Newnham et al. BMC Cancer 2011, 11:93 http://www.biomedcentral.com/1471-2407/11/93 Table 5 Details of genes with differential copy number and expression between K-Ras mutant and wild-type tumours Symbol Gene name Cytoband Difference in P value expression (log2 mutant - wild type) RGS2 NCAM1 Regulator of G-protein signaling 2, 24kDa Neural cell adhesion molecule 1 CD55 CD55 molecule, decay accelerating factor for complement (Cromer blood group) PTGS2/ Prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and COX-2 cyclooxygenase)/Cyclooxygenase-2 ECM1 Extracellular matrix protein 1 EXTL2 Exostoses (multiple)-like 2 HIST2H2BE Histone cluster 2, H2be H2AA Histone 2 CHEK1 CHK1 checkpoint homolog (S. pombe) GPX7 Glutathione peroxidase 7 RWDD2A RWD domain containing 2A HSF2 Heat shock transcription factor 2 BLR1 Burkitt lymphomas receptor 1, GTP binding protein (chemokine (CXC motif) receptor 5) MIZF MBD2-interacting zinc finger KPNA5 Karyopherin alpha 5 (importin alpha 6) LMO4 LIM domain only 4 MUTYH MutY homolog (E. coli) REV3L REV3-like, catalytic subunit of DNA polymerase zeta (yeast) EPHB2 Ephrin B2 DGKZ Diacylglycerol kinase, zeta 104kDa TSPYL4 TSPY-like 4 DBT Dihydrolipoamide branched chain transacylase E2 FOXO3 Forkhead box O3 PPP2R1B Protein phosphatase 2, regulatory subunit A, beta isoform PTPRK Protein tyrosine phosphatase, receptor type, kappa 1q31 11 ( multiple clusters) 1q32 1q25.2-q25.3 1q21 1p21 1q21-q23 1q21 11q24-q24 1p32 6q14.2 6q22.31 11q23.3 11q23.3 6q22.2 1p22.3 1p34.3-p32.1 6q21 1p36.1-p35 11p11.2 6q22.1 1p31 6q21 11q23.2 6q22.2-q22.3 1.99 -1.63 1.49 1.32 1.21 -1.08 1.07 0.95 -0.94 -0.88 -0.80 -0.78 -0.69 -0.69 -0.66 -0.66 -0.65 -0.65 -0.64 -0.64 -0.63 -0.58 -0.53 -0.51 -0.08 ratio in NSCLC, as has been described in head and neck SCC [46]. Specific genes linked to recurrence or survival include SMARCA2 (implicated in the regulation of gene expression cell cycle control and oncogenesis), MINK (linked to the JNK MAP kinase pathway) [47] and RECK, which has putative roles in the suppression of tumour growth, invasion, angiogenesis and metastasis [48]. KRAS mutation has been associated with reduced expression of RECK in NSCLC [49], consistent with the clinical observation of poor outcome in patients with KRAS mutation bearing NSCLC. Activation of the Ras pathway may reduce RECK expression and thereby increase tumour recurrence. Importantly, our prognostic gene signature was validated in an independent test set, suggesting that these findings may eventually yield prog- nostic markers in resected early-stage NSCLC to better select patients for adjuvant treatments. Conclusions Several molecular alterations have been identified in association with NSCLC histotype, KRAS mutation, TP53 mutation, metastatic potential, disease recur- rence and survival. Although the size of the current study is small, our findings are in many cases consis- tent with those of previous studies, and have been validated in the case of the prognostic classifier in an independent test set. In addition, several novel mole- cular changes associated with clinically relevant end- points have been demonstrated. It is hoped that these results will contribute to identifying new predictive markers and targets for novel therapies to improve treatment selection and better outcomes for patients with this deadly disease. Additional material Additional file 1: Protocol for extraction of RNA Additional file 2: Protocols for extraction of DNA Additional file 3: Transcriptional profiling Additional file 4: Genomic profiling Additional file 5: 40 matched transcripts between GSE11117 and our differential gene list for recurrence Page 9 of 11 5.9 E-3 1.5 E-3 6.9 E-4 3.1 E-3 5.9 E-3 4.2 E-3 2.7 E-3 1.2 E-3 6.1 E-3 5.6 E-3 8.7 E-4 1.6 E-3 7.4 E-3 5.9 E-3 8.7 E-3 3.2 E-3 4.9 E-4 8.8 E-3 6.7 E-3 9.2 E-3 1.6 E-3 5.8 E-3 5.7 E-3 2.7 E-3 4.3 E-4