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DNA damage results in activation of ATM and ATR, which results in stabilization of the TP53 protein causing increased levels of cell cycle inhibitors, including CDKN1A/p21 Cip , CDKN1B/p27 Kip1 , and CDKN1C/p57 Kip2 [33]

The dual modifications improve metabolic stability and extend peptide activity in experimental models

The expression of SLC1A5 increased after treatment with the EGFR TKI almonertinib (89), which may be related to secondary resistance since glutamine can activate the downstream signal of EGFR, such as mTOR

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