Quantitative Analysis of Musashi2-reporter positive and Musashi2-reporter negative KPf/fC pancreatic cancer cell transcriptomes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA473030 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Purpose: The goal of this study is to compare the transcriptome of pancreatic cancer stem cells (Musashi2-reporter positive) to pancreatic cancer non-stem cells (Musashi2-reporter negative). Methods: Musashi2-reporter mice contain a GFP-cassette knocked into the first exon of the endogenous Musashi2 locus; heterozygous mice are used to track cells expressing Musashi2. These mice were crossed to the KPf/fC (Ptf1a-Cre; KrasG12D; p53f/f) mouse model of pancreatic cancer. Tumors from endstage Musashi2-reporter KPf/fC mice were dissociated and FACS sorted for EpCAM+/GFP+ (Musashi2+ stem cells) and EpCAM+/GFP- (Musashi2- non-stem cells). For sequencing, mRNA libraries were generated from total RNA and sequenced with 50 basepair (bp) single end reads (SR50) to a depth of approximately 30 million reads per sample on an Illumina HiSeq2500 using V4 sequencing chemistry. Conclusions: Our study provides comparative transcriptomic data from primary isolated pancreatic cancer stem and non-stem cells in biologic replicates.
2019-06-18 | GSE114906 | GEO
Project description:ES derived Flk-1+ cells were separated by sorting into Hoxb6 positive and negative populations by Venus reporter. Gene expression was compared between these two groups. Duplicate analysis of Hoxb6-Venus positive and negative Flk-1+ cells.
2013-04-16 | E-GEOD-45191 | biostudies-arrayexpress
Project description:ES derived Flk-1+ cells were separated by sorting into Hoxb6 positive and negative populations by RFP Hoxb6 reporter. Gene expression was compared between these two groups. Duplicate analysis of Hoxb6-RFP positive and negative Flk-1+ cells.
2013-04-16 | E-GEOD-45192 | biostudies-arrayexpress
Project description:ES derived Flk-1+ cells were separated by sorting into Hoxb6 positive and negative populations by Venus reporter. Gene expression was compared between these two groups.
2013-04-16 | GSE45191 | GEO
Project description:ES derived Flk-1+ cells were separated by sorting into Hoxb6 positive and negative populations by RFP Hoxb6 reporter. Gene expression was compared between these two groups.
2013-04-16 | GSE45192 | GEO
Project description:Geitlerinema sp. FC II strain:FC II Genome sequencing and assembly
| PRJNA399071 | ENA
Project description:Inflammatory breast cancer (IBC) is the most aggressive type of advanced breast cancer and is associated with a poor prognosis. We have developed a new model of IBC derivated from the pleural effusion of a 49-year-old woman with metastatic secondary IBC. FC-IBC02 tumor cells were isolated from the pleural effusion and cultured under non-adherent conditions, resulting in the formation of spheroids or mammospheres. FC-IBC02 are triple negative (estrogen receptor negative, progesterone receptor negative and ErbB2 negative) and strongly positive for E-cadherin, beta-catenin and vimentin. FC-IBC02 cells developed breast tumors when they were injected into the mammary fat pad of SCID mice and characteristic tumor emboli were detected. Breast tumor xenografts were poorly differentiated triple negative carcinomas and all injected mice developed metastasis in the lungs and lymph nodes. These IBC tumor cells showed genomic alterations in all chromosomes, with the gains/amplifications more common than the deletions/losses. Duplicated regions were on 1q, 2p, 3q, 8q and 18p and chromosomes 7 and 9. The 8q chromosome arm where the MYC oncogene resides was amplified up to seven fold. Chromothripsis (local chromosome shattering) was observed on chromosome 11q and losses were found on 8p, 11q, 16q and 17p (location of TP53). FC-IBC-02 cells expressed the stem cell marker CD44, EpCAM and strongly expressed EGFR and ALK. In summary, this novel preclinical model demonstrated that IBC is a disease enriched for highly tumorigenic cells which harbor a stem cell phenotype. This IBC model is ideal for the study of the metastatic process and to evaluate targeting therapeutic modalities. Total RNA were isolated from IBC-02, IBC-02 in mammosphere growth, IBC3, SUM149, SUM190, MDA-MB231, and MDA-MB468 cell lines. Affymetrix Human U133 Plus 2.0 arrays were used for whole-genome gene expression assays. Duplicate samples were analyzed for each cell line.
2012-09-20 | E-GEOD-40464 | biostudies-arrayexpress
Project description:Inflammatory breast cancer (IBC) is the most aggressive type of advanced breast cancer and is associated with a poor prognosis. We have developed a new model of IBC derivated from the pleural effusion of a 49-year-old woman with metastatic secondary IBC. FC-IBC02 tumor cells were isolated from the pleural effusion and cultured under non-adherent conditions, resulting in the formation of spheroids or mammospheres. FC-IBC02 are triple negative (estrogen receptor negative, progesterone receptor negative and ErbB2 negative) and strongly positive for E-cadherin, beta-catenin and vimentin. FC-IBC02 cells developed breast tumors when they were injected into the mammary fat pad of SCID mice and characteristic tumor emboli were detected. Breast tumor xenografts were poorly differentiated triple negative carcinomas and all injected mice developed metastasis in the lungs and lymph nodes. These IBC tumor cells showed genomic alterations in all chromosomes, with the gains/amplifications more common than the deletions/losses. Duplicated regions were on 1q, 2p, 3q, 8q and 18p and chromosomes 7 and 9. The 8q chromosome arm where the MYC oncogene resides was amplified up to seven fold. Chromothripsis (local chromosome shattering) was observed on chromosome 11q and losses were found on 8p, 11q, 16q and 17p (location of TP53). FC-IBC-02 cells expressed the stem cell marker CD44, EpCAM and strongly expressed EGFR and ALK. In summary, this novel preclinical model demonstrated that IBC is a disease enriched for highly tumorigenic cells which harbor a stem cell phenotype. This IBC model is ideal for the study of the metastatic process and to evaluate targeting therapeutic modalities.
2012-09-20 | GSE40464 | GEO
Project description:Global Run-On has been performed in MLL2 F/F and FC/FC MEF cells. The aim of the experiment is to test how the lack of MLL2 affects nascent RNA transcription. Four samples were analyzed - 2 independent replicates. The experiments were performed using immortalized mouse embryonic fibroblasts (MEF) in which both MLL2 alleles were targeted by the loxp system (F/F cells). Tamoxifen treatment of the F/F cells for 24 hours results in the excision of both MLL2 alleles (FC/FC cells).
2016-04-13 | E-GEOD-73126 | biostudies-arrayexpress
Project description:Global Run-On has been performed in MLL2 F/F and FC/FC MEF cells. The aim of the experiment is to test how the lack of MLL2 affects nascent RNA transcription.
2016-04-13 | GSE73126 | GEO