Expression data of tumor and non-tumor samples from patients with esophageal cancer
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE33810 | GEO | 2011/11/19
SECONDARY ACCESSION(S): PRJNA148133
REPOSITORIES: GEO
Similar Datasets
Project description:We used cDNA microarray to study the gene expression profile between the tumor and non-tumor tissue samples from patients with esophageal cancer Pooled RNA from 10 pairs of primary ESCCs and their corresponding non-tumor tissues were compared by Affymetrix microarrays.
2011-11-19 | E-GEOD-33810 | biostudies-arrayexpress
Project description:Esophageal cancer is among the 10 most common malignancies and ranks as the 6th leading cause of death from cancer. It constitutes 7% of all gastrointestinal cancers and is one of the most lethal of all cancers. The large variation in the incidence of esophageal cancer in different geographic regions has often been thought to be due to variation in exposure to environmental factors; however, hereditary factors may also contribute to the variation in rates. A positive family history was found to be associated with an increased risk of esophageal cancer in several case-control and cohort studies in China. Familial aggregation also has been observed in Iran and Japan. The cancer data generated from six hospital based cancer registries in India under National Cancer Registry Programme (NCRP, Annual Report, 2003-2004) has revealed that the occurrence of esophageal cancer in Assam is highest in India. The aggregation of esophageal cancer in families is a long-observed and well-documented phenomenon in Assam of North-east part of India (AAR=32.6). In Assam high incidence of esophageal cancer with familial aggregation need investigation for etiology. The etiology of esophageal cancer in Northeast Indian population is different from other population at India due to wide variations in dietary habits or nutritional factors, tobacco chewing and alcohol habits. With in these high-risk regions, studies have shown a strong tendency toward familial aggregation, suggesting that genetic susceptibility, in conjunction with potential environmental exposures, may be involved in the etiology of esophageal cancer. Familial clustering of cancer has been one of the main avenues to the understanding of cancer etiology and the signal to the involvement of heritable genes. Familial clustering of cancer may be due to environmental factors shared by family members or due to shared genes. However, the familial aggregation of esophageal cancer among the population in northeast India may reflect the influence of environmental factors operating on individuals who are already genetically susceptible. Epidemiological studies indicate that tobacco smoking and alcohol consumption are the major factors for esophageal cancer, the role of genetic factors for familial aggregation has not been elucidated. In this study, tumor and matched normal tissue from esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer were analyzed using cDNA microarray containing 10,000genes to evaluate gene expression differences in esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer from a high- risk area in India. To identify alteration in genes and molecular functional pathways in esophageal cancer in a high incidence region of India where there is wide spread use of tobacco and betel quid with fermented areca nuts and familial aggregation cancer. Keywords: Gene Expression
2008-02-09 | GSE10127 | GEO
Project description:Esophageal cancer is among the 10 most common malignancies and ranks as the 6th leading cause of death from cancer. It constitutes 7% of all gastrointestinal cancers and is one of the most lethal of all cancers. The large variation in the incidence of esophageal cancer in different geographic regions has often been thought to be due to variation in exposure to environmental factors; however, hereditary factors may also contribute to the variation in rates. A positive family history was found to be associated with an increased risk of esophageal cancer in several case-control and cohort studies in China. Familial aggregation also has been observed in Iran and Japan. The cancer data generated from six hospital based cancer registries in India under National Cancer Registry Programme (NCRP, Annual Report, 2003-2004) has revealed that the occurrence of esophageal cancer in Assam is highest in India. The aggregation of esophageal cancer in families is a long-observed and well-documented phenomenon in Assam of North-east part of India (AAR=32.6). In Assam high incidence of esophageal cancer with familial aggregation need investigation for etiology. The etiology of esophageal cancer in Northeast Indian