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. 2010 Jan 6;115(10):2077–2087. doi: 10.1182/blood-2009-03-211375

Table 4.

Only AML patients develop NuSAP1 Ab and CHAF1b antibody after HCT

Yes No P
NuSAP1 antibody n = 24 n = 96
    Median patient age, y 46 50 .88
    Median donor age, y 40 50 .44
    Conditioning .36
        Myeloablative 13 40
        Nonmyeloablative 11 56
    Donor .16
        Related 16 78
        Unrelated 8 18
    IgG levels 907 mg/dL 643 mg/dL < .001
    Acute GVHD 1.00
        0-I 20 81
        II-IV (15%) 4 15
    Chronic GVHD .64
        Yes (66%) 17 62
        No 7 34
    Relapse .007
        Yes (28%) 1 29
        No 23 67
    Disease < .001
        AML 24 13
        Other diseases 0 83
CHAF1b antibody n = 10 n = 110
    Median patient age, y 40 50 .44
    Median donor age, y 48 48 .70
    Conditioning .75
        Myeloablative 5 48
        Nonmyeloablative 5 62
    Donor .052
        Related 5 87
        Unrelated 5 23
    IgG levels 850 mg/dL 682 mg/dL < .001
    Acute GVHD 1.00
        0-I 9 93
        II-IV (15%) 1 17
    Chronic GVHD .49
        Yes (66%) 8 71
        No 2 39
    Relapse 1.00
        Yes (28%) 2 29
        No 8 81
    Disease .001
        AML 8 29
        Other diseases 2 81

One hundred twenty patients were screened for antibodies against NuSAP1 and CHAF1b. The patients were segregated into 2 groups. The first group shows patients with antibody and the second group was detected with no antibody responses. These 2 groups are correlated with variables as shown.