Anthony Davis

Assistant Professor

University of Texas Southwestern Medical Center

United States

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Dr. Anthony Davis is an Assistant Professor at the University of Texas Southwestern Medical Center in the United States. His research focuses on the molecular mechanisms of cancer therapy resistance, particularly in relation to DNA repair pathways and radiosensitization strategies. Recent publications highlight his work on various cancer types, including prostate and breast cancer, as well as advancements in radiobiology and particle beam therapy.

Articles (12)

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2025

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2025

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2024

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2024

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2024

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2024

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2024

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2023

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2023

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2023

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2022

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2021

Collaborators (9)

Jui-Chung Chiang

University of Texas Southwestern Medical Center

UNITED STATES

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Zeng-Fu Shang

Assistant Professor

University of Texas Southwestern Medical Center

UNITED STATES

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Benjamin PC Chen

UNITED STATES

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Bret Mobley

Assistant Professor

Vanderbilt University Medical Center

UNITED STATES

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Guo-Min Li

Professor

University of Texas Southwestern Medical Center

UNITED STATES

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Yuanyuan Zhang

University of Texas Southwestern Medical Center

UNITED STATES

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Peter Ly

Assistant Professor

University of Texas Southwestern Medical Center

UNITED STATES

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Ling Cai

University of Texas Southwestern Medical Center

UNITED STATES

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Daniel Sanchez-Parcerisa

Associate Professor

Universidad Complutense de Madrid

SPAIN

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Anthony Davis

Research Interests

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About

Articles (12)

Lipoylation inhibition enhances radiation control of lung cancer by suppressing homologous recombination DNA damage repair

Dual inhibition of ATR and DNA-PKcs radiosensitizes ATM-mutant prostate cancer

Non-homologous end joining shapes the genomic rearrangement landscape of chromothripsis from mitotic errors.

Particle Beam Radiobiology Status and Challenges: A PTCOG Radiobiology Subcommittee Report

AXL/WRNIP1 Mediates Replication Stress Response and Promotes Therapy Resistance and Metachronous Metastasis in HER2+ Breast Cancer

BUB1 regulates non-homologous end joining pathway to mediate radioresistance in triple-negative breast cancer

Current trends and future perspectives in hadron therapy: radiobiology

ATM phosphorylates the FATC domain of DNA-PKcs at threonine 4102 to promote non-homologous end joining

DNA‐PKcs and ATM modulate mitochondrial ADP‐ATP exchange as an oxidative stress checkpoint mechanism

DNA-PK is activated by SIRT2 deacetylation to promote DNA double-strand break repair by non-homologous end joining

DNA-PKcs-dependent phosphorylation of RECQL4 promotes NHEJ by stabilizing the NHEJ machinery at DNA double-strand breaks

Ablating putative Ku70 phosphorylation sites results in defective DNA damage repair and spontaneous induction of hepatocellular carcinoma

Collaborators (9)

Jui-Chung Chiang

Zeng-Fu Shang

Benjamin PC Chen

Bret Mobley

Guo-Min Li

Yuanyuan Zhang

Peter Ly

Ling Cai

Daniel Sanchez-Parcerisa

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