population is different from other population at India due to wide variations in dietary habits or nutritional factors, tobacco chewing and alcohol habits. With in these high-risk regions, studies have shown a strong tendency toward familial aggregation, suggesting that genetic susceptibility, in conjunction with potential environmental exposures, may be involved in the etiology of esophageal cancer. Familial clustering of cancer has been one of the main avenues to the understanding of cancer etiology and the signal to the involvement of heritable genes. Familial clustering of cancer may be due to environmental factors shared by family members or due to shared genes. However, the familial aggregation of esophageal cancer among the population in northeast India may reflect the influence of environmental factors operating on individuals who are already genetically susceptible. Epidemiological studies indicate that tobacco smoking and alcohol consumption are the major factors for esophageal cancer, the role of genetic factors for familial aggregation has not been elucidated. In this study, tumor and matched normal tissue from esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer were analyzed using cDNA microarray containing 10,000genes to evaluate gene expression differences in esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer from a high- risk area in India. To identify alteration in genes and molecular functional pathways in esophageal cancer in a high incidence region of India where there is wide spread use of tobacco and betel quid with fermented areca nuts and familial aggregation cancer. Low RNA Input Fluorescent Linear Amplification Kit (Agilent, Santa Clara, CA) was used for labeling. Briefly, both first and second strand cDNA were synthesized by incubating 500ng of total RNA with 1.2ul of oligo dT-T7 Promoter Primer in nuclease-free water at 65 â¦C for 10 min followed by incubation with 4.0ul of 5à First strand buffer, 2ul of 0.1M DTT, 1 ul of 10mM dNTP mix, 1ul of 200 U/ul MMLV-RT, and 0.5ul of 40U/ul RNaseOUT, at 40 â¦C for 2 hour. Immediately following cDNA synthesis, the reaction mixture was incubated with 2.4 ul of 10 mM Cyanine-3-CTP or 2.4 ul of 10 mM Cyanine-5-CTP (Perkin-Elmer, Boston, MA), 20ul of 4X Transcription buffer, 8 ul of NTP mixture, 6 ul of 0.1M DTT, 0.5 ul of RNaseOUT, 0.6ul of Inorganic pyrophosphatase, 0.8 ul of T7 RNA polymerase, and 15.3ul of nuclease-free water at 40 â¦C for 2 hour. Qiagenâs RNeasy mini spin columns were used for purifying amplified aRNA samples. The quantity and specific activity of cRNA was determined by using NanoDrop ND-1000 UV-VIS Spectrophotometer version3.2.1. Samples with specific activity >8 were used for hybridization. 825ng of each Cyanine 3 or Cyanine 5 labeled cRNA in a volume of 41.8ul were combined with 11ul of 10x Blocking agent and 2.2ul of 25x Fragmentation buffer (Agilent), and incubated at 60deg C for 30 minutes in dark. The fragmented cRNA were mixed with 55ul of 2x Hybridization Buffer (Agilent). About 110ul of the resulting mixture was applied to the Microarray and hybridized at 65degC for 17 hours in an Agilent Microarray Hybridization Chamber (SureHyb: G2534A) with Hybridization Oven. After hybridization, slides were washed with Agilent Gene expression Wash Buffer I for 1 minute at room temperature followed by a 1 min wash with Agilent Gene expression Wash Buffer II for 37C. Slides were finally rinsed with Acetonitrile for cleaning up and drying. Microarrays were scanned on an Agilent scanner (G2565AA) at 100% laser power, 30% PMT.Data extraction was carried out with Agilent Feature Extraction software (version 9.1), and normalization was done using linear per array algorithm according to the manufacturerâs protocol. The data was analysed by GeneSpring GX and Biointerpreter software from Genotypic Technology, Bangalore. The differential expression was considered if the Log 2 mean of at least -1 for the down regulated genes and +1 for the upregulated genes. We considered only the genes that were reproducible from all replicates.
2010-06-25 | E-GEOD-10127 | biostudies-arrayexpress
Project description:Esophageal cancer is one of the common malignant tumors, and the mortality rate ranks fourth among all malignant tumors in China. Radiotherapy is one of the main methods for the treatment of esophageal cancer, and radiation resistance is one of the important factors of tumor recurrence and metastasis. Therefore, the study of radioresistance related markers of esophageal cancer is of great significance to improve the radiosensitivity of esophageal cancer. We used microarrays to detail to find critical prognostic factors for esophageal cancer patients after radiotherapy.
