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This exhausted state renders T cells dysfunctional and reversing or preventing this phenotype is a major goal in cancer immunotherapy ( IFNG and GZMB ) and a gain of ChARs at exhaustion gene loci ( PDCD1 , HACVR2, and BATF ) compared with non-exhausted T cells ( thymocyte selection-associated HMG BOX ( TOX ) locus ( Figure 2 )

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E-cadhedrin contributes to tumor progression by increasing proliferation, invasion, and metastasis [19]

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