Relationships among additional chromosome abnormalities in chronic myelocytic leukemia (CML) with translocation 9;22 [Philadelphia chromosome (Ph1)-positive CML] were analyzed by log-linear models on 709 karyotypes reported in the literature. Additional abnormalities, such as the gain of chromosome 8 (+8), gain of Philadelphia chromosome (+Ph1), isochromosome of the long arm (q) of chromosome 17 [i(17q)], and the gain of chromosome 19 (+19), were frequently observed. A four-way 2 x 2 x 2 x 2 contingency table was considered with respect to the appearance of these four abnormalities, then the hierarchical log-linear models having at least four main effects were fitted to the observed contingency table. Akaike's information criteria of the models reflected the fitness of the model very well. Parameter estimates of the interaction terms indicated that the combinations of two abnormalities, '+8 and +19', '+Ph1 and +19', and '+8 and i(17q)' were positively associated, while '+Ph1 and i(17q)', and '+19 and i(17q)' were negatively associated. Based on the results of the data analysis, an inference was made on the route of karyotypic evolution in Ph1-positive CML; it statistically supports the hypothesis presented by Heim and Mitelman.
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机译：通过对数线性模型对文献报道的709个核型分析了慢性粒细胞白血病（CML）的其他染色体异常与易位9; 22 [费城染色体（Ph1）阳性CML]之间的关系。其他异常，例如8号染色体（+8）的增益，费城染色体（+ Ph1）的增益，17号染色体的长臂（q）的同染色体[i（17q）]和19号染色体的增益（+ 19），经常被观察到。考虑到这四个异常的出现的四向2 x 2 x 2 x 2列联表，然后将具有至少四个主要作用的分层对数线性模型拟合到观察到的列联表中。 Akaike的模型信息准则很好地反映了模型的适用性。相互作用项的参数估计表明，两个异常的组合“ +8和+19”，“ + Ph1和+19”以及“ +8和i（17q）”正相关，而“ + Ph1和i （17q）”和“ +19和i（17q）”负相关。根据数据分析的结果，推断Ph1阳性CML的核型进化途径。它在统计学上支持海姆（Heim）和米特尔曼（Mitelman）提出的假设。
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