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. 2010 Jan 14;115(12):2462–2472. doi: 10.1182/blood-2009-08-239822

Table 1.

Distribution of GFI136N in AML patients and healthy control patients

Population AA GA GG Frequency allele A OR P* 95% CI
German and Dutch patients and control patients
    Patients 1 195 1610 0.054 ± 0.005 1.6 < 8 × 10−5 1.3-2
    Control patients 1 118 1572 0.035 ± 0.003
Patients by location
    Germany patients 1 134 1129 0.053 ± 0.004 1.6 < 2 × 10−3 1.2-2
    Germany control patients 1 87 1162 0.035 ± 0.004
    The Netherlands patients 0 61 481 0.056 ± 0.007 1.6 .02 1.1-2.6
    The Netherlands control patients 0 31 410 0.035 ± 0.006
According to smoking status
    Smokers AML 0 9 39 0.09 ± 0.028 3.4 .04 1.1-11.8
    Smokers control patients 0 4 59 0.03 ± 0.015
    Nonsmokers AML 0 13 41 0.12 ± 0.016 4.3 .003 1.5-12.2
    Nonsmokers control patients 0 6 82 0.03 ± 0.013

Allele frequencies for the GFI136N variant among white AML patients and control patients in Germany and in The Netherlands. GFI136N was enriched 1.6-fold in AML patients (P < 8 × 10−5) compared with the control population, which was confirmed after adjusting for age and sex.

AML indicates acute myeloid leukemia; CI, confidence interval; GFI1, Growth Factor Independence 1; and OR, odds ratio.

*

The Hardy-Weinberg equilibrium was tested and fit expectation with the exception that the frequency of genotype AA was lower than expected (1 vs 5; P = .01).

With reference to Essen and Marburg.