BMC Cancer 2009, 9:11 http://www.biomedcentral.com/1471-2407/9/11 Table 3: Differentially expressed genes associated with cervical lymph node and pathologic stage status (Continued) Number present t-score Accession: Definition/Description or EST name 3.782 X62055: H. sapiens PTP1C mRNA for protein-tyrosine phosphate 3.514 AB023135: Homo sapiens mRNA for activation-inducible lymphocyte p-value Number present t-score Accession: Definition/Description or EST name 3.698 3.761 3.501 3.709 3.824 3.023 3.952 3.565 3.271 2.955 3.512 2.843 3.215 3.319 2.979 3.542 immunomediatory molecule AILIM A1828166: wk32h09 U85773: Human phosphomannomutase (PMM2) mRNA S67970: ZNF75 = KRAB zinc finger [human, lung fibroblast, mRNA M81750: H. sapiens myeloid cell nuclear differentiation antigen mRNA AA121509:zk88c10.s1 Z11697: Homo sapiens mRNA for HB15 D67031: Homo sapiens ADDL mRNA for adducin-like protein J02923: Human 65-kilodalton phosphoprotein (p65) mRNA L10717: Homo sapiens T cell-specified tyrosine kinase mRNA AL031228:dJ1033B10. 10/Membrane protein with histidine rich charge clusters AB011102: Homo sapiens mRNA for KIAA0530 protein M80482: Human subtilisin-like protein (PACE4) mRNA AF072099: Homo sapiens immunoglobulin-like transcript 3protein variant 1 gene J03037: Human carbonic anhydrase II mRNA D21261: Human mRNA for KIAA0120 gene L06797: HUMGPCR Human (clone L5) orphan G protein-coupled receptor mRNA 0.043% p-value 0.062% 0.062% 0.073% 0.085% 0.104% 0.104% 0.104% 0.104% 0.123% 0.123% 0.145% 0.145% 0.170% 0.199% 0.199% 0.199% 0.199% B 5 11 31 31 6 16 31 21 31 29 21 26 24 25 19 28 31 31 The 20 patients were grouped into early-stage (Stage I and II disease) category and late-stage (Stage III and IV disease) category. A; Similarly, patients without cervical nodal metastasis (N0) were compared to those with nodal disease (N1–N3). B; Genes whose expression in tumor was different in normal mucosa and which were most different between the clinical stage and nodal disease subgroups were identified by statistical regression analysis (t test). The genes identified within the two subgroups are listed. Note that HSAL2 were identified in both subgroups. Only genes that were present in at least 5 samples were included. often lack predictive power. Two important limitations of the studies to date are the heterogeneity in subsites ana- lyzed and the small number of study samples. Our study as well as that of others addressed the former by focusing only on oral tongue SCC [36-38]. Carinci et al. analyzed gene expression in 9 specimens with dysplasia, 8 with oral tongue SCC with no metastasis, and 11 with metastatic oral tongue SCC. Several genes were identified as poten- tial markers of oral tongue progression and metastasis [36]. Shimada and colleagues identified 16 genes that were upregulated in 4 oral tongue SCC specimens. One gene, RabIA, a member of the Ras oncogene, was chosen and validated at the RNA and protein levels [37]. In a study by Zhou et al., 25 primary oral tongue SCC were Page 11 of 13 (page number not for citation purposes)