Expression data of tongue mucosa from normal mice and mice treated by the 4-NQO
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE75421 | GEO | 2016/12/06
SECONDARY ACCESSION(S): PRJNA304168
REPOSITORIES: GEO
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Project description:We hypothesized that the expression of many genes are dysregulated during oral cancer carcinogenesis. We examined genome-wide transcript levels in normal mouse tongues and the tongue squamous cell carcinomas induced by 4-NQO. The results will provide important information for the diagnosis, prevention, and treatment of human oral cancers, including tongue cancer. Total RNA obtained from normal tongues (not treated with 4-NQO) and tongue squamous cell carcinomas induced by 4-NQO.
2014-07-01 | E-GEOD-54246 | biostudies-arrayexpress
Project description:We hypothesized that the expression of many genes are dysregulated during oral cancer carcinogenesis. We examined genome-wide transcript levels in normal mouse tongues and the tongue squamous cell carcinomas induced by 4-NQO. The results will provide important information for the diagnosis, prevention, and treatment of human oral cancers, including tongue cancer.
2014-07-01 | GSE54246 | GEO
Project description:The 4-NQO induced rat tongue carcinogenesis model presenting considerable histologic and molecular similarity to oral cancers commonly seen in humans is very useful for investigating oral carcinogenesis. In order to understand the molecular basis of oral carcinogenesis and identify gene biomarkers and potential chemopreventive targets for future studies, we characterized the molecular changes in oral squamous cell carcinoma (SCC) samples generated from this model system using F344 rats by performing gene expression microarray and methylation analysis of selected genes. Microarray studies identified 1735 genes to be upregulated by at least 2 fold (p<0.05, n=11) and 1803 genes to be downregulated by at least 50% (p<0.05, n=11) in SCC in comparison to the adjacent normal tissues and 28 KEGG pathways to be altered in SCC (p<0.01). Among the altered genes, keratins and keratin associated proteins were found to be differentially regulated and the keratin profile appeared to an important biomarker for oral SCC. PTGS2 and PTGS2 relevant genes, which are potential targets of chemoprevention and therapy, were also found to be upregulated in SCC and confirmed by qRT-PCR. The upregulation of PTGS2 appeared to correlate with hypomethylation of its proximal promoter. Methylation analysis of other selected genes showed that the first exon of APC2 was methylated in normal tissues, and the methylation level increased moderately in SCC samples (p<0.01, n=8). These results demonstrate that 4-NQO induced tongue carcinogenesis in F344 rats is accompanied by alteration of multiple gene expression, hypomethylation of PTGS2 and increased methylation of APC2. Gene expression in untreated normal vs.4-NQO induced tongue tumors in F344 rats (n=11).
2014-08-04 | E-GEOD-51125 | biostudies-arrayexpress
Project description:The 4-NQO induced rat tongue carcinogenesis model presenting considerable histologic and molecular similarity to oral cancers commonly seen in humans is very useful for investigating oral carcinogenesis. In order to understand the molecular basis of oral carcinogenesis and identify gene biomarkers and potential chemopreventive targets for future studies, we characterized the molecular changes in oral squamous cell carcinoma (SCC) samples generated from this model system using F344 rats by performing gene expression microarray and methylation analysis of selected genes. Microarray studies identified 1735 genes to be upregulated by at least 2 fold (p<0.05, n=11) and 1803 genes to be downregulated by at least 50% (p<0.05, n=11) in SCC in comparison to the adjacent normal tissues and 28 KEGG pathways to be altered in SCC (p<0.01). Among the altered genes, keratins and keratin associated proteins were found to be differentially regulated and the keratin profile appeared to an important biomarker for oral SCC. PTGS2 and PTGS2 relevant genes, which are potential targets of chemoprevention and therapy, were also found to be upregulated in SCC and confirmed by qRT-PCR. The upregulation of PTGS2 appeared to correlate with hypomethylation of its proximal promoter. Methylation analysis of other selected genes showed that the first exon of APC2 was methylated in normal tissues, and the methylation level increased moderately in SCC samples (p<0.01, n=8). These results demonstrate that 4-NQO induced tongue carcinogenesis in F344 rats is accompanied by alteration of multiple gene expression, hypomethylation of PTGS2 and increased methylation of APC2.
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Project description:Tobacco use and alcohol consumption are two major contributing factors for head and neck squamous cell carcinoma (HNSCC) carcinogenesis. We combined the 4-nitroquinoline-1-oxide (4-NQO) oral carcinogenesis mouse model and the Meadows-Cook alcohol mouse models and performed next generation genome-wide RNA-sequencing of tongues. We determined changes in transcript levels in four groups: 4-NQO followed by ethanol treatment (4-NQO/EtOH), 4-NQO followed by normal drinking water (4-NQO/Untr.), vehicle control followed by ethanol treatment (V.C./EtOH), and vehicle control followed by normal drinking water (V.C./Untr.). We found that the 494 gene transcripts were significantly changed (at least a 2-fold change where p<0.05) in the V.C./EtOH group compared to the V.C./Untr. group. The 4-NQO/Untr. group had 1,808 transcripts significantly changed compared to the V.C./Untr group, while the 4-NQO/EtOH group had 3,606 significantly changed transcripts as compared to the V.C/Untr. group. This study is the first to show that 4-NQO followed by ethanol cause the largest number of changes in transcript levels in the tongue.
