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While these metabolic effects were likely to have been mediated by compensatory upregulation of FGF19 and/or FGF21 (308), they were clearly independent of FGFR4 agonism, instead being mediated by agonism of FGFR1c, 2c or 3c
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ICI D1694, a quinazoline antifolate thymidylate synthase inhibitor that is a potent inhibitor of L1210 tumor cell growth in vitro and in vivo: a new agent for clinical study
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