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TGFβ inhibition with Galunisertib combined with anti PD-L1 antibodies (Ab) exploits a vulnerability created in highly mesenchymal CRC, like those from the serrated origin, by alleviating the stromal activation and boosting the antitumor response. Also, inhibition of PHGDH and/or DNMT activity with azacytidine (aza) can exploit a vulnerability created in therapy-resistant PCa to block NEPC differentiation and tumorigenesis.
