Toxicity mechanism in hematopoietic stem/progenitor-derived signaling via aryl hydrocarbon receptors induced by benzene exposure

我们已经发现，第一，最简单和基本的芳烃，苯，可以诱导异生物反应，通过激活的芳烃受体（AhR），第二，AhR的功能定位影响生态位功能相关的发育生物维持未分化的祖细胞。通过AhR活化在原始造血/祖细胞水平上的苯诱导的异生物质反应可以根据基因表达谱的模式进行分类：苯诱导的共同基因表达谱（BICGEP），即同一组试验小鼠之间特异性和共同表达的基因表达谱，以及苯诱导的随机基因表达谱（BISGEP），其是在同一组中的每只测试小鼠中概率上不同的随机基因表达谱。

We have discovered that, first, the simplest and fundamental aromatic hydrocarbon, benzene, can induce xenobiotic responses through the activation of the aryl hydrocarbon receptor(AhR) and that, second, the functional localization of AhRs affects niche function related to the developmental biological maintenance of undifferentiated progenitor cells. The benzene-induced xenobiotic responses through AhR activation at the primitive hematopoietic/progenitor level can be classified on the basis of the pattern of gene expression profile : benzene-induced common gene expression profiles(BICGEP), which are the specifically and commonly expressed profiles among the test mice in the same group, and benzene-induced stochastic gene expression profiles(BISGEP), which are the stochastic gene expression profiles that are probabilistically different in each of the test mice in the same group.