RT Journal Article SR Electronic T1 Topological Network Analysis of Differentially Expressed Genes in Cancer Cells with Acquired Gefitinib Resistance JF Cancer Genomics - Proteomics JO Cancer Genomics Proteomics FD International Institute of Anticancer Research SP 153 OP 166 VO 12 IS 3 A1 YOUNG SEOK LEE A1 SUN GOO HWANG A1 JIN KI KIM A1 TAE HWAN PARK A1 YOUNG RAE KIM A1 HO SUNG MYEONG A1 KANG KWON A1 CHEOL SEONG JANG A1 YUN HEE NOH A1 SUNG YOUNG KIM YR 2015 UL http://cgp.iiarjournals.org/content/12/3/153.abstract AB Background/Aim: Despite great effort to elucidate the process of acquired gefitinib resistance (AGR) in order to develop successful chemotherapy, the precise mechanisms and genetic factors of such resistance have yet to be elucidated. Materials and Methods: We performed a cross-platform meta-analysis of three publically available microarray datasets related to cancer with AGR. For the top 100 differentially expressed genes (DEGs), we clustered functional modules of hub genes in a gene co-expression network and a protein-protein interaction network. We conducted a weighted correlation network analysis of total DEGs in microarray dataset GSE 34228. The identified DEGs were functionally enriched by Gene Ontology (GO) function and KEGG pathway. Results: We identified a total of 1,033 DEGs (510 up-regulated, 523 down-regulated, and 109 novel genes). Among the top 100 up- or down-regulated DEGs, many genes were found in different types of cancers and tumors. Through integrative analysis of two systemic networks, we selected six hub DEGs (Pre-B-cell leukemia homeobox1, Transient receptor potential cation channel subfamily C member 1, AXL receptor tyrosine kinase, S100 calcium binding protein A9, S100 calcium binding protein A8, and Nucleotide-binding oligomerization domain containing 2) associated with calcium homeostasis and signaling, apoptosis, transcriptional regulation, or chemoresistance. We confirmed a correlation of expression of these genes in the microarray dataset. Conclusion: Our study may lead to comprehensive insights into the complex mechanism of AGR and to novel gene expression signatures useful for further clinical studies.