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In short, the above studies provide ample evidence that LSH, as an oncogene, is participated in ferroptosis and is a possible therapeutic target for lung cancer due to its key effect in ferroptosis

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[2] Supporting preclinical work showed that once-daily CJC-1295 normalized growth in a GHRH-knockout mouse model, evidence at the animal tier that the molecule engages the GH axis productively in vivo