| Budget Amount *help |
¥4,020,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Research Abstract |
In this study, the low-molecular-weight proteome, peptidome, is a source of potential biomarkers for the disease. However, almost all detected peptides in previous reports are fragments originating from highly abundant plasma proteins, probably through the activities of disease-associated proteases and the ex vivo coagulation and complement degradation pathways in the collected blood. In addition, the major plasma proteins abundant in blood mask the presence of circulating peptide biomarkers indicative of the disease state, making the discovery of such biomarkers challenging. In present study, we established the methodology for differential and quantitative serum peptidome profiling that is efficient in the discovery of these peptides. Comprehensive fractionation by 2 dimensional LC-MALDI-TOF MS, non-labeling quantification and multi-sample comparison data analysis were performed. Numerous reports claim that the use of surface-enhanced laser desorption/ionization (SELDI)-TOF MS or MALD
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I-TOF MS has identified mass peaks or combinations of mass peaks that are capable of diagnosing disease with high sensitivity and specificity. However, most of these studies are pattern-based without identification of each of such mass peaks and, therefore, present analytical platform must be powerful tool for differential proteomics to reveal signaling pathways in carcinogenesis and cancer progression. We also analyzed signaling pathways involved in cancer progression and drug-resistance in clear cell carcinoma of kidney. To identify genomic alterations involved in progression of clear cell renal cell carcinoma (CRCC) and figure out the oncogenic pathways of renal cell. Twenty-three tumors and their corresponding normal tissues were collected and genomic DNA and RNA were isolated. The 50 K SNP mapping array U133 Plus 2.0 array was used. Individual copy numbers on chromosome and gene expression patterns at corresponding loci were analyzed. We have identified novel homozygous deletion at 4q24 including CXXC4 by using SNP array in renal cell carcinoma. The CXXC4 gene encodes the Idax protein that whose functions as is a negative regulator of the Wnt signaling by binding to the PDZ domain of Dvl Here we report a possible role of CXXC4 in development and progression of RCC. Present data suggest that the decrease of CXXC4 might play an important role for tumor progression in RCC. Its loss in RCC may result in constitutively activate Writ signaling, and induce the expression of genes that function downstream of beta-catenin. Less
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