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. 2008 Dec 17;100(24):1792–1803. doi: 10.1093/jnci/djn416

Table 1.

Characteristics of patients in the German Cooperative Study Group for Childhood Acute Lymphoblastic Leukemia COALL-92/97 and the ALL-IX Dutch Childhood Oncology Group discovery cohort and in the St. Jude validation cohort*

No. of patients
Variable COALL-DCOG (n = 177) St. Jude (n = 95) P value
Age, y .13
    1–10 130 78
    >10 47 17
Subtype .97
    B-lineage other 47 22
    BCR-ABL 5 3
    E2A-PBX1 8 5
    MLL-AF4 3 1
    TEL-AML1 44 22
    Hyperdiploid 43 28
    T cell 28 14
WBCs, No. × 109 per liter .66
    <10 42 28
    10–49 67 36
    50–100 28 15
    >100 39 16
*

COALL-DCOG = German Cooperative Study Group for Childhood Acute Lymphoblastic Leukemia COALL-92/97 and the ALL-IX Dutch Childhood Oncology Group (the discovery cohort); St. Jude = validation cohort; WBCs = white blood cells.

Fisher exact test. All statistical tests were two-sided.

The BCR-ABL gene fusion is a translocation of parts of chromosomes 9 and 22, t(9;22), and involves the gene break point cluster region protein and Abelson murine leukemia viral (v-abl) oncogene homolog 1.The t(1;19) translocation creates E2A-PBX1 fusion gene and involves pre-B-cell leukemia homeobox 1 and E2A immunoglobulin enhancer-binding factor E12/E47. The t(4;11) translocation creates the MLL-AF4 fusion gene involving the mixed-lineage leukemia and the AF4–FMR2 family member 1 gene. The t(12;21) translocation creates the TEL-AML1 fusion gene, involving the ets variant gene 6 (TEL oncogene) and the runt-related transcription factor 1 (acute myeloid leukemia 1; aml1 oncogene). Hyperdiploid cells were identified by cytogenetics as having more than 51 chromosomes.