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Project description:Understanding the dynamics of the immune microenvironment is critical to the development of immuno-prevention strategies for the prevention of oral potentially malignant disorders transformation to oral squamous cell carcinoma (OSCC). We generated gene expression profiles of the microdissected epithelial and stromal compartments normal mucosa, hyperplasia, dysplasia and invasive tumors in the 4-nitroquinolein (4-NQO) murine model of oral carcinogenesis. Most gene expression changes were observed in the stromal compartment and related to immune biological processes. Immune cell deconvolution identified infiltration by the macrophage population as the most important quantitatively especially at the stage of dysplasia. In 86 patients with oral leukoplakia, three M2 macrophages signatures were independently associated and highly predictive of improved oral cancer-free survival.
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Project description:To identification of genome wide DNA methylation profiling during lingual tumorigenesis, tongue cancer was induced by oral delivery of 4-nitroquinoline-1-oxide (4NQO) at a dose of 50mg/L for 16weeks in C57BL/6J female mice. Nine samples of lingual mucosa from 0 (encoded as C in experiment), 12 (encoded as M in experiment) and 28 (encoded as E in experiment) week, which were supposed as normality, early and advanced stage during lingual tumorigenesis, were harvested for methylated DNA Immunoprecipitation sequencing. Illumina HiSeq 2000 was used to obtain DNA methylation profiles across 16023 CpG Islands including 26600 promoters and 21625 genebodies in murine tongue samples. Samples included 3 normal lingual mucosa,3 lingual mucosa with hyperplasia, mild and moderate dysplasia, 3 lingual mucosa with carcinoma in situ and invasive cancer.
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Project description:Gene expression profiles of oral tongue squamous cell carcinoma tissues. Keywords: human tongue cancer, brachytherapy, biopsy sample, primary tissues
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Project description:The mucosae of the oral cavity are different at the histological level but are all exposed to common genotoxic agents. As a result of this exposure, changes in the mucosal epithelia develop giving rise to Oral Potentially Malignant Lesions (OPMLs), which with time may in turn progress to Oral Squamous Cell Carcinomas (OSCCs). Therefore, much effort should be devoted to identify features able to predict the likeliness of progression associated with an OPML. Such features may be helpful in assisting the clinician to establish both appropriate therapies and follow-up schedules. Here, we report a pilot study that compared the anatomical subsites of OPMLs development with occurrence of DNA aneuploidy and chromosomal copy number aberrations (CNAs). Multiple samples from histologically diagnosed OPMLs were processed for high resolution DNA flow cytometry (hr DNA-FCM) in order to determine the relative DNA content expressed by the DNA index (DI). Additionally, array-Comparative Genomic Hybridization (a-CGH) analysis was performed on FCM-sorted nuclei subpopulations based on DI values. Tongue OPMLs were more frequently associated with DNA aneuploidy and CNAs than OPMLs arising from all the other mucosal subsites. We suggest that the follow-up and the management of the patients with tongue OPMLs should receive a distinctive special attention. Clearly, this conclusion should be validated in a prospective clinical study. exposed to common genotoxic agents. As a result of this exposure, changes in the mucosal epithelia develop giving rise to Oral Potentially Malignant Lesions (OPMLs), which with time may in turn progress to Oral Squamous Cell Carcinomas (OSCCs). Therefore, much effort should be devoted to identify features able to predict the likeliness of progression associated with an OPML. Such features may be helpful in assisting the clinician to establish both appropriate therapies and follow-up schedules. Here, we report a pilot study that compared the anatomical subsites of OPMLs development with occurrence of DNA aneuploidy and chromosomal copy number aberrations (CNAs). Multiple samples from histologically diagnosed OPMLs were processed for high resolution DNA flow cytometry (hr DNA-FCM) in order to determine the relative DNA content expressed by the DNA index (DI). Additionally, array-Comparative Genomic Hybridization (a-CGH) analysis was performed on FCM-sorted nuclei subpopulations based on DI values. Tongue OPMLs were more frequently associated with DNA aneuploidy and CNAs than OPMLs arising from all the other mucosal subsites. We suggest that the follow-up and the management of the patients with tongue OPMLs should receive a distinctive special attention. Clearly, this conclusion should be validated in a prospective clinical study. We analyzed: 19 samples (4 aneuploid and 15 diploid components) deriving from oral potentially malignant lesions without dysplasia obtained of 16 patients; 14 samples (2 aneuploid and 12 diploid components) deriving from oral potentially malignant lesions with dysplasia obtained from 11 patients (two patients had multiple dysplastic lesions); 2 samples from visually normal mucosa in the near field obtained from two patients with dysplastic lesions. All the aneuploid samples had a purity of at least 90%.
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Project description:This study aims to compare the global expression signature of protein coding genes between oral cancers from carcinogen-induced mice and human patients. Combinatorial treatment of 4NQO and arecoline for 8 weeks consistently induced the formation of mouse oral cancer with morphology and pathology resembling human oral squamous cell carcinoma. In this dataset, 5 mouse normal tongue and 7 tumor samples were used and Illumina Mouse Ref-8 cDNA microarray was conducted. To identify protein coding genes differentially expressed in mice oral cancers, 7 tumor tissues from carcinogen-treated mice and 5 normal tongue tissues from control mice were used in a microarray-based analysis for protein-coding gene expression patterns.
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