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previous findings have highlighted a decrease in H2AX levels and activation of TP53 upon radiation treatment, pointing them out as indicators of DNA damage response and radiosensitivity [46, 47]
A mismatch between the proposed mechanism and the selected endpoint can make a biologically active therapy appear clinically neutral
RHD) and the Canadian Institutes of Health Research (RHD), and graduate scholarship from NSERC (SLG)
In preclinical rodent models, it has demonstrated modulation of adipose tissue and lipid metabolism through indirect mechanisms involving 3-adrenergic receptor pathways, without activating growth hormone or IGF-1-related proliferative effects (Heffernan et al
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