Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
Project description:We characterized the epigenetic landscape of human colorectal cancer (CRC). To this extent, we performed gene expression profiling using high throughput sequencing (RNA-seq) and genome wide binding/occupancy profiling (ChIP-seq) for histone modifications correlated to transcriptional activity, enhancers, elongation and repression (H3K4me3, H3K4me1, H3K27Ac, H3K36me3, H3K27me3) in patient-derived organoids (PDOs), and in normal and tumoral primary colon tissues. We also generated ChIP-seq data for transcription factors YAP/TAZ in human CRC PDOs.
Project description:We characterized the epigenetic landscape of human colorectal cancer (CRC). To this extent, we performed gene expression profiling using high throughput sequencing (RNA-seq) and genome wide binding/occupancy profiling (ChIP-seq) for histone modifications correlated to transcriptional activity, enhancers, elongation and repression (H3K4me3, H3K4me1, H3K27Ac, H3K36me3, H3K27me3) in patient-derived organoids (PDOs), and in normal and tumoral primary colon tissues. We also generated ChIP-seq data for transcription factors YAP/TAZ in human CRC PDOs.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
Project description:The patients who underwent surgery for primary lesions were examined. All patients had metastatic or recurrent CRC and received bevacizumab therapy as first line or second line treatment. Responders and nonresponders were determined based on RECIST and confirmed by CT or MRI. Gene-expression profiles of primary CRC were determined using Human Genome GeneChip arrays U133. Colorectal cancer patients who had undergone surgical resection of colorectal cancer were studied. To identify molecular signatures to predict response to bevacizumab, gene expression profiles were compared between Reponder and Non-responder.
Project description:The patients who underwent surgery for primary lesions were examined. All patients had metastatic or recurrent CRC and received modified FOLFOX6. Responders and nonresponders were determined based on the best observed response at the end of the first-line treatment, mFOLFOX6. Gene-expression profiles of primary CRC were determined using Human Genome GeneChip arrays U133. Colorectal cancer patients who had undergone surgical resection of colorectal cancer were studied. To identify molecular signatures to predict response to mFOLFOX6 regimen, gene expression profiles were compared between Reponder and Non-responder. Some patients are overlapped with Bevacizumab therapy.
Project description:DNA methylation profiling of matched primary tumor (CRC), cancer-associated mucosa (CAM) and blood from two colorectal cancer patients to identify cancer-specific methylation targets.
Project description:Colorectal cancer (CRC) with high rate of mortality is one of the most commonly diagnosed cancers in worldwide. Advanced colorectal cancer is often accompanied by malignant proliferation of tumor cells. Further researches on colorectal cancer proliferation to find new targets and develop new therapeutic regimen are an important direction for colorectal cancer treatment. In this study, genome-wide RNAi screening was used to discover the essential genes associated with colorectal cancer cell proliferation. We found DKC1 (dyskerin pseudouridine synthase 1) promoted CRC proliferation through binding and modifying ribosomal proteins (RPL10A, RPL22L1, RPL34, RPS3) mRNA to increase the mRNAs stability and eventually increasing their expression. Besides, DKC1 is highly expressed in colorectal cancer and its aberrantly high expression is associated with poor prognosis of colorectal cancer patients. These results suggest that DKC1 could be a new therapeutic target for colorectal cancer.