Project description:array CGH (244K) of liver tumors and unaffected liver controls from mice conditionally deficient for Mad2 and p53 in hepatocytes aCGH of sample DNA was hybridized with sex mismatched control DNA from a different mouse. Tumor and unaffected liver tissues were tested for each mouse. 19 tissue samples, 10 tumors, 9 normal samples
Project description:Tumor samples and matching healthy tissue from 23 human hepatocellular carcinoma (HCC) patients and one hepatocellular adenoma patient were collected after surgical resection. Total RNA was harvested and sequenced with a strand-specific single-end RNA-seq protocol.
Project description:Hepatocellular adenomas (HCA) are rare benign tumors that constitute a heterogeneous entity, divided into 5 groups based on molecular features (1) H-HCA with inactivating mutations of Hepatocyte Nuclear Factor 1A (HNF1α), (2) inflammatory HCA (IHCA) with diverse mutations activating the JAK/STAT pathway, (3) b-HCA with activating β-catenin mutation (4) recently identified sh-HCA presenting a Sonic Hedgehog pathway activation and finally, (5) the unclassified HCA (UHCA)). Risk of bleeding of sh-HCA and UHCA is their main clinical feature with malignant transformation. Nowadays, no specific biomarker exists to evaluate this hemorrhage risk. The objective of this study was to combine laser microdissection and mass spectrometry analysis to define Hepatocellular Adenoma proteome in the purpose of identifying specific biomarkers able to predict this bleeding risk.
Project description:AIM: To analyze the expression profiles of premalignant and/or preclinical lesions of gastric cancers. METHODS: We analyzed the expression profiles of normal gastric pit, tubular adenoma and carcinoma in situ using microdissected cells from routine gastric biopsies. For the DNA microarray analysis of formalin-fixed samples, we developed a simple and reproducible RNA extraction and linear amplification procedure applying two polymerase-binding sites. The amplification procedure took only 8 h and yielded comparable DNA microarray data between formalin-fixed tissues and unfixed controls. RESULTS: In comparison with normal pit, adenoma/carcinoma showed 504 up-regulated and 29 down-regulated genes at the expected false significance rate 0.15%. The differential expression between adenoma and carcinoma in situ was subtle: 50 and 22 genes were up-, and down-regulated in carcinomas at the expected false significance rate of 0.61%, respectively. Differentially expressed genes were grouped according to patterns of the sequential changes for the 'tendency analysis' in the gastric mucosa-adenoma-carcinoma sequence. CONCLUSION: Groups of genes are shown to reflect the sequential expression changes in the early carcinogenic steps of stomach cancer. It is suggested that molecular carcinogenic pathways could be analyzed using routinely processed biopsies. Keywords: other