Results: 3

1.
Figure 1

Figure 1. From: ATF5 polymorphisms influence ATF function and response to treatment in children with childhood acute lymphoblastic leukemia.

ATF5, ASNS, and ASS1 gene polymorphisms and derived haplotypes. Haploview LD displays, linear representation and derived haplotypes for the selected ATF5 (A), ASNS (B), and ASS1 (C) polymorphisms. The linear display refers to all initially selected SNPs, and haploview LD (with pairwise r2) refers to SNPs with MAF ≥ 5%. MAF in the control population is given below the position of each SNP. SNPs excluded from the analysis of ALL patients because of pairwise r2 ≥ 87% are indicated by asterisks, and those retained in the analysis are indicated by arrows. Haplotypes (with a frequency ≥ 3%) derived from tag SNPs are arbitrarily numbered. The frequency in controls is given next to each haplotype. Note that for ATF5, only the haplotypes in the promoter and 5′UTR are listed (the allele defining each haplotype is underlined) because of their correspondence with functional assay performed (see Figure 3).

Julie Rousseau, et al. Blood. 2011 November 24;118(22):5883-5890.
2.
Figure 2

Figure 2. From: ATF5 polymorphisms influence ATF function and response to treatment in children with childhood acute lymphoblastic leukemia.

EFS for patients with ALL according to ATF5, ASNS, and ASS1 genotypes. (A) EFS according to genotypes of ATF5 C1562T polymorphism. EFS curves are shown for patients who were carriers (T+; dark gray) or not (T; light gray) of the T1562 allele. EFS curves are presented for HSJ patients (test set) on the 91-01 protocol (HSJ/91-01, left panel), HSJ patients on 95-01 protocol (HSJ/95-01) randomized to E coli or Erwinia asparaginase (2 plots of the middle panel), and for all HSJ and DFCI patients (validation set) who were assigned to E coli asparaginase (2 plots on the right panel, HSJ/E coli and DFCI/E coli, respectively). The number of all patients in each curve (with the number of cases with an event in brackets) is indicated next to the curve. The EFS difference between patients with and without the T1562 allele is estimated by the log-rank test and the P value is indicated on each plot. Risk of an event for T allele carriers, expressed as a univariable HR with the 95% CI in brackets, is indicated below each plot. (B) EFS curves according to ASNS genotypes. EFS for all HSJ patients (left plot) and those assigned to E coli asparaginase (middle plot), with (+; dark gray line) and without (-; light gray line) ASNS haplotype *1. Haplotype *1 is defined in Figure 1B. EFS for HSJ patients (right plot) assigned to E coli asparaginase who are homozygous (22+; dark gray line) or not (22-; light gray line) for the 2R allele of the ASNS tandem repeat. The number of patients within each curve, the number of cases with an event, the P value, and the genotype-associated risk of an event is labeled as in panel A. (C) EFS curves according to genotypes of ASS1 G1343T and G34T polymorphisms. Left plot is EFS for HSJ patients assigned to E coli asparaginase who are carriers (T+; dark gray line) or not (T-; light gray line) of the ASS1 T1343 allele and the right plot is EFS for HSJ patients assigned to E coli asparaginase who are carriers (TT+, dark gray line) or not (TT-, light gray line) of the ASS1 TT34 genotype. The number of cases within the curve, the number of patients with an event, the P value, and the genotype-associated risk of an event is labeled as in panel A.

Julie Rousseau, et al. Blood. 2011 November 24;118(22):5883-5890.
3.
Figure 3

Figure 3. From: ATF5 polymorphisms influence ATF function and response to treatment in children with childhood acute lymphoblastic leukemia.

Genomic structure of ATF5 regulatory region and polymorphism-related function. (A) Genomic structure of 2 ATF5 regions used in the luciferase assay. Exonic and coding sequences are represented by open and gray boxes, respectively, and SNPs are represented by gray dots. Alternatively spliced 5′UTRα and 5′UTRβ, as determined by Watatani et al,32 are indicated by the dark gray and black boxes, respectively. Note that 2 SNPs in LD, C-514T and A321T SNPs, which defines haplotype *3, are present in the first and the second fragment, respectively; 2 other SNPs in LD (C-270A/C1562T), which define haplotype *5, are both present in fragment 2. The black and gray arrows indicate the transcription and translation start sites, respectively, estimated according to Wei et al23 and Watatani et al32 and reference sequence NM012068. (B) Relative promoter activity of ATF5 haplotype *1,*2,*3, and *4 derived from fragment 1 (top panel) and haplotypes*2,*3, and *5 derived from fragment 2 (bottom panel) in 3 cell lines (HeLa, Jeg3, and HepG2). The haplotype numbers correspond to the haplotypes of the proximal promoter and 5′UTR given in Figure 1A. The haplotypes *1, *2, *3, *4, and *5 are defined by A-1072, G-34, T-514 (or T321 in correlation), C-670, and T1562 (or A-270 in correlation), respectively. Haplotypes showing a significant increase in promoter activity (P ≤ .02, ANOVA posthoc) compared with low-expression haplotypes are indicated by asterisks. (C) Relative mRNA levels in HapMap lymphoblastoid cell lines for individuals who are carriers or not of indicated alleles of ATF5 polymorphisms, which are defining haplotypes *1 to *5, respectively. Mean values ± SE are given. The number of individuals represented by each bar and the P value obtained by the Mann-Whitney test are indicated on the plots.

Julie Rousseau, et al. Blood. 2011 November 24;118(22):5883-5890.

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