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

Fengfeng Wang, Wing Chi Chan, William C.S. Cho, Petrus Tang, Jun Yu, Chi Ren Shyu, Nancy B.Y. Tsui, Sze Chuen Cesar Wong, Parco M. Siu, Shea Ping Yip, Yat Ming Yung

Research output: Journal article publicationJournal articleAcademic researchpeer-review

5 Citations (Scopus)

Abstract

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 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.
Original languageEnglish
Article number439840
JournalBioMed Research International
Volume2014
DOIs
Publication statusPublished - 1 Jan 2014

ASJC Scopus subject areas

  • General Biochemistry,Genetics and Molecular Biology
  • General Immunology and Microbiology

Fingerprint

Dive into the research topics of 'Novel approach for coexpression analysis of E2F1-3 and MYC target genes in chronic myelogenous leukemia'. Together they form a unique fingerprint.

Cite this