No significant associations were observed between specific copy number changes and different mutation subgroups. Tumors with PDGFRA mutations showed the same overall pattern of alterations seen in those with KIT mutations, even if genomic complexity was much lower in the former. Therapeutic selleckbio correlations and survival data Follow up data was available in 74 cases. During this period, 26 patients showed disease progression and were subsequently treated with imatinib. According with the most recent clinical records, six of these patients died from their cancer. Most of the samples from the progres sion group showed KIT mutations, namely in exon 11 and exon 9, with only two patients showing no mutations in either gene.

The 48 patients that received no adjuvant therapy are currently alive without evidence of disease, with the exception of three non disease related deaths. Within this group, 41 tumors harbored muta tions, namely Inhibitors,Modulators,Libraries in KIT exon 11, KIT exon 9, PDGFRA exon 12, PDGFRA exon 14, and PDGFRA exon 18. Disease specific survival curves were uninformative due to the reduced number of death from disease events, and five year disease free survival curves were thus com puted. Stratification according Inhibitors,Modulators,Libraries to tumor location showed that lesions in the stomach progressed Inhibitors,Modulators,Libraries much less frequently than those in other locations. Regarding risk groups, most progression events were seen in lesions cat egorized as high risk. When patients were categorized based on genetic variables, a more aggressive outcome was seen in patients with KIT mutations Inhibitors,Modulators,Libraries compared to those with PDGFRA mutations.

Based on previous literature reports, patients were additionally categorized according to specific Inhibitors,Modulators,Libraries mutations associated with worse prognosis. Patients with KIT exon 9 or KIT exon 11 deletions delins showed a tendentiously worse progression free survival than those showing mutations in PDGFRA most or other mutations in KIT. Within the subgroup of patients with KIT exon 11 muta tions, the number of progression events in tumors with deletions delins was significantly higher than those with other mutations. In multivariate analysis including risk groups and genotype, a high risk at diagnosis was the strongest predictor of relapse In the subgroup of patients with CGH data and com plete follow up information, genomic complexity was very strongly associated with a worse outcome. The presence of genomic gains or deletions at 1p or 22q were also sig nificantly associated with a shorter progression free period. Multivariate survival analysis in this subset showed that the best predictor of progression was genomic complexity. Discussion Recent years have seen important breakthroughs that resulted in better diagnostic, prognostic and therapeutic tools for patients with GIST.