Fig. 2

TrkA amplification associates with primary MM thickness and metastatic outcome. a genomic qPCR detection of copy number levels of TrkA gene in primary MM samples (n = 64), reported as fold-change over a diploid control of pooled healthy DNA (mean ± SD of n = 2 independent experiments, each of three replicates). Two additional samples of benign nevi were used as further accuracy control for diploidy. Samples are arranged according to increasing tumor thickness. Genomic amplification is depicted in red. b comparison of TrkA copy number levels for 29 primary MM samples from the aCGH dataset showing significant correlation between aCGH and qPCR. Log2-transformed fold changes (sample/control) of qPCR results are plotted with the corresponding aCGH log2 ratio mean values (Pearson’s correlation: p < 0.01; Pearson’s correlation coefficient, r = 0.5). c box and whiskers graph of the association between TrkA amplification and tumor thickness in primary MM samples analyzed by genomic qPCR (n = 64; Mann-Whytney U test: *, p < 0.05). d Kaplan–Meier curves for metastasis free survival in patient cohorts with TrkA amplification (n = 32) or TrkA diploidy (n = 12), as detected by genomic qPCR of primary MM genome (*, p < 0.05 by log-rank test). e Kaplan–Meier curves of overall survival for patients with TrkA amplification (n = 32) or diploid TrkA (n = 12), as detected by qPCR on primary MM genome (n.s., not statistically significant by log-rank test). Dipl, diploid copy number; Amp, amplification