Cytogenetics of Hispanic and White Children with Acute Lymphoblastic Leukemia in California
Epidemiologic studies of childhood leukemia have made limited use of tumor genetic characteristics, which may be related to disease etiology. We characterized the cytogenetics of 543 childhood leukemia patients (0-14 years of age) enrolled in the Northern California Childhood Leukemia Study, an appr...
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Published in | Cancer epidemiology, biomarkers & prevention Vol. 15; no. 3; pp. 578 - 581 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Philadelphia, PA
American Association for Cancer Research
01.03.2006
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Subjects | |
Online Access | Get full text |
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Summary: | Epidemiologic studies of childhood leukemia have made limited use of tumor genetic characteristics, which may be related to
disease etiology. We characterized the cytogenetics of 543 childhood leukemia patients (0-14 years of age) enrolled in the
Northern California Childhood Leukemia Study, an approximately population-based study comprised primarily of Hispanics (42%)
and non-Hispanic Whites (41%), and compared the cytogenetic profiles between these two ethnic groups. Subjects were classified
by immunophenotype, conventional cytogenetic characteristics, and fluorescence in situ hybridization findings. The ploidy levels most frequently observed among acute lymphoblastic leukemia patients were high
hyperdiploidy (51-67 chromosomes) and pseudodiploidy (34% and 27%, respectively). No ethnic differences in the frequency of
11q23/ MLL rearrangements were observed between Hispanics and non-Hispanic Whites. Among B-lineage acute lymphoblastic leukemia patients,
the percentage of TEL-AML1 translocations was significantly lower in Hispanics (13%) than in non-Hispanic Whites (24%; P = 0.01). This is the first time that this ethnic variation has been observed in a large number of patients in a defined geographic
region, which is consistent with findings from smaller international studies. The mechanistic basis for this 2-fold variation
in frequency of TEL-AML1 may be due to ethnic-specific risk factors or genetics and should be explored further. (Cancer Epidemiol Biomarkers Prev
2006;(15)3:578–81) |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1055-9965 1538-7755 |
DOI: | 10.1158/1055-9965.EPI-05-0833 |