Using Affymetrix U133A oligonucleotide microarrays, screening was done for genes that were differentially expressed in gastric cancer (T) and normal gastric mucosa (C), and their chromosome location was characterized by bioinformatics. A total of 270 genes were found to have a difference in expression levels of more than eight times. Of them 157 were up-regulated (Signal Log Ratio [SLR] > or = 3), and 113 were down-regulated (SLR< or = -3). Except for, four genes with unknown localization, a vast majority of the genes were sporadically distributed over every chromosome. However, chromosome 1 contained the most differentially expressed genes (26 genes, or 9.8%), followed by chromosomes 11 and 19 (both 24 genes, or 9.1%). These genes were also more likely to be on the short-arm of the chromosome (q), which had 173 (65%). When these genes were classified according to their functions, it was found that most (67 genes, 24.8%) belonged to the enzymes and their regulators groups. The next group was the signal transduction genes group (43 genes, 15.9%). The rest of the top three groups were nucleic acid binding genes (17, 6.3%), transporter genes (15, 5.5%), and protein binding genes (12, 4.4%). These made up 56.9% of all the differentially expressed genes. There were also 50 genes of unknown function (18.5%). Therefore it was concluded that differentially expressed genes in gastric cancer seemed to be sporadically distributed across the genome, but most were found on chromosomes 1, 11 and 19. The five groups associated genes abnormality were important genes for further study on gastric cancer.
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http://dx.doi.org/10.1016/S0379-4172(06)60066-8 | DOI Listing |
Curr Opin Genet Dev
January 2025
Department of Biochemistry and Molecular Biophysics, Program for Mathematical Genomics, Columbia University Irving Medical Center, New York, NY 10032, USA. Electronic address:
Enhancers in metazoan genomes are known to activate their target genes across both short and long genomic distances. Recent advances in chromosome conformation capture assays and single-cell imaging have shed light on the underlying chromatin contacts and dynamics. Yet the relationship between 3D physical enhancer-promoter (E-P) interactions and transcriptional activation remains unresolved.
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Laboratory of Immunogenetics and Tissue Immunology, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
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Department of Hepatobiliary Pancreatic Surgery, Changhai Hospital, Naval Medical University (Second Military Medical University), 168 Changhai Road, Shanghai 200433, China. Electronic address:
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