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In the context of SCLC, MYC has been shown to be regulated by both initiation and attenuation of transcription, MYCN appears to be regulated at the level of initiation of transcription, and MYCL has been shown to be regulated by attenuation of transcription ( In normal cells, MYC expression is tightly regulated by transcription factors CNBP, FuBP1, and TCF as well as structural DNA elements ( In mouse models, MYC withdrawal has led to tumor regression, indicating that MYC may be a valuable target in SCLC

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Evidence collected via WES, WGS, and NGS [9] suggests a correlation between several genes implicated in the pathogenesis of PFIC, adult cholestasis (RIC, LPAC, ICP), and the risk of developing HCC and CCA in both children and adults: TJP2, FXR, MYO5B, SLC51B, SLC25A13, NOTCH2, JAG1, TGR5, ABCB11, ABCB4, and HNF1B [9]