Ffect the proper estimation of the parameters. In the modified version of the algorithm, these limits are updated at each iteration to account for their credible values based on the current estimation of sample purity. All the modifications brought to the version 1.8.0 of genoCN (http://www.bioconductor.org/packages/2.10/bioc/ html/genoCN.html) are reported in supporting file. Only segments with at least 10 SNPs were retained. For each segment, the association of its loss (LOH) or gain with each phenotypic 1676428 variable was estimated using Fisher’s exact test for the factors or by the t-test for the quantitative variables. The false discovery rate was controlled using the Benjamini and Hochberg control of p-values [22]. Age and Karnofsky performance status (KPS) were compared using a two-sample t-test. Sex distribution among groups was compared using Chi-squared test with Yates’ correction. Progression free survival and overall survival curves were drawn using the Kaplan-Meier method and compared using a log-rank test. A pvalue,0.05 was considered as significant.All tumors were validated as AOD after a central pathological review.Genomic pattern and IDH mutational statusIn the entire cohort, 68/83 (82 ) of the tumors contained the 1p/19q-co-deletion with the chromosome 1 and 19 centromeric breakpoints used as a surrogate marker of t(1;19)(q10;p10) (Figure 1, Panel A), while 15/83 (18 ) of the order Tubastatin-A samples exhibited other genomic patterns (Figure 1, Panel B). Interestingly, in the latter group, three tumors harbored a whole-chromosome-arm 1p loss without the concurrent whole-chromosome-arm 19q loss, a chromosome 1p centromeric breakpoint or a chromosome 19q centromeric breakpoint. In the same group, an additional three tumors exhibited a whole-chromosome-arm 19q loss without the combined whole-chromosome-arm 1p loss. In the 1p/19q-co-deleted tumors, the most frequent gain was an 11q gain in 19.1 of the cases. The most frequent losses were the deletion of whole chromosome arm 9p, 4p, 4q, 9q and 15q in 32.4 , 17.6 , 16.2 , 14.7 , and 10.3 of the cases, respectively (Figure 2, Panel A, Top part). MedChemExpress Biotin NHS Sixty-one samples were assessable for IDH1, and 53 of them (86.8 ) were IDH1 mutated. The IDH2 mutation was found in 4/8 of the IDH1-intact tumors. Overall, 57/61 (93.4 ) of the tumors were IDH1 or IDH2 mutated. In the non-1p/19q-co-deleted group, the most frequent chromosome arm imbalances were a 9p loss, a 7q gain, a 1p loss, a 10p loss or a 10q loss in 40.0 , 26.7 , 20.0 , 20.0 and 20.0 of the samples, respectively (Figure 2, Panel A, Bottom part). All of the samples were assessable for IDH1, and 5/15 (33.3 ) were IDH1 mutated. The IDH2 mutation was found in 1/ 10 of the IDH1-intact tumors. Overall, 6/15 (40.0 ) of the tumors were IDH1 or IDH2 mutated. The IDH1 or IDH2 mutations were more frequently observed in the 1p/19q-co-deleted tumors when compared to the non-1p/19q-co-deleted tumors (p,0.0001) and were mutually exclusive.Candidate genomic abnormalities: homozygous deletion and gene amplificationIn the 1p/19q-co-deleted samples, a limited number 
of recurring homozygous deletions were detected (Figure 2-Panel B-Top part and Table 1). Eight loci were found to be homozygously deleted in at least two patients. Interestingly, in one case, a homozygous deletion of FUBP1 was observed. Additionally, CDKN2A was homozygously deleted in one case in the SNP-array analysis and was validated by qPCR. Similarly, recurring gene amplification was rare in the non-.Ffect the proper estimation of the parameters. In the modified version of the algorithm, these limits are updated at each iteration to account for their credible values based on the current estimation of sample purity. All the modifications brought to the version 1.8.0 of genoCN (http://www.bioconductor.org/packages/2.10/bioc/ html/genoCN.html) are reported in supporting file. Only segments with at least 10 SNPs were retained. For each segment, the association of its loss (LOH) or gain with each phenotypic 1676428 variable was estimated using Fisher’s exact test for the factors or by the t-test for the quantitative variables. The false discovery rate was controlled using the Benjamini and Hochberg control of p-values [22]. Age and Karnofsky performance status (KPS) were compared using a two-sample t-test. Sex distribution among groups was compared using Chi-squared test with Yates’ correction. Progression free survival and overall survival curves were drawn using the Kaplan-Meier method and compared using a log-rank test. A pvalue,0.05 was considered as significant.All tumors were validated as AOD after a central pathological review.Genomic pattern and IDH mutational statusIn the entire cohort, 68/83 (82 ) of the tumors contained the 1p/19q-co-deletion with the chromosome 1 and 19 centromeric breakpoints used as a surrogate marker of t(1;19)(q10;p10) (Figure 1, Panel A), while 15/83 (18 ) of the samples exhibited other genomic patterns (Figure 1, Panel B). Interestingly, in the latter group, three tumors harbored a whole-chromosome-arm 1p loss without the concurrent whole-chromosome-arm 19q loss, a chromosome 1p centromeric breakpoint or a chromosome 19q centromeric breakpoint. In the same group, an additional three tumors exhibited a whole-chromosome-arm 19q loss without the combined whole-chromosome-arm 1p loss. 
In the 1p/19q-co-deleted tumors, the most frequent gain was an 11q gain in 19.1 of the cases. The most frequent losses were the deletion of whole chromosome arm 9p, 4p, 4q, 9q and 15q in 32.4 , 17.6 , 16.2 , 14.7 , and 10.3 of the cases, respectively (Figure 2, Panel A, Top part). Sixty-one samples were assessable for IDH1, and 53 of them (86.8 ) were IDH1 mutated. The IDH2 mutation was found in 4/8 of the IDH1-intact tumors. Overall, 57/61 (93.4 ) of the tumors were IDH1 or IDH2 mutated. In the non-1p/19q-co-deleted group, the most frequent chromosome arm imbalances were a 9p loss, a 7q gain, a 1p loss, a 10p loss or a 10q loss in 40.0 , 26.7 , 20.0 , 20.0 and 20.0 of the samples, respectively (Figure 2, Panel A, Bottom part). All of the samples were assessable for IDH1, and 5/15 (33.3 ) were IDH1 mutated. The IDH2 mutation was found in 1/ 10 of the IDH1-intact tumors. Overall, 6/15 (40.0 ) of the tumors were IDH1 or IDH2 mutated. The IDH1 or IDH2 mutations were more frequently observed in the 1p/19q-co-deleted tumors when compared to the non-1p/19q-co-deleted tumors (p,0.0001) and were mutually exclusive.Candidate genomic abnormalities: homozygous deletion and gene amplificationIn the 1p/19q-co-deleted samples, a limited number of recurring homozygous deletions were detected (Figure 2-Panel B-Top part and Table 1). Eight loci were found to be homozygously deleted in at least two patients. Interestingly, in one case, a homozygous deletion of FUBP1 was observed. Additionally, CDKN2A was homozygously deleted in one case in the SNP-array analysis and was validated by qPCR. Similarly, recurring gene amplification was rare in the non-.