Anthony Tao
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Anthony Tao has a total of 45 co-authors. Here are the top co-authors by number of shared publications:
- Cynthia A. Loomis
Laura and Isaac Perlmutter Cancer Center 1 New York, New York
11 shared publications - Diana Erenburg
Department of Pathology, NYU Grossman School of Medicine, New York, New York
11 shared publications - Elizabeth F. Sher
Department of Pathology, NYU Grossman School of Medicine, New York, New York
11 shared publications - Hannan Mir
Regeneron Pharmaceuticals , Tarrytown, New York
11 shared publications - Jiehui Deng
New York University Langone Medical Center 3 New York, NY
11 shared publications - Kelly V. Ruggles
Institute for Systems Genetics, New York University Grossman School of Medicine, New York, NY, USA
11 shared publications
Latest Publications
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 5 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Impact of POLE inhibition on xenograft and allograft TNBC models.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 5 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Impact of POLE inhibition on xenograft and allograft TNBC models.
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 3 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Quantifies immunoblots from Figure 2 and provides corroborating data showing the impact of POLE suppression in additional cell line models.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 3 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Quantifies immunoblots from Figure 2 and provides corroborating data showing the impact of POLE suppression in additional cell line models.
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 2 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Analysis of the ISPY2 Breast Cancer Data Resource for the gene expression signature of POLE suppression reported in Figure 1.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 2 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Analysis of the ISPY2 Breast Cancer Data Resource for the gene expression signature of POLE suppression reported in Figure 1.
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 4 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Reports the effect of suppressing pathways upstream of NF-kB on NF-kB signaling triggered by replication stress.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 4 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Reports the effect of suppressing pathways upstream of NF-kB on NF-kB signaling triggered by replication stress.
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 3 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
67 gene POLE TNBC Signature Reported in Figure 1G and Data Reported in Figure 1J.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 3 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
67 gene POLE TNBC Signature Reported in Figure 1G and Data Reported in Figure 1J.
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 1 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Effect of POLE Suppression as a function of mutation and the CUT&RUN-Seq Analysis of the transcriptomic data reported in Figure 1.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 1 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Effect of POLE Suppression as a function of mutation and the CUT&RUN-Seq Analysis of the transcriptomic data reported in Figure 1.
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
TPM Raw Data underlying Figure 1.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
TPM Raw Data underlying Figure 1.
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 4 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Data Supporting Supplementary Figure 2 (I-SPY II Trial Analysis).
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 4 from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Data Supporting Supplementary Figure 2 (I-SPY II Trial Analysis).
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Data from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Breast cancer remains the second leading cause of cancer-related mortality among women, with triple-negative breast cancer (TNBC) exhibiting a particularly poor 5-year prognosis. In this study, we have demonstrated that among genetic and pharmacologic perturbations targeting DNA replication, suppression of the DNA polymerase epsilon catalytic subunit (POLE) induced a potent, TNBC-specific gene expression signature enriched in inflammatory cytokines that are transcriptional targets of NF-κB. TNBC cells exhibited markedly higher levels of DNA damage and canonical NF-κB activation compared with luminal breast cancer cells. Notably, NF-κB activation in this context depended on the canonical component RELA but not on the noncanonical component RELB. Mechanistically, ataxia–telangiectasia mutated, stimulator of IFN genes, and retinoic acid–inducible gene I each contributed to NF-κB activation following POLE suppression. POLE suppression in an in vivo murine TNBC model led to cancer cell–intrinsic elimination of tumor burden and increased immune cell infiltration. Together, these findings support a model in which replication stress from POLE inhibition triggers robust NF-κB–mediated inflammation and immune microenvironment remodeling in TNBC and can independently trigger tumor eradication. These results suggest a potential therapeutic avenue for targeting POLE in TNBC.Significance:DNA replication protein POLE can be selectively targeted in triple-negative breast cancer to activate signaling pathways that increase expression of inflammatory genes dependent on canonical NF-κB signaling and to eradicate tumors.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessData from Targeting DNA Polymerase Epsilon Induces Tumor Clearance and Activates an NF-κB–Mediated Inflammatory Response in Triple-Negative Breast Cancer
Breast cancer remains the second leading cause of cancer-related mortality among women, with triple-negative breast cancer (TNBC) exhibiting a particularly poor 5-year prognosis. In this study, we have demonstrated that among genetic and pharmacologic perturbations targeting DNA replication, suppression of the DNA polymerase epsilon catalytic subunit (POLE) induced a potent, TNBC-specific gene expression signature enriched in inflammatory cytokines that are transcriptional targets of NF-κB. TNBC cells exhibited markedly higher levels of DNA damage and canonical NF-κB activation compared with luminal breast cancer cells. Notably, NF-κB activation in this context depended on the canonical component RELA but not on the noncanonical component RELB. Mechanistically, ataxia–telangiectasia mutated, stimulator of IFN genes, and retinoic acid–inducible gene I each contributed to NF-κB activation following POLE suppression. POLE suppression in an in vivo murine TNBC model led to cancer cell–intrinsic elimination of tumor burden and increased immune cell infiltration. Together, these findings support a model in which replication stress from POLE inhibition triggers robust NF-κB–mediated inflammation and immune microenvironment remodeling in TNBC and can independently trigger tumor eradication. These results suggest a potential therapeutic avenue for targeting POLE in TNBC.Significance:DNA replication protein POLE can be selectively targeted in triple-negative breast cancer to activate signaling pathways that increase expression of inflammatory genes dependent on canonical NF-κB signaling and to eradicate tumors.