Gene expression of mouse oral cancer cell lines
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ABSTRACT:
PROVIDER: PRJNA579101 | ENA |
REPOSITORIES: ENA
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Project description:A comparative microarray analysis of indolent or aggressive mouse oral cancer cell lines was performed to identify gene expression signatures and specific molecules involved in aggressive tumor growth.
2014-04-13 | GSE50041 | GEO
Project description:A comparative microarray analysis of indolent or aggressive mouse oral cancer cell lines was performed to identify gene expression signatures and specific molecules involved in aggressive tumor growth. We compared 3 indolent cell lines (MOC1, MOC22, MOC23) to 1 aggressive line and it's derivatives (MOC2, MOC2-7 and MOC2-10). We also included a cell line generated from a lymph node metastasis of the MOC2 tumor. The lines were all analyzed in triplicated except for MOC1 which was done in quadruplicate. Finally, we included duplicate samples of primary, normal C57BL/6 oral keratinocytes grown in the same media as the MOC cell lines.
2014-04-13 | E-GEOD-50041 | biostudies-arrayexpress
Project description:To genome-wide screening for the genes whose expression are responsible for the promoter DNA methylation, we performed the cDNA microarray with oral cancer cells before and after a DNA methyltransferase inhibitor, 5-aza-2’-deoxycytidine (AzC), treatment. Total RNA was collected from four oral cancer cell lines before or after AzC treatment.
2015-04-01 | E-GEOD-38823 | biostudies-arrayexpress
Project description:We established two murine OSCC cell lines, named M1-2 and M2-3, from a mouse tumor induced by 4-nitroquinoline 1-oxide (4-NQO)/arecoline. After in vitro selection using sphere culture, NHRI-HN1 and NHRI-HN2 were derived from M1-2 and M2-3 cells, respectively. Only NHRI-HN1 cells are capable of generating orthotopic tumors in syngeneic mice.
2022-09-21 | GSE139282 | GEO
Project description:Patients with oral preneoplastic lesion (OPL) have high risk of developing oral cancer. Although certain risk factors such as smoking status and histology are known, our ability to predict oral cancer risk remains poor. The study objective was to determine the value of gene expression profiling in predicting oral cancer development. Gene expression profile was measured in 86 of 162 OPL patients who were enrolled in a clinical chemoprevention trial that used the incidence of oral cancer development as a prespecified endpoint. The median follow-up time was 6.08 years and 35 of the 86 patients developed oral cancer over the course. Gene expression profiles were associated with oral cancer-free survival and used to develope multivariate predictive models for oral cancer prediction. We developed a 29-transcript predictive model which showed marked improvement in terms of prediction accuracy (with 8% predicting error rate) over the models using previously known clinico-pathological risk factors. Based on the gene expression profile data, we also identified 2182 transcripts significantly associated with oral cancer risk associated genes (P-value<0.01, single variate Cox proportional hazards model). Functional pathway analysis revealed proteasome machinery, MYC, and ribosomes components as the top gene sets associated with oral cancer risk. In multiple independent datasets, the expression profiles of the genes can differentiate head and neck cancer from normal mucosa. Our results show that gene expression profiles may improve the prediction of oral cancer risk in OPL patients and the significant genes identified may serve as potential targets for oral cancer chemoprevention.
2011-02-01 | GSE26549 | GEO
Project description:Patients with oral preneoplastic lesion (OPL) have high risk of developing oral cancer. Although certain risk factors such as smoking status and histology are known, our ability to predict oral cancer risk remains poor. The study objective was to determine the value of gene expression profiling in predicting oral cancer development. Gene expression profile was measured in 86 of 162 OPL patients who were enrolled in a clinical chemoprevention trial that used the incidence of oral cancer development as a prespecified endpoint. The median follow-up time was 6.08 years and 35 of the 86 patients developed oral cancer over the course. Gene expression profiles were associated with oral cancer-free survival and used to develope multivariate predictive models for oral cancer prediction. We developed a 29-transcript predictive model which showed marked improvement in terms of prediction accuracy (with 8% predicting error rate) over the models using previously known clinico-pathological risk factors. Based on the gene expression profile data, we also identified 2182 transcripts significantly associated with oral cancer risk associated genes (P-value<0.01, single variate Cox proportional hazards model). Functional pathway analysis revealed proteasome machinery, MYC, and ribosomes components as the top gene sets associated with oral cancer risk. In multiple independent datasets, the expression profiles of the genes can differentiate head and neck cancer from normal mucosa. Our results show that gene expression profiles may improve the prediction of oral cancer risk in OPL patients and the significant genes identified may serve as potential targets for oral cancer chemoprevention. Gene expression profile was measured in 86 of 162 OPL patients who were enrolled in a clinical chemoprevention trial that used the incidence of oral cancer development as a prespecified endpoint. The median follow-up time was 6.08 years and 35 of the 86 patients developed oral cancer over the course. Gene expression profiles were associated with oral cancer-free survival and used to develope multivariate predictive models for oral cancer prediction.
2011-02-01 | E-GEOD-26549 | biostudies-arrayexpress
Project description:Three types of oral cancer cell lines (HSC3,Sa3 and SAS) and human normal oral keratinocytes(HNOKs) were used to identify a circular RNA specifically. expressed in oral cancer
2020-02-21 | GSE145608 | GEO
Project description:expression of human and mouse breast cancer cell lines
| PRJNA135447 | ENA
Project description:miRNA expression of human cancer and mouse cell lines
| PRJNA116139 | ENA
Project description:BACKGROUND: Cell lines have been developed for modeling cancer and cancer progression. The molecular background of these cell lines is often unknown to those using them to model disease behaviors. As molecular alterations are the ultimate drivers of cell phenotypes, having an understanding of the molecular make-up of these systems is critical for understanding the disease biology modeled. METHODS: Six immortalized normal, one immortalized dysplasia, one self-immortalized dysplasia, and two primary normal cell lines derived from oral tissues were analyzed for DNA copy number changes and changes in both mRNA and miRNA expression using SMRT-v.2 genome-wide tiling comparative genomic hybridization arrays, Agilent Whole Genome 4x44k expression arrays, and Exiqon V2.M-RT-PCR microRNA Human panels. RESULTS: DNA copy number alterations were detected in both normal and dysplastic immortalized cell lines—as well as in the single non-immortalized dysplastic cell line. These lines were found to have changes in expression of genes related to cell cycle control as well as alterations in miRNAs that are deregulated in clinical oral squamous cell carcinoma tissues. Immortal lines—whether normal or dysplastic—had increased disruption in expression relative to primary lines. All data are available as a public resource. CONCLUSIONS: Molecular profiling experiments have identified DNA,mRNA,andmiRNAalterations for a panel of normal and dysplastic oral tissue cell lines. These data are a valuable resource to those modeling diseases of the oral mucosa, and give insight into the selection of model cell lines and the interpretation of data from those lines. Total RNA from oral cancer cell lines were hybridized to Agilent 4x44k gene expression microarray
2014-07-10 | E-GEOD-59238 | biostudies-arrayexpress