Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/28431
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dc.contributorDepartment of Health Technology and Informatics-
dc.creatorWang, F-
dc.creatorChan, LWC-
dc.creatorCho, WCS-
dc.creatorTang, P-
dc.creatorYu, J-
dc.creatorShyu, CR-
dc.creatorTsui, NBY-
dc.creatorWong, SCC-
dc.creatorSiu, PM-
dc.creatorYip, SP-
dc.creatorYung, BYM-
dc.date.accessioned2014-12-30T08:38:27Z-
dc.date.available2014-12-30T08:38:27Z-
dc.identifier.issn2314-6133en_US
dc.identifier.urihttp://hdl.handle.net/10397/28431-
dc.language.isoenen_US
dc.publisherHindawi Publishing Corporationen_US
dc.rightsCopyright © 2014 Fengfeng Wang 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.en_US
dc.rightsThe following article: Fengfeng Wang, Lawrence W. C. Chan, William C. S. Cho, et al., “Novel Approach for Coexpression Analysis of E2F1–3 and MYC Target Genes in Chronic Myelogenous Leukemia,” BioMed Research International, 439840, 2014, is available at https//doi.org/10.1155/2014/439840en_US
dc.titleNovel approach for coexpression analysis of E2F1-3 and MYC target genes in chronic myelogenous leukemiaen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.volume2014en_US
dc.identifier.doi10.1155/2014/439840en_US
dcterms.abstractBackground. Chronic myelogenous leukemia (CML) is characterized by tremendous amount of immature myeloid cells in the blood circulation. E2F1-3 and MYC are important transcription factors that form positive feedback loops by reciprocal regulation in their own transcription processes. Since genes regulated by E2F1-3 or MYC are related to cell proliferation and apoptosis, we wonder if there exists difference in the coexpression patterns of genes regulated concurrently by E2F1-3 and MYC between the normal and the CML states. Results. We proposed a method to explore the difference in the coexpression patterns of those candidate target genes between the normal and the CML groups. A disease-specific cutoff point for coexpression levels that classified the coexpressed gene pairs into strong and weak coexpression classes was identified. Our developed method effectively identified the coexpression pattern differences from the overall structure. Moreover, we found that genes related to the cell adhesion and angiogenesis properties were more likely to be coexpressed in the normal group when compared to the CML group. Conclusion. Our findings may be helpful in exploring the underlying mechanisms of CML and provide useful information in cancer treatment.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationBioMed research international, 2014, v. 2014, 439840-
dcterms.isPartOfBioMed research international-
dcterms.issued2014-
dc.identifier.scopus2-s2.0-84907387237-
dc.identifier.pmid25180182-
dc.identifier.eissn2314-6141en_US
dc.identifier.rosgroupid2014001190-
dc.description.ros2014-2015 > Academic research: refereed > Publication in refereed journalen_US
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_IR/PIRAen_US
dc.description.pubStatusPublisheden_US
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