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Article: Novel approach for coexpression analysis of E2F1-3 and MYC target genes in chronic myelogenous leukemia

TitleNovel approach for coexpression analysis of E2F1-3 and MYC target genes in chronic myelogenous leukemia
Authors
Issue Date2014
Citation
BioMed Research International, 2014, v. 2014 How to Cite?
AbstractCopyright © 2014 Fengfeng Wang et al. Background. 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 prolifera tion 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.
Persistent Identifierhttp://hdl.handle.net/10722/244175
ISSN
2021 Impact Factor: 3.246
2020 SCImago Journal Rankings: 0.772
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Fengfeng-
dc.contributor.authorChan, Lawrence W.C.-
dc.contributor.authorCho, William C.S.-
dc.contributor.authorTang, Petrus-
dc.contributor.authorYu, Jun-
dc.contributor.authorShyu, Chi Ren-
dc.contributor.authorTsui, Nancy B.Y.-
dc.contributor.authorWong, S. C.Cesar-
dc.contributor.authorSiu, Parco M.-
dc.contributor.authorYip, S. P.-
dc.contributor.authorYung, Benjamin Y.M.-
dc.date.accessioned2017-08-31T08:56:15Z-
dc.date.available2017-08-31T08:56:15Z-
dc.date.issued2014-
dc.identifier.citationBioMed Research International, 2014, v. 2014-
dc.identifier.issn2314-6133-
dc.identifier.urihttp://hdl.handle.net/10722/244175-
dc.description.abstractCopyright © 2014 Fengfeng Wang et al. Background. 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 prolifera tion 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.-
dc.languageeng-
dc.relation.ispartofBioMed Research International-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleNovel approach for coexpression analysis of E2F1-3 and MYC target genes in chronic myelogenous leukemia-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1155/2014/439840-
dc.identifier.pmid25180182-
dc.identifier.scopuseid_2-s2.0-84907387237-
dc.identifier.volume2014-
dc.identifier.spagenull-
dc.identifier.epagenull-
dc.identifier.eissn2314-6141-
dc.identifier.isiWOS:000340761200001-
dc.identifier.issnl2314-6133-

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