Newnham et al. BMC Cancer 2011, 11:93 http://www.biomedcentral.com/1471-2407/11/93 Table 1 Demographic and pathologic details for 69 NSCLC patients Variable (number of patients assessed) Gender (69) Male Female Age at definitive treatment (years) (69) Median (range) Histology (69) AC SCC LCC Smoking status (69) Never Current/Ex Stage (69) IA IB IIA IIB IIIA IIIB IV Unknown Primary tumour size (mm) (69) 0 - 20 21 - 30 31 - 50 51 - 70 >70 Unknown T < 40 mm, N1 &/or M1 (69) T > 40 mm, N0M0 (69) T > 70 mm, N0M0 (69) K-Ras mutation (46)** EGFR mutation (46)** P53 mutation (69) Definite Possible Recurrence (68)+ Death from NSCLC (68)+ Time from surgery to death (months) (23) Median (range) Number Percentage (95% CI) 70 (29 - 85) 42 27 30 23 16 16 53 16 26 3 7 8 3 5* 1# 23 10 22 5 7 2^ 13 11 4 10 5 26 +/- 17 26 17 28 23 19 (7 - 73) 61 (49-72) 39 (28-51) 43 (32-55) 33 (23-45) 23 (14-34) 23 (14-34) 77 (66-86) 23 (14-34) 38 (27-49) 4 (1-11) 10 (5-19) 12 (6-20) 4 (1-11) 12 (6-20) 1 (0-7) 33 (23-45) 15 (8-24) 32 (22-43) 7 (3 - 16) 10 (5 - 20) 3 (0-9) 19 (11-29) 16 (9-26) 6 (2-13) 21 (11-34) 11 (4-22) 38 (27-49) 25 (16-36) 41 (30-53) 34 (23-45) AC = adenocarcinoma; LCC = large cell carcinoma; SCC = squamous cell carcinoma. *3 patients had solitary cerebral metastases resected at diagnosis, 1 patient had 2 separate lung lesions (unclear if synchronous primary lesions or pulmonary metastasis), 1 patient had disseminated disease. # Stage unable to be determined in 1 patient after wedge resection without nodal dissection. ^ Tumour size unable to be assessed in 1 patient who underwent incomplete tumour resection after combined chemoradiation, and one who had incomplete resection of an obstructing stage IIIA tumour followed by definitive radiotherapy. ** Only AC and LCC samples were tested for mutations of K-Ras and EGFR. +One patient with disseminated disease at diagnosis excluded from recurrence and survival analysis. Page 3 of 11 groups (Table 2). Specifically, neither prognosis, degree of histologic differentiation, K-Ras or TP53 status was associated with evidence of greater aneuploidy. Histotype comparisons Charts documenting the averaged standardised copy numbers at each BAC location were generated to enable visual comparisons of genomic profiles between AC (23) and SCC (17) (figure 1). Regions of shared change (amplification of 5p15.33-p13.13, loss of 3p26.3-p13) and several regions of difference (SCC: gains at 3q12.1- q28 and 12p13.33-p12.1, losses of chromosome 4 (4pter-4qter); AC: gains of 6p25.1-p21.31, losses of 6q13-27, and a greater magnitude of change in several regions of shared loss (9p, 13q, 17p, 18q, 19p, 19q and 22q) or gain (7p, 7q, 8q)) were identified. These findings are consistent with previous studies [9-16]. Associations with mutation status in TP53, KRAS and EGFR pathways Clinical data demonstrated a trend to greater rate of TP53 mutation in SCC than AC (TP53 mutation in 9/12 (75%) SCC and 9/18 (50%) AC, p = 0.083). Amplification of 3q Table 2 Comparisons of average number of breakpoints for NSCLC subgroups Subgroup Ave. No. Ratio of comparison (p value) Breakpoints Histotype AC 45.7 SCC 43.1 LCC 39.5 Gender Male (M) 44.9 Female (F) 41.2 Smoking Smokers (S) 44.5 Never smokers (N) 41.1 Recurrence Recurrent (R) 44.7 Non-recurrent (NR) 43.3 Survival Non-survivors (NS) 46.5 Survivors (S) 42.8 Metastasis Metastatic (M) 40.0 Non-metastatic (NM) 46.8 EGFR status Mutant (m) 38.6 Wild-type (wt) 44.6 K-Ras status Mutant (m) 42.3 Wild-type (wt) 43.9 p53 status Mutant (m) 46.8 Wild-type (wt) 40.8 ACC:SCC = 1.1 (1.0) M:F = 1.1 (1.0) S:N = 1.1 (1.0) R:NR = 1.0 (1.0) NS:S = 1.1 (0.9) M:NM = 0.9 (0.9) m:wt = 0.9 (0.9) m:wt = 1.0 (1.0) m:wt = 1.1 (0.9)