Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA205252 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Human breast cancer SKBr-3 cells selected with trastuzumab for 6 month compared with parental SKBr-3 cells; Goal was to screen for microRNAs involved in development of trastuzumab resistance. Human breast cancer SKBr-3 cells were continuously cultured in the presence ofM-BM- 5M-BM-5g/ml trastuzumab for 6 months, and the resulting alive cells were regarded as trastuzumab-resistant. Total RNAs were prepared from these cells and cells cultured in parallel in control media, and were subjected to hybridization on the miRCURY LNA Array (Exiqon, version 11.0).
2013-05-25 | E-GEOD-47011 | biostudies-arrayexpress
Project description:Human breast cancer SKBr-3 cells selected with trastuzumab for 6 month compared with parental SKBr-3 cells; Goal was to screen for microRNAs involved in development of trastuzumab resistance.
2013-05-25 | GSE47011 | GEO
Project description:RNA-seq of human ovarian cancer cell line OVSAHO parental and CB-5083-resistant cells
2025-01-23 | E-MTAB-7328 | ExpressionAtlas
Project description:Networking of differentially expressed genes in human MCF7 breast cancer cells resistant to methotrexate
2025-01-24 | E-GEOD-16070 | ExpressionAtlas
Project description:Networking of differentially expressed genes in human MDA-MB-468 breast cancer cells resistant to methotrexate
2025-01-24 | E-GEOD-16080 | ExpressionAtlas
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:Breast cancer cell lines - palmitate vs control
2025-01-23 | E-MTAB-2601 | ExpressionAtlas
Project description:Acquired resistance to trastuzumab, a rationally designed HER-2 targeting antibody, remains a major hurdle in management of HER-2 positive breast cancer (HER-2+ BC) patients. Potential resistance mechanisms are numerous, derived primarily from studies where HER-2 positive cell lines are chronically exposed to trastuzumab. Recent evidence suggests a role for epithelial-mesenchymal transition (EMT) in trastuzumab resistance, but a definitive link between the two has been difficult to establish because relevant model systems are lacking. When sub-populations of trastuzumab sensitive SKBR-3 cells were isolated using cloning rings, an (EMT) occurred spontaneously in several (3/8) clones. SKBR-3 EMT-clones featured increased spindle morphology, expressed N-glycosylated M-NM-21-integrin, and decreased HER-2, all characteristics shared by JIMT-1, a cell lines with intrinsic resistance to trastuzumab. SKBR-3 EMT-clones were characterized by gene expression profiling and mammosphere formation. The N-glycosylated isoform of M-NM-2-itnegrin was targeted with M-NM-2-integrin inhibiting antibody, AIIB2. Transcriptional profiling revealed that SKBR-3 EMT-clones underwent a shift from a luminal molecular subtype to a more aggressive mesenchymal/ basal phenotype. Isolating clones from SKBR-3 cells with enforced expression of a M-NM-2-integrin isoform lacking extensive N-glycosylation failed to increase the likelihood for spontaneous EMT in SKBR-3. However, specific inhibition of the heavily N-glycosylated variant of M-NM-21-integrin expressed by SKBR-3 EMT-clones restored epithelial morphology and impaired mammosphere formation. Furthermore, when SKBR-3 EMT-clones were treated with relevant doses of trastuzumab and lapatinib, they showed M-bM-^@M-^\spontaneousM-bM-^@M-^] resistance. In this study we describe a model of spontaneous EMT following clonal selection in HER-2+ cell line, SKBR-3. Using this model we establish the first direct link between EMT and resistance to HER-2 targeted therapies. We also identify the N-glycosylated isoform of M-NM-2-integrin as a potential biomarker and target in HER-2+ BC refractory to HER-2 targeted therapies. RNA was isolated from 10 breast cancer cell lines in triplicate. Pairwise gene expression differences were compared between each of the SKBR-3 cell lines (SKBR-3/ b1, SK-EV-C4, and SK-B1-C1). Features selected had at least a 2X difference in at least one comparison, with a one-way ANOVA corrected p-value of >0.05. In addition, expression profiles from SKBR-3/ EV and SK-B1-C1 cell were compared and a differential gene list was generated to include genes that differed by at least 1.5X, with a t-test p-value of >0.02 (unpaired, Bonferroni corrected). A total of 1940 entities met these criteria and the expression of these genes was investigated in all breast cancer cell lines.
2015-01-01 | E-GEOD-40152 | biostudies-arrayexpress
Project description:Transcription profiling by array of human MCF-7 breast cancer cells
2025-01-16 | E-GEOD-11791 | ExpressionAtlas
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.
2015-04-21 | GSE55005 | GEO