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BioMed Research International
Volume 2014, Article ID 834087, 9 pages
http://dx.doi.org/10.1155/2014/834087
Research Article

Gene Expression Profiling of Biological Pathway Alterations by Radiation Exposure

1Institute of Medical Sciences, Tzu Chi University, Hualien 970, Taiwan
2Laboratory for Cytogenetics, Center for Genetic Counseling, Buddhist Tzu Chi General Hospital, Hualien 970, Taiwan
3Innovation Center for Big Data and Digital Convergence, Yuan Ze University, Chungli 32003, Taiwan
4Department of Computer Science and Engineering, Yuan Ze University, Chungli 32003, Taiwan
5Bioinformatics Core Laboratory, Institute of Molecular Biology, Academia Sinica, Taipei 11529, Taiwan
6Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan
7Department of Computer Science & Information Engineering, Tamkang University, New Taipei City 25137, Taiwan

Received 9 April 2014; Accepted 21 July 2014; Published 8 September 2014

Academic Editor: Tzong-Yi Lee

Copyright © 2014 Kuei-Fang Lee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Gene ontology enrichment analysis results are given in Table 2 and supplementary table 1. It appears that, starting at a dosage of 0.5 Gy 60Co radiation, cells may have already been affected in terms of nucleotide metabolism and signaling pathways responsive to external apoptotic signals.

Beginning at 1 Gy, increasing radiation exposure induces changes in a significant number of genes involved in the immune system processes and programmed cell death pathways. These genes are mostly mapped to chromosomes 2, 11, 16, 17, and 19 (supplementary Table 2). It is likely that these chromosomes are particular sensitive to radiation-induced damages. Most of the genes were affected by 60Co radiation, regardless of the dosage, appeared to be enriched on chromosomes 11, 17, 19, 16, and 2.

  1. Supplementary Material