Lei Shi (0000-0003-1149-0474)

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I am a scientist with interest in linking hard-core biochemistry and practical cancer therapy. With more than ten years of study in biochemistry and metabolism, I am currently investigating the reprogrammed metabolism by specific oncogenic mutations in both cholangiocarcinoma and pancreatic ductal adenocarcinoma, two deadly human cancer types. Metabolism to a cell is like gas to a car, only more complex. By elucidating the mechanisms of oncogenic induced metabolic reprogramming, novel metabolic drugs can be discovered to improve patient outcomes.

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Massachusetts General Hospital: Boston, Massachusetts, US

2020-04-26 to present | Instructor in Medicine (Center for Cancer Research)

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Lei Shi

https://orcid.org/0000-0003-1149-0474

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Biography

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Employment (6)

Massachusetts General Hospital: Boston, Massachusetts, US

Harvard Medical School: Boston, Massachusetts, US

Broad Institute: Cambridge, MA, US

Massachusetts General Hospital: Boston, MA, US

Harvard Medical School: Boston, MA, US

University of Texas Southwestern Department of Biochemistry: Dallas, TX, US

Education and qualifications (3)

University of Texas Southwestern Department of Biochemistry: Dallas, TX, US

China Agricultural University: Beijing, CN

Purdue University: West Lafayette, IN, US

Professional activities (2)

American Association for Cancer Research: Philadelphia, PA, US

American Chemical Society: Washington, DC, US

Funding (1)

EXPLOITING METABOLIC REPROGRAMMING TO TARGET IDH1 MUTATED CHOLANGIOCARCINOMA

Works (36)

Mutant IDH1 inhibition induces dsDNA sensing to activate tumor immunity

Systematic identification of anticancer drug targets reveals a nucleus-to-mitochondria ROS-sensing pathway

Data from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

Data from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

Data from Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma

Data from Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma

Supplementary Figure from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

Supplementary Figure from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

Supplementary Figure from Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma

Supplementary Figure from Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma

Supplementary Table from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

Supplementary Table from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

Supplementary Table from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

Supplementary Table from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

Supplementary table from Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma

Supplementary table from Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma

Supplementary table from Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma

Supplementary table from Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma

NRF2 activation induces NADH-reductive stress, providing a metabolic vulnerability in lung cancer

SULT1A1-dependent sulfonation of alkylators is a lineage-dependent vulnerability of liver cancers

Identification of chemotherapy targets reveals a nucleus-to-mitochondria ROS sensing pathway

Reprogramming Intrahepatic Cholangiocarcinoma Immune Microenvironment by Chemotherapy and CTLA-4 Blockade Enhances Anti-PD1 Therapy

Biology of IDH mutant cholangiocarcinoma

EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

Mutant IDH Inhibits IFNγ–TET2 Signaling to Promote Immunoevasion and Tumor Maintenance in Cholangiocarcinoma

FGFR2 Extracellular Domain In-Frame Deletions Are Therapeutically Targetable Genomic Alterations That Function as Oncogenic Drivers in Cholangiocarcinoma

TAS-120 Overcomes Resistance to ATP-Competitive FGFR Inhibitors in Patients with FGFR2 Fusion–Positive Intrahepatic Cholangiocarcinoma

Cycloheximide can distort measurements of mRNA levels and translation efficiency

GATOR1 regulates nitrogenic cataplerotic reactions of the mitochondrial TCA cycle

Isocitrate dehydrogenase mutations confer dasatinib hypersensitivity and SRC dependence in intrahepatic cholangiocarcinoma

Cycling Transcriptional Networks Optimize Energy Utilization on a Genome Scale

Acetyl-CoA and the regulation of metabolism: mechanisms and consequences

Npr2 inhibits TORC1 to prevent inappropriate utilization of glutamine for biosynthesis of nitrogen-containing metabolites

Protein acetylation as a means to regulate protein function in tune with metabolic state

Acetyl-CoA induces transcription of the key G1 cyclin CLN3 to promote entry into the cell division cycle in Saccharomyces cerevisiae

Trehalose Is a Key Determinant of the Quiescent Metabolic State That Fuels Cell Cycle Progression upon Return to Growth