Professor Emeritus
P_Bioengineering
+1 415 502-6526
My lab studies molecular genetics and signaling pathways during hepatic carcinogenesis. Specifically, using genomic approaches including expression arrays and array based CGH, we have identified large numbers of genes which are deregulated during liver cancer development. Using murine models, we are studying how these genetic alterations contribute to malignant transformation and progression in vivo. Our current studies focus on AKT/mTOR and Notch pathways and how they regulate cancer metabolism and cancer cell proliferation. In addition, using the novel mouse models as preclinical models, we are testing the therapeutic potentials of PI3K/mTOR or Notch inhibitors in treating liver cancers.
Publications
Identifying strategies to target the metabolic flexibility of tumours.
Nature metabolism
Mammalian Target of Rapamycin Complex 2 Signaling Is Required for Liver Regeneration in a Cholestatic Liver Injury Murine Model.
The American journal of pathology
Publisher Correction: Harnessing big 'omics' data and AI for drug discovery in hepatocellular carcinoma.
Nature reviews. Gastroenterology & hepatology
Oncogene-dependent function of BRG1 in hepatocarcinogenesis.
Cell death & disease
SNAI1 Promotes the Cholangiocellular Phenotype, but not Epithelial-Mesenchymal Transition, in a Murine Hepatocellular Carcinoma Model.
Cancer research
The mTORC2-Akt1 Cascade Is Crucial for c-Myc to Promote Hepatocarcinogenesis in Mice and Humans.
Hepatology (Baltimore, Md.)
Loss of Fbxw7 synergizes with activated Akt signaling to promote c-Myc dependent cholangiocarcinogenesis.
Journal of hepatology
Axis inhibition protein 1 (Axin1) Deletion-Induced Hepatocarcinogenesis Requires Intact ß-Catenin but Not Notch Cascade in Mice.
Hepatology (Baltimore, Md.)
Hippo Cascade Controls Lineage Commitment of Liver Tumors in Mice and Humans.
The American journal of pathology
Efficacy of MEK inhibition in a K-Ras-driven cholangiocarcinoma preclinical model.
Cell death & disease
Loss of Pten synergizes with c-Met to promote hepatocellular carcinoma development via mTORC2 pathway.
Experimental & molecular medicine
Pan-mTOR inhibitor MLN0128 is effective against intrahepatic cholangiocarcinoma in mice.
Journal of hepatology
Glucose Catabolism in Liver Tumors Induced by c-MYC Can Be Sustained by Various PKM1/PKM2 Ratios and Pyruvate Kinase Activities.
Cancer research
A functional mammalian target of rapamycin complex 1 signaling is indispensable for c-Myc-driven hepatocarcinogenesis.
Hepatology (Baltimore, Md.)
Both de novo synthetized and exogenous fatty acids support the growth of hepatocellular carcinoma cells.
Liver international : official journal of the International Association for the Study of the Liver
Differential requirement for de novo lipogenesis in cholangiocarcinoma and hepatocellular carcinoma of mice and humans.
Hepatology (Baltimore, Md.)