into immunodeficient NSG mice to generate an immunocompetent NSG/BM-GFP+ (NSG-R) mouse model. Treatment with the antiprogestin Mifepristone (MFP) inhibited growth of 59-2-HI tumors with similar kinetics in both animal models. Interestingly, MFP treatment reshaped the tumor microenvironment, enhancing the production of proinflammatory cytokines and chemokines. Tumors in MFP-treated immunocompetent mice showed increased infiltration of F4/80+ macrophages, NK, and CD8 T cells, displaying a central memory phenotype. Mechanistically, MFP induced immunogenic cell death in vivo and in vitro, as depicted by the expression and subcellular localization of the alarmins calreticulin and HMGB-1 and the induction of an immunogenic cell death gene program. Moreover, MFP-treated tumor cells efficiently activated immature dendritic cells, evidenced by enhanced expression of MHC-II and CD86, and induced a memory T cell response, attenuating tumor onset and growth after re-challenge. Finally, MFP treatment increased the sensitivity of HR+ 59-2-HI tumor to PD-L1 blockade, suggesting that antiprogestins may improve immunotherapy response rates. These results contribute to a better understanding of the mechanisms underlying the antitumor effect of hormonal treatment and the rational design of therapeutic combinations based on endocrine and immunomodulatory agents in HR+ breast cancer.

2020-11-07 | GSE161012 | GEO

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