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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: Mol Cancer Res. 2011 Jul 20;9(9):1209–1221. doi: 10.1158/1541-7786.MCR-10-0424

Table 3.

SAM analysis was conducted on microarray data

Gene ID Symbol Gene description Fold change q (%)
228729 at CCNB1 Cyclin B1 9.91 3.85
228069 at FAM54A Family with sequence similarity 54, member A 9.30 3.85
203362 s at MAD2L1 MAD2 mitotic arrest deficient-like 1 (yeast) 5.44 0.00
209408 at KIF2C Kinesin family member 2C 5.03 3.85
218009 s at PRC1 Protein regulator of cytokinesis 1 4.99 0.00
218875 s at FBXO5 F-box protein 5 4.95 3.85
219148 at PBK PDZ-binding kinase 4.85 0.00
219918 s at ASPM asp (abnormal spindle) homolog, microcephaly associated (Drosophila) 4.44 3.85
203213 at CDK1 Cyclin-dependent kinase 1 4.13 3.85
214710 s at CCNB1 Cyclin B1 3.88 0.00
208808 s at HMGB2 High-mobility group box 2 3.81 0.00
208079 s at AURKA Aurora kinase A 3.55 0.00

NOTE: SAM identifies 12 genes that are statistically upregulated in both tumor and TAHN-1 cells with the highest hTERT promoter activity. Telomerase high data sets from both tumor and TAHN-1 were compared with telomerase low data sets from tumor and TAHN-1 in a paired analysis. The arrays were median centered, a minimum fold change of 3 was set, and a delta value of 6.23 was set to establish a false discovery rate of 3.85% (q value). Using these values, 12 genes were identified that were statistically significantly overexpressed in the cells with high telomerase promoter activity in both tumor and TAHN-1 cells. No genes were found to be significantly underexpressed in these cells.