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Tos effect. This observation suggests that the suppressive effect of asbestos on TUSC2 expression is mediated via ROS. Indeed, generation of ROS by asbestos was documented in many studies [25]. A yet another source of ROS that may keep the TUSC2 level down in normal and malignant tissues are inflammatory cells attracted to the site of asbestos lodging [31]. We previously showed that TUSC2 is expre
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Y is consistent with the haploinsufficient effect of the gene observed in our mouse KO model. Indeed, mice hetero- or homozygous on the Tusc2 deletion shared similar immunological and tumorigenic phenotypes at comparable frequencies. These data suggest that even partial loss of the TUSC2 dosage is sufficient to trigger pathological inflammation and increase susceptibility to cancer [15]. We consid