QL
Qi Liu
Shenzhen Bay Laboratory, Shenzhen University, UCSF Helen Diller Family Comprehensive Cancer Center
Research areas: Biochemistry, Genetics and Molecular Biology · Molecular Biology · DNA Repair Mechanisms · Head and Neck Cancer Studies · TGF-β signaling in diseases
0000-0002-3285-7864
Employment
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Shenzhen Bay Laboratory Research associate professor2019 - Present
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UCSF Helen Diller Family Comprehensive Cancer Center Research Scientist2016 - 2020
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Harvard Medical School Postdoc researcher2012 - 2015
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Shenzhen University Associate Professor
Education
Education history is unavailable.
Projects & Funding
Projects & funding information is unavailable.
Publications (31)
- The Effects of Combining Two Digital Systems for Preclinical Prosthodontic Education on Tooth Preparation Save
- Bioorthogonal Diels–Alder Click Chemistry-Based Pretargeted PET Imaging Strategy for Monitoring Programmed Death-Ligand 1 Expression Save
- Molecular PET/CT mapping of rhACE2 distribution and quantification in organs to aid in SARS‐CoV‐2 targeted therapy Save
- Development and Preclinical Evaluation of [68Ga]BMSH as a New Potent Positron Emission Tomography Tracer for Imaging Programmed Death-Ligand 1 Expression Save
- Boron-peptide conjugates with angiopep-2 for boron neutron capture therapy Save
- Human papillomavirus associated XPF deficiency increases alternative end joining and cisplatin sensitivity in head and neck squamous cell carcinoma Save
- Data from Subjugation of TGFβ Signaling by Human Papilloma Virus in Head and Neck Squamous Cell Carcinoma Shifts DNA Repair from Homologous Recombination to Alternative End Joining Save
- Data from Subjugation of TGFβ Signaling by Human Papilloma Virus in Head and Neck Squamous Cell Carcinoma Shifts DNA Repair from Homologous Recombination to Alternative End Joining Save
- Liu CCR-18-1236 Revised SD from Subjugation of TGFβ Signaling by Human Papilloma Virus in Head and Neck Squamous Cell Carcinoma Shifts DNA Repair from Homologous Recombination to Alternative End Joining Save
- Liu CCR-18-1236 Revised SD from Subjugation of TGFβ Signaling by Human Papilloma Virus in Head and Neck Squamous Cell Carcinoma Shifts DNA Repair from Homologous Recombination to Alternative End Joining Save
- A Boronated Derivative of Temozolomide Showing Enhanced Efficacy in Boron Neutron Capture Therapy of Glioblastoma Save
- Targeting the DNA replication stress phenotype of KRAS mutant cancer cells. Save
- Loss of TGFβ signaling increases alternative end-joining DNA repair that sensitizes to genotoxic therapies across cancer types. Save
- Technical note: factors affecting dose distribution in the overlap region of two-segment total body irradiation by helical tomotherapy Save
- Misrepair in Context: TGFβ Regulation of DNA Repair. Save
- Acquired Resistance of EGFR-Mutated Lung Cancer to Tyrosine Kinase Inhibitor Treatment Promotes PARP Inhibitor Sensitivity. Save
- A HYPOTHESIS OF RADIORESISTANCE AND CELL-SURVIVAL CURVE SHAPE BASED ON CELL-CYCLE PROGRESSION AND DAMAGE TOLERANCE. Save
- Subjugation of TGFβ Signaling by Human Papilloma Virus in Head and Neck Squamous Cell Carcinoma Shifts DNA Repair from Homologous Recombination to Alternative End Joining. Save
- PARP-1 inhibition with or without ionizing radiation confers reactive oxygen species-mediated cytotoxicity preferentially to cancer cells with mutant TP53. Save
- Radiation Resistance in KRAS-Mutated Lung Cancer Is Enabled by Stem-like Properties Mediated by an Osteopontin-EGFR Pathway. Save