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Transcriptional profilng of CCNE1 overexpressing hTERT-immortalized p53-R175H fallopian tube cell lines (FT282)

ABSTRACT: Transcriptional profilng of CCNE1 overexpressing hTERT-immortalized p53-R175H fallopian tube cell lines (FT282)

PROVIDER: PRJNA719673 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14141259_1.fastq.gz	Fastqsanger.gz
	SRR14141259_2.fastq.gz	Fastqsanger.gz
	SRR14141260_1.fastq.gz	Fastqsanger.gz
	SRR14141260_2.fastq.gz	Fastqsanger.gz
	SRR14141261_1.fastq.gz	Fastqsanger.gz

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Transcriptional profilng of CCNE1 overexpressing hTERT-immortalized p53-R175H fallopian tube cell lines (FT282)

Project description:In this study we used RNA-seq to profile transcriptional changes in two clones of FT282-hTERT p53-R175H cells engineered to overexpress CCNE1. We compared the differential gene expression (DGE) of CCNE1 OE to their wild type counterparts and identified that CCNE1 OE increases expression of genes involved in G2/M progression. Subsequent gene set enrichment analysis (GSEA) revealed significant enrichment of genes co-regulated by MYBL2 and FOXM1 transcription factors.

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Gene signatures of normal hTERT immortalized ovarian epithelium and fallopian tube epithelium (paired cultures from 2 donor patients)

Project description:Most epithelial ovarian cancers are thought to arise from different cells in the ovarian or fallopian tube epithelium. We hypothesized that these distinct cells-of-origin may play a role in determining ovarian tumor phenotype and also could inform the molecular classification of ovarian cancer. To test this hypothesis, we developed new methods to isolate and culture paired normal human ovarian (OV) and fallopian tube (FT) epithelial cells from multiple donors without cancer and identified a cell-of-origin gene expression signature that distinguished these cell types within the same patient. Application of the OV versus FT cell-of-origin gene signature to gene expression profiles of primary ovarian cancers permitted identification of distinct OV and FT-like subgroups among these cancers. Importantly, the normal FT-like tumor classification correlated with a significantly worse disease-free survival. This work describes a new experimental method for culture of normal human OV and FT epithelial cells from the same patient. These findings provide new evidence that cell-of-origin is an important source of ovarian tumor heterogeneity and the associated differences in tumor phenotype. We analyzed 12 samples from two donor patients and established cultures of both ovarian epithelium and fallopian tube epithelium (hTERT immortalized), each with 3 replicates (different culture passages).

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Array CGH reveals genetic homogeneity and frequent copy number increases encompassing CCNE1 in Fallopian tube carcinoma

Project description:Fallopian tube carcinoma (FTC) is a rare, poorly studied and aggressive cancer, associated with poor survival. Since tumorigenesis is related to acquisition of genetic changes, we used genome-wide array CGH to analyze copy number aberrations occurring in FTC in order to obtain a better understanding of FTC carcinogenesis and to identify prognostic events and targets for therapy. We used arrays of 2464 genomic clones, providing ~1.4 Mb resolution across the genome to quantitatively map genomic DNA copy number aberrations from fourteen FTC onto the human genome sequence. All tumors showed a high frequency of copy number aberrations with recurrent gains on 3q, 6p, 7q, 8q, 12p, 17q, 19 and 20q, and losses involving chromosomes 4, 5q, 8p, 16q, 17p, 18q and X. Recurrent regions of amplification included 1p34, 8p11-q11, 8q24, 12p, 17p13, 17q12-q21, 19p13, 19q12-q13 and 19q13. Candidate, known oncogenes mapping to these amplicons included CMYC (8q24), CCNE1 (19q12-q21) and AKT2 (19q13), whereas PIK3CA and KRAS, previously suggested to be candidate driver genes for amplification mapped outside copy number maxima on 3q and 12p, respectively. The FTC were remarkably homogeneous, with some recurrent aberrations occurring in more than 70% of samples, which suggests a stereotyped pattern of tumor evolution. Keywords: array CGH, CCNE1, AKT2, Fallopian tube cancer

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Gene signatures of normal hTERT immortalized ovarian epithelium and fallopian tube epithelium (paired cultures from 2 donor patients)

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CCNE1 interactome analysis in HEK293T cells under the treatment of different CCNE1(:CDK2) ligands

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