Shigeaki Umeda
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Shigeaki Umeda has a total of 180 co-authors. Here are the top co-authors by number of shared publications:
- Christine Iacobuzio-Donahue
The David M Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, New York, NY
113 shared publications - Eileen Mary O'Reilly
Weill Cornell Medicine
91 shared publications - Wungki Park
Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, USA
91 shared publications - Akimasa Hayashi
Department of Pathology, Kyorin University School of Medicine, Tokyo, Japan
85 shared publications - Jungeui Hong
Memorial Sloan Kettering Cancer Center 1 David M. Rubenstein Center for Pancreatic Cancer Research New York, New York
62 shared publications - Elias-Ramzey Karnoub
David M. Rubenstein Center for Pancreas Cancer Research, Memorial Sloan Kettering Cancer Center, New York, USA
36 shared publications
Latest Publications
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S6 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 6 showing AMIGO2 promotes HIF1a nuclear retention via specific HIF1a residues
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S6 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 6 showing AMIGO2 promotes HIF1a nuclear retention via specific HIF1a residues
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S3 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 3 showing NPTX1 is over-expressed in human primary and metastatic PDAC tumors
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S3 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 3 showing NPTX1 is over-expressed in human primary and metastatic PDAC tumors
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S1 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 1 showing NPTX1 is highly expressed in both human and murine highly metastatic PDAC models.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S1 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 1 showing NPTX1 is highly expressed in both human and murine highly metastatic PDAC models.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S5 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 5 showing AMIGO2 as a cell surface receptor for NPTX1 and a driver of PDAC metastasis
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S5 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 5 showing AMIGO2 as a cell surface receptor for NPTX1 and a driver of PDAC metastasis
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Key Resource Table from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Key resource table with cat numbers
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessKey Resource Table from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Key resource table with cat numbers
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S2 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 2 showing NPTX1 drives liver metastasis of PDAC
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S2 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 2 showing NPTX1 drives liver metastasis of PDAC
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S4 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 4 showing NPTX1 promotes cell growth under hypoxic conditions
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S4 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. Figure 4 showing NPTX1 promotes cell growth under hypoxic conditions
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S7 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. figure 7 showing therapeutic targeting of NPTX1 with monoclonal NPTX1 antibody
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S7 from A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention
Suppl. figure 7 showing therapeutic targeting of NPTX1 with monoclonal NPTX1 antibody
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Table S3 from Transcriptomic Plasticity Is a Hallmark of Metastatic Pancreatic Cancer
Differentially expressed and modular genes for each archetype cluster, including upregulated genes (log₂ fold change > 1, p < 0.05) and Hotspot-identified informative genes with significant autocorrelation (FDR < 0.05)
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessTable S3 from Transcriptomic Plasticity Is a Hallmark of Metastatic Pancreatic Cancer
Differentially expressed and modular genes for each archetype cluster, including upregulated genes (log₂ fold change > 1, p < 0.05) and Hotspot-identified informative genes with significant autocorrelation (FDR < 0.05)