Cytogenetics of Hispanic and white children with acute lymphoblastic leukemia in California
Cytogenetics of Hispanic and white children with acute lymphoblastic leukemia in California
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DOI：
10.1158/1055-9965.epi-05-0833
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发表时间：
2006-03-01
影响因子：
3.8
通讯作者：
Buffler, PA
中科院分区：
文献类型：
--
作者：
Aldrich, MC;Zhang, LP;Buffler, PA
儿童白血病的流行病学研究对肿瘤遗传特征的利用有限，而肿瘤遗传特征可能与疾病病因有关。我们描述了参加北方加州儿童白血病研究的543例儿童白血病患者（0-14岁）的细胞遗传学特征，并比较了这两个种族群体之间的细胞遗传学特征。受试者通过免疫表型、常规细胞遗传学特征和荧光原位杂交结果进行分类。在急性淋巴细胞白血病患者中最常见的倍体水平是高超二倍体（51-67条染色体）和假二倍体（分别为34%和27%）。在西班牙裔和非西班牙裔白人之间没有观察到11 q23/MLL重排频率的种族差异。在B系急性淋巴细胞白血病患者中，AML 1.西班牙裔（13%）显著低于非西班牙裔白人（24%; P = 0.01）。这是第一次在确定的地理区域的大量患者中观察到这种种族差异，这与较小的国际研究结果一致。TEL-AML 1频率2倍变异的机制基础可能是种族特异性风险因素或遗传学，应进一步探索。
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 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.