OBJECTIVES: To explore the underlying molecular mechanisms of childhood B-precursor acute lymphoblastic leukemia (ALL) by bioinformatics analysis and find potential targets for childhood ALL diagnosis and treatment. METHODS: Gene expression profile GSE28460 was downloaded from the Gene Expression Omnibus, including 49 diagnostic and relapse bone marrow samples with childhood B-precursor ALL. The differentially expressed genes (DEGs) were identified by paired t-test. Pathway enrichment analysis of DEGs and transcription factors (TFs) enrichment analysis were performed, followed by construction of co-expressed, DEGs, and susceptibility gene protein-protein interaction (PPI) network. Based on these three networks, relevant regulatory network modules and the important DEGs in the modules were identified. RESULTS: Total of 947 DEGs were identified. Up-regulated DEGs enriched 20 pathways including cell cycle, and down-regulated DEGs significantly enriched Jak-STAT signaling pathways. CDK1 and BRCA1 were found to have more hubs in both co-expressed network and PPI network. Besides, total of five modules in INTS10, MCM, BRCA1, GYPA, and VCAN1 families were identified and a pathway of INTS10-INTS6-POLR2A-MAGI2 was selected. CONCLUSION: Cell cycle and Jak-STAT signaling pathway were closely associated with relapse of childhood B-precursor ALL. The DEGs, such as PTTG1, PIK3CA, CDK1, and BRCA1 may be the potential targets for childhood ALL diagnosis and treatment.
OBJECTIVES: To explore the underlying molecular mechanisms of childhood B-precursor acute lymphoblastic leukemia (ALL) by bioinformatics analysis and find potential targets for childhood ALL diagnosis and treatment. METHODS: Gene expression profile GSE28460 was downloaded from the Gene Expression Omnibus, including 49 diagnostic and relapse bone marrow samples with childhood B-precursor ALL. The differentially expressed genes (DEGs) were identified by paired t-test. Pathway enrichment analysis of DEGs and transcription factors (TFs) enrichment analysis were performed, followed by construction of co-expressed, DEGs, and susceptibility gene protein-protein interaction (PPI) network. Based on these three networks, relevant regulatory network modules and the important DEGs in the modules were identified. RESULTS: Total of 947 DEGs were identified. Up-regulated DEGs enriched 20 pathways including cell cycle, and down-regulated DEGs significantly enriched Jak-STAT signaling pathways. CDK1 and BRCA1 were found to have more hubs in both co-expressed network and PPI network. Besides, total of five modules in INTS10, MCM, BRCA1, GYPA, and VCAN1 families were identified and a pathway of INTS10-INTS6-POLR2A-MAGI2 was selected. CONCLUSION: Cell cycle and Jak-STAT signaling pathway were closely associated with relapse of childhood B-precursor ALL. The DEGs, such as PTTG1, PIK3CA, CDK1, and BRCA1 may be the potential targets for childhood ALL diagnosis and treatment.
Authors: Stephin J Vervoort; Sarah A Welsh; Jennifer R Devlin; Elisa Barbieri; Deborah A Knight; Sarah Offley; Stefan Bjelosevic; Matteo Costacurta; Izabela Todorovski; Conor J Kearney; Jarrod J Sandow; Zheng Fan; Benjamin Blyth; Victoria McLeod; Joseph H A Vissers; Karolina Pavic; Ben P Martin; Gareth Gregory; Elena Demosthenous; Magnus Zethoven; Isabella Y Kong; Edwin D Hawkins; Simon J Hogg; Madison J Kelly; Andrea Newbold; Kaylene J Simpson; Otto Kauko; Kieran F Harvey; Michael Ohlmeyer; Jukka Westermarck; Nathanael Gray; Alessandro Gardini; Ricky W Johnstone Journal: Cell Date: 2021-05-17 Impact factor: 66.850