Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151529 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Microparticles (MPs) comprise the major source of systemic RNA including microRNA (miRNA), the aberrant expression of which appears to be associated with stage, progression and spread of many cancers. We have shown MPs to transfer multidrug resistance proteins accross both haematological and and non-haematological cancers. using microarray miRNA profiling analysis we now analyze changes in miRNA profiles of both cancer types following microparticle transfer. We identified certain upregulated miRNAs in both cancer types. Total RNA was extracted and pooled from duplicate experiments for hybridization on Affymetrix microarrays from (i) the parental drug sensitive leukaemia (CEM) or breast cancer (MCF-7) cells, (ii) their Multidrug Resistant strains leukaemia (VLB100) or breast cancer ( DX cells), (iii) the microparticles isolated from the resistant cells: VLBMP or DXMP, and (iv) the cocultured samples: sensitive cell co-incubated with MPs from their resistant cells ( leukaemia: CEM+VLBMP) or(breast cancer: MCF-7+DXMP). We sought to examine the miRNA profiles of the drug sensitve cells after MP transfer from drug resistant cells across leukaemia nd breact cancer cell lines.
2012-06-08 | E-GEOD-34560 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE28968: MRNA expression data from human breast cancer cell lines after demethylation treatment. GSE28969: MicroRNA expression data from human breast cancer cell lines after demethylation treatment. Refer to individual Series
2012-01-24 | E-GEOD-28976 | biostudies-arrayexpress
Project description:MicroRNA expression data from human breast cancer cell lines after demethylation treatment.
| PRJNA142859 | ENA
Project description:To understand the the effect of microparticles conjugated with vascular endothelial growth factor (VEGF) on human endothelial cells derived from human umbilical cord blood (UCB) CD34+ hematopoietic stem cells, we have employed microRNA microarray profiling. The microparticles used in this study were purchased from Invitrogen (Dynal magnetic microparticles coated with streptavidin, 4.5 micron in size) and modified in our lab. Cell suspensions were mixed with blank microparticles (without VEGF), soluble VEGF or VEGF-conjugated microparticles and seeded as hanging drops to prepare endothelial cell aggregates. Cell aggregates without any treatments were used as control. After 2 h or 8 h, the cell aggregates were collected and miRNA expression profiles were detected.
2017-07-07 | GSE75899 | GEO
Project description:MicroRNA analysis of breast cancer cell lines
| PRJNA230102 | ENA
Project description:The intention was to detect genes that are determining trastuzumab efficiency in HER2-positive breast cancer cell lines with different resistance phenotypes. While BT474 should be sensitive to the drug treatment, HCC1954 is expected to be resistant due to a PI3K mutation. The cell line BTR50 has been derived from BT474 and was cultured to be resistant as well. Based on RNA-Seq data, we performed differential expression analyses on these breast cancer cell lines with and without trastuzumab treatment. In detail, five separate tests were performed, namely resistant cells vs. wild type, i.e. HCC1954 and BTR50 vs. BT474, respectively, and untreated vs. drug treated cells. The significant genes of the first two tests should contribute to resistance. The significant genes of the test BT474 vs. its drug treated version should contribute to the trastuzumab effect. To exclude false positives from the combined gene set (#64), we removed ten genes that were also significant in the test BTR50 vs. its drug treated version. This way we ended up with 54 genes that are very likely to determine trastuzumab efficiency in HER2-positive breast cancer cell lines. mRNA profiles of human breast cancer cell lines were generated by deep sequencing using Illumina HiSeq 2000. The cell lines BT474 and HCC1954 were analyzed with and without trastuzumab treatment. HCC1954 is known to be trastuzumab resistant. Additionally, the cell line BTR50 was generated as resistant version of BT474, and was analyzed with and without trastuzumab as well.
2015-04-21 | E-GEOD-55005 | biostudies-arrayexpress
Project description:Hormone treatment of ER+ breast cancer cell lines
| PRJNA807655 | ENA
Project description:All-trans retinoic acid (atRA) regulates gene expression and is used to treat acute promyelocytic leukemia. Attempts to use atRA for breast cancer treatment without a stratification strategy have resulted in limited overall effectiveness. To identify biomarkers for the treatment of triple-negative breast cancer (TNBC) with atRA, we characterized the effects of atRA on the tumor growth of 13 TNBC cell lines. This resulted in a range of tumor growth effects that was not predictable based on the levels of retinoid signaling molecules and transcriptional responses that were mostly independent of retinoic acid response elements. Given the importance of DNA methylation in regulating gene expression, we hypothesized that differential DNA methylation could predict the response of TNBCs to atRA. We identified over 1400 CpG sites that were differentially methylated between atRA resistant and sensitive cell lines. These CpG sites predicted the response of four TNBC patient-derived xenografts to atRA treatment and we utilized these xenografts to refine the profile to 6 CpGs. We identify as many as 17% of TNBC patients who could benefit from atRA treatment. These data illustrate that differential DNA methylation of specific sites may predict the response of patient tumors to atRA treatment. This study characterizes the gene expression of 2 triple-negative patient-derived breast cancer xenografts
2018-10-22 | GSE118002 | GEO