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M.KouretasD.VeskoukisA.et al (2019a)

Yamamura S, Izumiya Y, Araki S, Nakamura T, Kimura Y, Hanatani S, et al

10.1007/s00726-011-0867-5 38 CramerS

KRAS mutations in pancreatic cancer cells rely on both endogenous TNF -related apoptosis-inducing ligands (TRAILs) as well as their receptors to promote tumor growth and metastasis ( KRAS mutations evaded immune therapy by upregulating programmed cell death 1 ligand 1 (PD-L1) transcription and protein expression ( KRAS mutation could also enhance the recycling of PD-L1 molecules in pancreatic cancer cells to the cell surface to promote the immune escape of pancreatic cancer cells ( KRAS mutation-containing PDAC tumors displayed high m6A scores, suggesting a correlation between KRAS , m6A, and immune escape (Figure 7)

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