2021-06-16 | GSE137867 | GEO
Project description:Jaridon 6, an ent-kaurene diterpenoid derivative from Rabdosia rubescens (Hemsl.) Hara, possesses strong antitumor activity in esophageal cancer cells. This study explored the underlying molecular events of Jaridon 6’s anti-tumor activity in esophageal cancer cells through the cDNA microarray.
2019-12-31 | GSE94012 | GEO
Project description:Downregulation is a common feature of tumor suppressor gene (TSG), which can be caused by allele deletion, promoter hypermethylation, histone deacetylation and posttranscriptional silencing by microRNA. Therefore, comparison of expression profiles by cDNA microarray between tumor and non-tumor tissues and characterization of downregulated genes in tumor specimens is a useful strategy to identify TSGs. To identify deregulated genes during ESCC development, Affemetrix cDNA microarray was applied to compare differentially expressed genes between 4 pairs of ESCC tumors and corresponding adjacent non-tumor tissues (#301, #327, #351 and #363), and one pair of esophageal dysplasia tissue and adjacent normal tissue (#314).
2017-07-15 | GSE100942 | GEO
Project description:We demonstrate that blood and esophageal tissues shared similar DNA methylation patterns within the same individual,suggesting an influence of genetic background on DNA methylation. Recent studies have shown a genetic influence on gene expression variation, chromatin, and DNA methylation. However, the effects of genetic background and tissue types on DNA methylation at the genome-wide level have not been characterized extensively. To study the effect of genetic background and tissue types on global DNA methylation, we performed DNA methylation analysis using the Affymetrix 500K SNP array on tumor, adjacent normal tissue, and blood DNA from 30 patients with esophageal squamous cell carcinoma (ESCC). The use of multiple tissues from 30 individuals allowed us to evaluate variation of DNA methylation states across tissues and individuals. Our results demonstrate that blood and esophageal tissues shared similar DNA methylation patterns within the same individual, suggesting an influence of genetic background on DNA methylation. Furthermore, we showed that tissue types are important contributors of DNA methylation states. Methylation and gDNA intensity data derived from Affymetrix 500k array. 30 individuals with blood, normal and tumor esophageal tissues.
2010-08-02 | E-GEOD-20123 | biostudies-arrayexpress
Project description:We demonstrate that blood and esophageal tissues shared similar DNA methylation patterns within the same individual,suggesting an influence of genetic background on DNA methylation. Recent studies have shown a genetic influence on gene expression variation, chromatin, and DNA methylation. However, the effects of genetic background and tissue types on DNA methylation at the genome-wide level have not been characterized extensively. To study the effect of genetic background and tissue types on global DNA methylation, we performed DNA methylation analysis using the Affymetrix 500K SNP array on tumor, adjacent normal tissue, and blood DNA from 30 patients with esophageal squamous cell carcinoma (ESCC). The use of multiple tissues from 30 individuals allowed us to evaluate variation of DNA methylation states across tissues and individuals. Our results demonstrate that blood and esophageal tissues shared similar DNA methylation patterns within the same individual, suggesting an influence of genetic background on DNA methylation. Furthermore, we showed that tissue types are important contributors of DNA methylation states.
2010-07-06 | GSE20123 | GEO
Project description:We detected the expression of miRNA in an esophageal NEC sample and the corresponding normal esophagus tissue. Then, we identified the differentially expressed miRNAs in this rare disease.
2018-04-28 | GSE113776 | GEO
Project description:In the past decades, the incidence of esophageal adenocarcinoma has increased dramatically in Western populations. Better understanding of disease etiology along with the identification of novel prognostic and predictive biomarkers are urgently needed to improve the dismal survival probabilities. Here, we performed comprehensive RNA (both coding and non-coding) profiling in various samples from 17 patients diagnosed with esophageal adenocarcinoma, high-grade dysplastic or non-dysplastic Barrett’s esophagus. Per patient, a blood plasma sample, and a healthy esophageal and disease tissue sample were included. In total, this comprehensive dataset consists of 102 RNA-seq libraries from 51 samples. The raw data for this study have been deposited to the controlled access archive EGA under submission EGAS00001004939.
2022-01-01 | E-MTAB-10004 | biostudies-arrayexpress