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Human Tissues: pancreatic cancer vs. pancreatic non-tumoral tissues

ABSTRACT: Transcriptional profiling of pancreatic tumors comparing to adjacent non-tumoral pancreatic tissue by two strategies. The first strategy implies a traditional microarray assay, while the second involves a previous Suppression Subtractive Hybridization (SSH) and then the traditional microarray assay. Goal was to determine differences in gene expression profile in tumor samples by both strategies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE39751 | GEO | 2012/07/31

SECONDARY ACCESSION(S): PRJNA171578

REPOSITORIES: GEO

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Human Tissues: pancreatic cancer vs. pancreatic non-tumoral tissues

Project description:Transcriptional profiling of pancreatic tumors comparing to adjacent non-tumoral pancreatic tissue by two strategies. The first strategy implies a traditional microarray assay, while the second involves a previous Suppression Subtractive Hybridization (SSH) and then the traditional microarray assay. Goal was to determine differences in gene expression profile in tumor samples by both strategies. Two-condition experiment, tumoral vs. non-tumoral tissues. Biological replicates: 6 tumoral replicates, 6 non-tumoral replicates. The same replicates for both strategies.

2012-07-30 | E-GEOD-39751 | biostudies-arrayexpress

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Project description:Transcriptional profiling of colonic tumors compared to paired adjacent non-tumoral colonic tissue by two strategies. The first strategy is a conventional microarray assay, while the second strategy involves a previous Suppression Subtractive Hybridization (SSH) followed by a conventional microarray assay. We applied subtractive hybridization followed by microarray analysis to identify tumor-specific low-abundance transcripts. The goal was to determine differences in gene expression profile in tumor samples by both strategies. Two-condition experiment: tumoral vs. adjacent non-tumoral tissues. Biological replicates: 10 tumoral replicates, 10 non-tumoral replicates. The same replicates were used for both strategies (conventional, SSH). Human Universal Reference RNA (Clontech) was used as the reference.

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2012-06-27 | GSE38939 | GEO

Expression data of gastric cancer by conventional microarray and by suppressive subtractive hybridization coupled to microarray

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Gene expression data from advanced gastric and colon cancers: tumoral vs. matched non-tumoral tissues

Project description:This SuperSeries is composed of the following subset Series: GSE38932: Expression data of gastric cancer by conventional microarray and by suppressive subtractive hybridization coupled to microarray GSE38939: Expression data of colon cancer by conventional microarray and by suppressive subtractive hybridization coupled to microarray Refer to individual Series

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Human Tissues: pancreatic cancer vs. pancreatic non-tumoral tissues

Project description: Not available

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Schistosoma japonicum gender-associated differentially expressed genes

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Project description:Pancreatic cancer is one of the deadliest human malignancies, with a survival rate less than 10%. Traditional modes of therapy have proven ineffective in the treatment of pancreatic cancer, highlighting the need to further understand the basic biology of the disease in order to identify new treatment modalities. Previously, our group showed that the epigenetic regulator Bmi1 is required for the initiation of pancreatic cancer in mice. In murine models of PDAC, mice lacking pancreatic Bmi1 expression do not develop precancerous lesions, despite oncogene expression. In this work, we sought to determine the role of Bmi1 in later stages of pancreatic tumor development. Using a CRISPR/Cas9 strategy, we deleted Bmi1 in primary human pancreatic caner cells and created clonal lines. When used in a subcutaenous tumor growth assay, those cells lacking BMI1 expression formed tumors that grew significantly smaller than controls. To query the mechanism of BMI1 action in pancreatic cancer growth, we used RNA sequencing to compare those pancreatic cancer cells with and without BMI1 expressed. This revealed that Bmi1 controls the gene expression of glycolysis and cell proliferation pathways, likely the reason for its requirement in pancreatic tumor growth. Overall, we found that Bmi1 is required in pancreatic tumor progression, and that it controls gene expression in both glycolysis and cell proliferation.

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