Crane M M, Strom S S, Halabi S, Berman E L, Fueger J J, Spitz M R, Keating M J
Division of Medical Education and Research, Greenville Hospital System, South Carolina 29605, USA.
Cancer Epidemiol Biomarkers Prev. 1996 Aug;5(8):639-44.
Many bone marrow cytogenetic abnormalities in acute myelogenous leukemia (AML) are tumor specific, clonal, nonrandom, and related to prognosis; it has been hypothesized that they may be markers of exposure to etiological agents. A previous report from our institution revealed several such associations; the purpose of the current study was to determine whether previous findings were present in a new group of patients. Subjects included 84 newly diagnosed AML patients (French-American-British M1 and M2); exposure data were gathered using self-report questionnaires at the time of registration. Two sets of comparisons were made: (a) patients with all (AA) or some (AN) cytogenetically abnormal cells versus those with normal karyotypes (NN) and (b) patients with specific abnormalities [-5/5q-, -7/7q-, +8, t(8;21)] versus all others. Odds ratios (ORs) were 4.64 for the association between prior cytotoxic therapy and -5/5q- and 6.38 for the association with -7/7q-, but were <1.00 for +8 and t(8;21). There were no ORs > 2.0 for specific abnormalities in any of the other exposures evaluated (cigarette smoking, alcohol use, occupational exposure to organic chemicals, paints, or pesticides/herbicides), with the exception of exposure to paints and -7/7q- (OR, 7.50). The ORs for AA/AN versus NN patients were 1.43 and 3.81 for smoking and alcohol use, and weak dose-response trends were present. The most consistent positive associations between the two series were for prior cytotoxic therapy (-5/5q-; -7/7q-), cigarette smoking (AA/AN versus NN) and alcohol use (AA/AN versus NN). Reasoning from the known association between prior cytotoxic therapy and -7/7q-, we would have predicted relatively high ORs (> 4.0) if specific abnormalities acted as markers for the exposures assessed, but none were present. However, in both series, AA/AN patients were more likely to smoke and use alcohol than were NN patients, and weak dose-response patterns were present for both. This finding suggests that both smoking and alcohol use may play a role in the pathogenesis of cytogenetic abnormalities in AML-M1/M2; however, the mechanism by which they work and whether they are involved in the etiology of these diseases remain unclear.
急性髓系白血病（AML）中的许多骨髓细胞遗传学异常具有肿瘤特异性、克隆性、非随机性且与预后相关；据推测，它们可能是接触致病因子的标志物。我们机构之前的一份报告揭示了几种此类关联；本研究的目的是确定这些先前的发现是否存在于一组新的患者中。研究对象包括84例新诊断的AML患者（法美英协作组分类的M1和M2型）；在登记时通过自我报告问卷收集暴露数据。进行了两组比较：（a）具有所有（AA）或部分（AN）细胞遗传学异常细胞的患者与核型正常（NN）的患者，以及（b）具有特定异常[-5/5q-、-7/7q-、+8、t(8;21)]的患者与所有其他患者。先前细胞毒性治疗与-5/5q-之间关联的优势比（OR）为4.64，与-7/7q-之间关联的OR为6.38，但与+8和t(8;21)相关的OR<1.00。在评估的任何其他暴露因素（吸烟、饮酒、职业接触有机化学品、油漆或杀虫剂/除草剂）中，除了接触油漆与-7/7q-（OR，7.50）外，特定异常的OR均未>2.0。AA/AN患者与NN患者相比，吸烟和饮酒的OR分别为1.43和3.81，并且存在微弱的剂量反应趋势。两个系列之间最一致的阳性关联是先前的细胞毒性治疗（-5/5q-；-7/7q-）、吸烟（AA/AN与NN相比）和饮酒（AA/AN与NN相比）。根据先前细胞毒性治疗与-7/7q-之间已知的关联，如果特定异常作为所评估暴露的标志物，我们会预测相对较高的OR（>4.0），但实际均未出现。然而，在两个系列中，AA/AN患者比NN患者更有可能吸烟和饮酒，并且两者都存在微弱的剂量反应模式。这一发现表明，吸烟和饮酒可能在AML-M1/M2细胞遗传学异常的发病机制中起作用；然而，它们起作用的机制以及是否参与这些疾病的病因仍不清楚。
