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Screening of differential expressed genes from gene chip and sequencing data and evaluate its prognostic values in males with digestive system neoplasms

  
@article{TCR32527,
	author = {Kai Fang and Caixia Hu and Xiufen Zhang and Zijian Guo and Lihua Li},
	title = {Screening of differential expressed genes from gene chip and sequencing data and evaluate its prognostic values in males with digestive system neoplasms},
	journal = {Translational Cancer Research},
	volume = {8},
	number = {6},
	year = {2019},
	keywords = {},
	abstract = {Background: Digestive system neoplasm is a common cancer in males worldwide. This study aimed to explore the commonalities in males with digestive system neoplasms (MDSN) and its clinical relevance. 
Methods: A total of 46 differential expressed genes (DEGs) in MDSN were identified shared in TCGA and GEO databases. 
Results: These DEGs significantly affected a variety of cell function and signaling pathways. Of which, a hub of 7 genes (CCNB1, MAD2L1, BUB1, CHEK1, MCM2, CCNA2 and CDC25B) were interacted with each other in protein level and significantly enriched in cell cycle pathway. Further methylation analysis, we found that BUB1, MAD2L1 and MCM2 were hypomethylation via m6A modification. Besides, BUB1, MAD2L1 and MCM2 were co-expressed in mRNA level and up-regulation of them led to worse prognostic in hepatocellular carcinoma, while caused a better prognostic in stomach adenocarcinoma (STAD), and had a race difference between white and Asian people in STAD. Medicine molecules, I-threonine (ID: PA451673) and enzymes (ID: PA164712734) might be efficient medicines in BUB1, MAD2L1 and MCM2 up-regulated MDSN patients. 
Conclusions: Taken together, hypomethylation via m6A modification might cause BUB1, MAD2L1 and MCM2 up-regulation in MDSN. Dysregulation of BUB1, MAD2L1 and MCM2 function as contrast prognostic in liver hepatocellular carcinoma and STAD. Our study provides more accurate therapeutic targets and prognostic biomarkers for specific cancer types.},
	issn = {2219-6803},	url = {https://tcr.amegroups.org/article/view/32527}
}