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Identifying and overcoming a mechanism of resistance to Wee1 kinase inhibitor AZD1775 in high grade serous ovarian cancer cells (OVCAR8)

ABSTRACT: Identifying and overcoming a mechanism of resistance to Wee1 kinase inhibitor AZD1775 in high grade serous ovarian cancer cells (OVCAR8)

PROVIDER: PRJNA595516 | ENA |

REPOSITORIES: ENA

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Identifying and overcoming a mechanism of resistance to Wee1 kinase inhibitor AZD1775 in high grade serous ovarian cancer cells (OVCAR8)

Project description:Treatment of Human high grade serous ovarian cancer cell line, OVCAR8, with WEE1 kinase inhibitor AZD1775

2020-12-01 | GSE141990 | GEO

Identifying and overcoming a mechanism of resistance to Wee1 kinase inhibitor AZD1775 in high grade serous ovarian cancer cells (ES-2)

Project description:Treatment of Human high grade serous ovarian cancer cell line, ES-2, with WEE1 kinase inhibitor AZD1775

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Identifying and overcoming a mechanism of resistance to Wee1 kinase inhibitor AZD1775 in high grade serous ovarian cancer cells

Project description:Identifying and overcoming a mechanism of resistance to Wee1 kinase inhibitor AZD1775 in high grade serous ovarian cancer cells

| PRJNA595941 | ENA

Identifying and overcoming a mechanism of resistance to Wee1 kinase inhibitor AZD1775 in high grade serous ovarian cancer cells (ES-2)

Project description:Identifying and overcoming a mechanism of resistance to Wee1 kinase inhibitor AZD1775 in high grade serous ovarian cancer cells (ES-2)

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Identifying and overcoming a mechanism of resistance to Wee1 kinase inhibitor AZD1775 in high grade serous ovarian cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-01 | GSE142126 | GEO

Proteomics of high-grade serous ovarian cancer models reveals cancer associated fibroblast markers associated with outcome.

Project description:Here, we performed proteomics on whole cell lysate of three high-grade serous ovarian cancer patient derived cancer associated fibroblast (CAF) lines, four commercially available high-grade serous ovarian epithelial cancer cell lines (Kuramochi, PEO4, OVCAR8, ES2) and two immortalized normal Fallopian tube secretory epithelial cell lines (FT237, FT194). N-glycoproteomics using hydrazide-based enrichment was performed on 8/9 models. Integration of data from in vitro models with publicly available primary tissue data identified multiple novel CAF proteins that are associated with poor clinical outcomes in HGSC.

2022-11-28 | MSV000090794 | MassIVE

LncRNA and mRNA expression profiles in High-grade serous ovarian cancer, Low-grade serous ovarian cancer and Normal fallopian tube

Project description:Ovarian cancer is the most lethal gynecologic cancer. High-grade serous ovarian carcinoma (HGSOC) is the most common histologic subtype, accounting for three quarters of ovarian cancer. To clarify the changes of gene expression in serous ovarian cancer, we performed lncRNA and mRNA microarrays to identify differentially expressed lncRNAs and mRNAs in High-grade and Low-grade serous ovarian carcinoma compared with Normal fallopian tube.

2020-02-12 | GSE135886 | GEO

Genomic analysis of low-grade serous ovarian carcinomas [IL610Q]

Project description:Low-grade serous ovarian carcinomas are typically Ras-pathway mutated, TP53 wild-type, have limited chromosomal aberration, and are frequently associated with borderline tumors. By contrast, high-grade serous ovarian carcinoma lack Ras-pathway mutations, are invariably TP53 mutated, show widespread genomic change, and are commonly BRCA-pathway disrupted. We sought to identify differences in genomic copy number changes between co-existing borderline and invasive components of serous carcinoma. Paired co-existing borderline and invasive tumor components of ovarian serous carcinoma were sampled and profiled from tumors from 7 patients

2014-10-01 | E-GEOD-57279 | biostudies-arrayexpress

TRRAP-mediated regulation of Wee1

Project description:The G2 DNA damage checkpoint inhibits Cdc2 and mitotic entry through the dual regulation of Wee1 and Cdc25 by the Chk1 effector kinase. Up-regulation of Chk1 by mutation or overexpression bypasses the requirement for up-stream regulators or DNA damage to promote a G2 cell cycle arrest. We screened in fission yeast for mutations that rendered cells resistant to overexpressed Chk1. We identified a mutation in tra1, which encodes one of two homologs of TRRAP, an ATM/R-related pseudokinase that scaffolds several histone acetyltransferase (HAT) complexes. Inhibition of histone deacetylases reverts the resistance to overexpressed Chk1, suggesting this phenotype is due to a HAT activity, though expression of checkpoint and cell cycle genes is not greatly affected. Cells with mutant or deleted tra1 activate Chk1 normally and are checkpoint proficient. However, these cells are semi-wee even when overexpressing Chk1, and accumulate inactive Wee1 protein. The Cdr (changed division response) kinases Cdr1 and Cdr2 are negative regulators of Wee1, and while best characterized in the cellular response to limited nutrition, we show that they are required for the Tra1-dependent alterations to Wee1 function. This identifies Tra1 as another component controlling the timing of entry into mitosis via Cdc2 activation. Two and three independent microaaray experiments were done for wild type and the mutant (tra1-1) respectively.

2010-04-11 | E-GEOD-12674 | biostudies-arrayexpress

Genomic analysis of low-grade serous ovarian carcinomas [EXP]

Project description:Low-grade serous ovarian carcinomas are typically Ras-pathway mutated, TP53 wild-type, have limited chromosomal aberration, and are frequently associated with borderline tumors. By contrast, high-grade serous ovarian carcinoma lack Ras-pathway mutations, are invariably TP53 mutated, show widespread genomic change, and are commonly BRCA-pathway disrupted. We sought to identify differentially expressed genes between co-existing borderline and invasive components of serous carcinoma.

2014-10-01 | GSE56443 | GEO

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