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Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse

The restoration of mTOR signaling with Fer1 rescue treatment in the context of RSL3 effects, and the genetic knockdown of GPX4, reaffirm our in vitro findings that RSL3-mediated induction of ferroptosis, mTOR pathway suppression, DNA damage and failure of DNA repair, and autophagy are GPX4-dependent processes in thyroid cancer cells