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Common Human Cancers (common + human_cancers)

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Medical Sciences100%

Selected Abstracts

Mutational analysis of hypoxia-related genes HIF1, and CUL2 in common human cancers

APMIS, Issue 12 2009
SANG WOOK PARK
Hypoxia is a general feature of solid cancer tissues. Hypoxia upregulates hypoxia-inducible factor 1, (HIF1,) that transactivates downstream genes and contributes to cancer pathogenesis. HIF1, is upregulated not only by hypoxia but also by genetic alterations in HIF1,-related genes, including VHL. Cullin 2 (CUL2) interacts with the trimeric VHL-elongin B-elongin C complex and plays an essential role in the ubiquitinated degradation of HIF1,. The aim of this study was to explore whether HIF1, and CUL2 genes are somatically mutated, and contribute to HIF1, activation in common human cancers. For this, we have analyzed the coding region of oxygen-dependent degradation domain of HIF1, in 47 colon, 47 gastric, 47 breast, 47 lung, and 47 hepatocellular carcinomas, and 47 acute leukemias by a single-strand conformation polymorphism assay. In addition, we analyzed mononucleotide repeat sequences (A8) in CUL2 in 55 colorectal and 45 gastric carcinomas with microsatellite instability (MSI). We found one HIF1, mutation (p.Ala593Pro) in the hepatocellular carcinomas (1/47; 2.1%), but none in other cancers. We found two CUL2 frameshift mutations in colon cancers (p.Asn292MetfsX20), which were exclusively detected in high MSI cancers (4.9%; 2/41). Our data indicate that somatic mutation of HIF1, is rare in common cancers, and somatic mutation of CUL2 occurs in a fraction of colorectal cancers (colorectal cancers with high MSI). The data suggest that neither HIF1, nor CUL2 mutation may play a central role in HIF1, activation in gastric, colorectal, breast, lung and hepatocellular carcinomas, and acute leukemias. [source]

Somatic mutation of pro-cell death Bif-1 gene is rare in common human cancers,

APMIS, Issue 10 2008
Min Sung Kim
No abstract is available for this article. [source]

Search for new biomarkers of gastric cancer through serial analysis of gene expression and its clinical implications

CANCER SCIENCE, Issue 5 2004
Wataru Yasui
Gastric cancer is one of the most common human cancers and is the second most frequent cause of cancer-related death in the world. Serial analysis of gene expression (SAGE) is a powerful technique to allow genome-wide analysis of gene expression in a quantitative manner without prior knowledge of the gene sequences. SAGE on 5 samples of gastric cancer with different histology and clinical stages have created large SAGE libraries of gastric cancer that enable us to identify new cancer biomarkers. Commonly up-regulated genes in gastric cancer in comparison with normal gastric epithelia included CEACAM6, APOC1 and YF13H12. By comparing gene expression profiles of gastric cancers at early and advanced stages, several genes differentially expressed by tumor stage were also identified, including FUS, CDH17, COL1A1 and COL1A2, which should be novel genetic markers for high-grade malignancy. Regenerating gene type IV (REGIV) is one of the most up-regulated genes in a SAGE library of a scirrhous-type gastric cancer. In vitro studies using RegIV-transfected cells revealed that RegIV is secreted by cancer cells and inhibits apoptosis, suggesting that RegIV may serve as a novel biomarker and therapeutic target for gastric cancer. Production of RNA aptamers could be a useful approach to establish a detection system in blood. A custom-made array, named Ex-STO-MACHIP, consisting of 395 genes, including highly differentially expressed genes identified by our SAGE and other known genes related to carcinogenesis and chemosensitivity, is useful to study the molecular pathogenesis of gastric cancer and to obtain information about biological behavior and sensitivity to therapy in the clinical setting. Combined analyses of gene expression profile, genetic polymorphism and genetic instability will aid not only cancer detection, but also characterization of individual cancers and patients, leading to personalized medicine and cancer prevention. [source]