Douglas E. Biancur
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Douglas E. Biancur has a total of 42 co-authors. Here are the top co-authors by number of shared publications:
- Albert S. W. Sohn
Perlmutter Cancer Center, New York University Grossman School of Medicine; New York, NY 10016, USA
20 shared publications - Alec C. Kimmelman
Department of Radiation Oncology, New York University Grossman School of Medicine, New York, USA
20 shared publications - Elaine Y. Lin
Perlmutter Cancer Center, New York University Grossman School of Medicine; New York, NY 10016, USA
20 shared publications - Peter Y. Yu
Perlmutter Cancer Center, New York University Grossman School of Medicine, New York, New York
20 shared publications - Deborah Corcoran
Institute for Systems Genetics, NYU Grossman School of Medicine, New York, NY USA
19 shared publications - Jiehui Deng
New York University Langone Medical Center 3 New York, NY
19 shared publications
Latest Publications
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S6 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Higher density of CXCR2 positive macrophages was observed in autophagy-inhibited PDAC tumors compared to the control tumors.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S6 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Higher density of CXCR2 positive macrophages was observed in autophagy-inhibited PDAC tumors compared to the control tumors.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Data from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Pancreatic ductal adenocarcinoma (PDAC) relies on elevated autophagy to support metabolism, proliferation, and immune evasion. Inhibiting autophagy has been reported to improve response rates in patients with PDAC. In this work, we identified a mechanism to explain how the loss of autophagy in PDAC triggers reprogramming of the tumor microenvironment (TME) to ultimately stimulate an antitumor response. Autophagy inhibition in PDAC recruited macrophages via the CXCL1/2-CXCR2 axis. Simultaneously, the loss of autophagy resulted in a decrease in the canonical “don’t eat me” ligand CD47 on tumor cells, thereby inducing their susceptibility to macrophage phagocytosis. Although CD8+ T cells were critical to the antitumor immune response to autophagy inhibition in PDAC, they were not directly involved in cytotoxicity but played a critical role in stimulating macrophage phagocytosis of tumor cells. Taken together, this study strongly supports the implementation of autophagy inhibition in pancreatic cancer and highlights a crucial link between PDAC biology and the TME-macrophage cross-talk that effectively promotes tumor cell killing. Significance:Inhibition of autophagy in pancreatic cancer promotes antitumor immunity through a stepwise process of recruiting macrophages and enhancing phagocytosis of cancer cells, providing a potential therapeutic strategy for this deadly tumor type.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessData from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Pancreatic ductal adenocarcinoma (PDAC) relies on elevated autophagy to support metabolism, proliferation, and immune evasion. Inhibiting autophagy has been reported to improve response rates in patients with PDAC. In this work, we identified a mechanism to explain how the loss of autophagy in PDAC triggers reprogramming of the tumor microenvironment (TME) to ultimately stimulate an antitumor response. Autophagy inhibition in PDAC recruited macrophages via the CXCL1/2-CXCR2 axis. Simultaneously, the loss of autophagy resulted in a decrease in the canonical “don’t eat me” ligand CD47 on tumor cells, thereby inducing their susceptibility to macrophage phagocytosis. Although CD8+ T cells were critical to the antitumor immune response to autophagy inhibition in PDAC, they were not directly involved in cytotoxicity but played a critical role in stimulating macrophage phagocytosis of tumor cells. Taken together, this study strongly supports the implementation of autophagy inhibition in pancreatic cancer and highlights a crucial link between PDAC biology and the TME-macrophage cross-talk that effectively promotes tumor cell killing. Significance:Inhibition of autophagy in pancreatic cancer promotes antitumor immunity through a stepwise process of recruiting macrophages and enhancing phagocytosis of cancer cells, providing a potential therapeutic strategy for this deadly tumor type.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S2 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Autophagy inhibition in PDAC cells suppressed the growth of orthotopic implanted tumors and promoted macrophage and CD8+ T cell infiltration
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S2 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Autophagy inhibition in PDAC cells suppressed the growth of orthotopic implanted tumors and promoted macrophage and CD8+ T cell infiltration
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Video S5 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Timelapse videos of macrophage phagocytosis in the cocultures with control (mST) or autophagy-inhibited PDAC cells (4B).
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Video S5 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Timelapse videos of macrophage phagocytosis in the cocultures with control (mST) or autophagy-inhibited PDAC cells (4B).
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Video S4 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Timelapse videos of macrophage phagocytosis in the cocultures with control (mST) or autophagy-inhibited PDAC cells (4B).
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Video S4 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Timelapse videos of macrophage phagocytosis in the cocultures with control (mST) or autophagy-inhibited PDAC cells (4B).
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S8 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Macrophages killed autophagy-inhibited PDAC cells in coculture and phagocytosed multiple tumor cells in autophagy-inhibited PDAC tumors.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S8 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Macrophages killed autophagy-inhibited PDAC cells in coculture and phagocytosed multiple tumor cells in autophagy-inhibited PDAC tumors.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Video S2 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Timelapse videos of macrophage phagocytosis in the cocultures with control (mST) or autophagy-inhibited PDAC cells (4B).
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Video S2 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Timelapse videos of macrophage phagocytosis in the cocultures with control (mST) or autophagy-inhibited PDAC cells (4B).
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S1 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
ATG4BC74A expression in PDAC cells promoted the upregulation of P62 and LC3B-I in tumor cells.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S1 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
ATG4BC74A expression in PDAC cells promoted the upregulation of P62 and LC3B-I in tumor cells.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Video S1 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Timelapse videos of macrophage phagocytosis in the cocultures with control (mST) or autophagy-inhibited PDAC cells (4B).
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Video S1 from Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells
Timelapse videos of macrophage phagocytosis in the cocultures with control (mST) or autophagy-inhibited PDAC cells (4B).