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Since radiotherapy is generally applied in a course of multiple fractions, cancer cells that survived after initial cycles acquire resistance through multiple cellular mechanisms including activation of NF-B, phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), mammalian target of rapamycin (mTOR), and become less responsive to the later cycles of radiotherapy and/or chemotherapy (Baskar et al., 2014)

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The effect of p53 on ferroptosis is double-sided[37]

The PK-PD disconnect why short half-life doesnt limit efficacy The striking feature of BPC-157 research is the disparity between short serum presence and sustained tissue-level effects