HIGHLIGHTS
SUMMARY
Genetic modelling of HCC has indicated that blocking MYC leads to tumour regression, suggesting that HCC can become MYC oncogene-addicted Official journal of CDDpress 2. This clinical observation drove the authors to explore the functionality of MYC and MET co-occurrence in_vivo, combining hydrodynamic tail vein injection for MYC expression with the R26stopMet genetic setting, in which wild-type MET levels are enhanced following the deletion of the stop cassette by Cre recombinase. The authors demonstrated that MYC and MET cooperate to trigger liver tumorigenesis in_vivo, modelling the subgroup of HCC patients with . . .
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