Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA350567 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Copy number profiling of MKN45T 5-FU resistant gastric cancer cell lines and its parental cell line MKN45. We hypothesized that a detailed fine-scale survey of genomic CNAs might reveal the mechanism for acquired resistant to 5-FU in gastric cancer.
2017-06-09 | GSE89191 | GEO
Project description:To understand the molecular basis of the acquisition of 5-FU resistance in gastric cancer stem cells, we established 5-FU-resistant gastric cancer organoids. We used microarrays to detail the global program of gene expression underlying 5-FU resistance and maintenance of stem cell properties in gastric cancer.
2020-07-10 | GSE154127 | GEO
Project description:The genomic loci with copy number alterations are known to harbor cancer genes. We investigated a comprehensive panel of gastric cancer cell lines for their genome-wide copy number alterations. Eighteen gastric cancer cell lines were profiled using Affymetrix 500K SNP arrays. For copy number calculation, seven independent normal blood samples were profiled together. The copy numbers were calculated genome-wide, in these cell lines with high resolution and reveal the cell line specific amplification and copy number changes.
2015-08-04 | GSE51074 | GEO
Project description:In this study, we established a successive xenograft model to enrich Epstein-Barr virus-associated gastric carcinoma (EBVaGC) cancer stem cells (CSCs) through long-term treatment of EBVaGC cell line SNU719 with 5-Fluorouraci (5-Fu) in mice vivo passage. Simply, NOD/SCID mice injected in the subcutaneous with SNU719 were treated with 5-Fu weekly until xenografts reached 1.5 cm diameter and the mice were euthanizedand single-cell suspensions were obtainedby collagenasedigestion. Then the purified cells were passaged in 5-Fu-treated NOD/SCID mice as above. After four successive generations,we obtained theSNU-4th cells from the fourth passage xenografts treated with 5-Fu. Compared with parental SNU719 cells, SNU-4th cells possessed the stemness characters. Increasing evidence have proved that circular RNA (circRNA) play an important role in maintaining the tumor phenotype. So, we compared circRNAs expression between the fourth passage xenografts treated with 5-Fu and PBS by RNA-sequencing, hoping to find out which circRNAs were involved in the stemness regulation of EBVaGC. we established a highly malignant EBVaGC cell line SNU-4th through long-term treatment of EBVaGC cell line SNU719 with 5-Fluorouraci in vivo passage, then we compared circRNAs expression between the fourth passage xenografts treated with 5-Fu and PBS by RNA-sequencing
2020-02-26 | GSE145894 | GEO
Project description:Copy number analysis to compare parental colorectal cancer cell lines and their selumetinib-resistant derivatives and identify gene copy changes that might contribute to resistance
2019-03-11 | GSE126367 | GEO
Project description:Cisplatin is the first-line agent utilized for the clinical treatment of a wide variety of solid tumors including gastric cancer. However, the intrinsic or acquired cisplatin resistance is often occurred in patients with gastric cancer and resulted in failure of cisplatin therapy. In order to investigate if miRNA involves in cisplatin resistance of human gastric cancer, we first screened and compared the expression of miRNAs between cisplatin resistant gastric cancer cell lines SGC-7901/DDP and BGC-823/DDP and their sensitive parental cells by miRNAs microarray.
2016-09-05 | GSE86195 | GEO
Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed comparative Genome hybridization (arrayCGH) for DNA copy number analysis on four different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compared to the parental CCRF-CEM wildtype cell line and reference DNA.
2015-11-04 | E-GEOD-74633 | biostudies-arrayexpress
Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed micro-RNA on two different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compared to the parental CCRF-CEM wildtype cell line.
2015-11-04 | E-GEOD-74632 | biostudies-arrayexpress
Project description:To compare gene copy number in cell populations with acquired resistance to specified EGFR inhibitors to parental cell lines. The aim of the experiment was to determine whether gain or loss of copy number of particular genes was associated with resistance to particular EGFR inhibitors. Comparing gene copy number in PC9 parental cells to gene copy number in 5 cell populations resistant to AZD9291, 2 cell populations resistant to WZ4002, 2 cell populations resistant to afatinib and 4 cell populations resistant to gefitinib.
2015-04-14 | E-GEOD-59239 | biostudies-arrayexpress
Project description:Drug-tolerant persister (DTP) cells remain following chemotherapy and can cause cancer relapse. However, it is unclear when acquired resistance to chemotherapy emerges. Here, we compared the gene expression profiles of gastric cancer patient-derived cells (GC PDCs) and their respective xenograft tumors with different sensitivities to 5-fluorouracil (5-FU) by using immunodeficient female BALB/c-nu mice. RNA sequencing analysis of 5-FU-treated PDCs demonstrated that DNA replication/cell cycle-related genes were transiently induced in the earlier phase of DTP cell emergence, while extracellular matrix (ECM)-related genes were sustainably upregulated during long-term cell survival in 5-FU-resistant residual tumors. NicheNet analysis, which uncovers cell-cell signal interactions, indicated the transforming growth factor-β (TGF-β) pathway as the upstream regulator in response to 5-FU treatment. This induced ECM-related gene expression in the 5-FU-resistant tumor model. In the 5-FU-resistant residual tumors, there was a marked upregulation of cancer cell-derived TGF-β1 expression and increased phosphorylation of SMAD3, a downstream regulator of the TGF-β receptor. By contrast, these responses were not observed in a 5-FU-sensitive tumor model. We further found that TGF-β-related upregulation of ECM genes was preferentially observed in non-responders to chemotherapy with 5-FU and/or oxaliplatin among 22 patient-derived xenograft tumors. These observations suggest that chemotherapy-induced activation of the TGF-β1/SMAD3/ECM-related gene axis is a potential biomarker for the emergence of drug resistance in GCs.
2024-05-30 | GSE264144 | GEO