Author

D. F. Schaeffer

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 5 Immunology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 6 Organism:mouse· 5 Research Focus:cancer & tumor microenvironment· 4 Research Focus:cell type annotation· 2 Research Focus:development & morphogenesis· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1

Frequent Co-Authors

J. L. Kopp· 4 shared J. D. Johnson· 3 shared A. M. Y. Zhang· 2 shared A. M. Zhang· 2 shared S. Patil· 2 shared T. J. J. de Winter· 2 shared W. C. K. Wang· 2 shared X. Hu· 2 shared

Activity by Year

2019-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

4 shared papersCancer Biology

J. L. Kopp

Mutual co-authors in cluster

Author profile →

6 papers

Recent·Most cited

Acvr1b loss increases formation of pancreatic precancerous lesions from acinar and ductal cells of origin

K. Saeki, I. S. Wood, W. C. K. Wang, S. Patil, Y. Sun, D. F. Schaeffer, G. H. Su, J. L. Kopp

This study shows that Acvr1b loss in combination with Kras mutation promotes precancerous lesions from both acinar and ductal cells in the pancreas, but the IPMN-like phenotype differs when mutations occur in all cells.

bioRxiv · Jun 8, 2023 · PreprintCancer Biology

Hyperinsulinemia acts via acinar insulin receptors to initiate pancreatic cancer by increasing digestive enzyme production and inflammation

A. M. Y. Zhang, Y. H. Xia, J. S. H. Lin, K. H. Chu, W. C. K. Wang, T. J. J. Ruiter, J. C. C. Yang, N. Chen, J. Chhuor, S. Patil, H. H. Cen, E. Rideout, V. R. Richard, D. F. Schaeffer, R. P. Zahedi, , J. Kopp

bioRxiv · May 6, 2022Cancer Biology

Effects of hyperinsulinemia on pancreatic cancer development and the immune microenvironment revealed through single-cell transcriptomics

A. M. Zhang, T. J. J. de Winter, S. Wang, S. Flibotte, Y. B. Zhao, X. Hu, H. Li, D. F. Schaeffer, J. D. Johnson, J. L. Kopp

This study uses single-cell transcriptomics to show hyperinsulinemia affects pancreatic cancer development and immune microenvironment by altering immune cell pathways and reducing pre-cancerous lesions.

bioRxiv · Mar 10, 2021Cancer Biology

Recombinant T cell receptors specific for HLA-A*02:01-restricted neoepitopes containing KRAS codon 12 hotspot mutations

C. M. Rive, E. Yung, C. S. Hughes, S. D. Brown, G. Sharma, L. Dreolini, N. M. Mawji, C. Warren, J. Karasinska, J. M. Loree, D. T. Yapp, G. B. Morin, D. J. Renouf, D. F. Schaeffer, S. Turcotte, R. A. Holt

The paper identifies and characterizes T cell receptors specific for HLA-A*02:01-restricted KRAS codon 12 mutations in cancer, showing their reactivity and cytotoxic activity against tumor cells.

bioRxiv · Jun 15, 2020 · PreprintImmunology

PRDM3 attenuates pancreatitis and pancreatic tumorigenesis by regulating inflammatory response

J. Ye, A. Huang, H. Wang, A. M. Y. Zhang, X. Huang, Q. Lan, T. Sato, S. Goyama, M. Kurokawa, C. Deng, M. Sander, D. F. Schaeffer, W. Li, J. L. Kopp, R. Xie

This study shows PRDM3 suppresses pancreatitis and pancreatic tumorigenesis by modulating inflammation and Kras-driven oncogenesis in acinar cells.

bioRxiv · Dec 18, 2019Cancer Biology

Endogenous insulin contributes to pancreatic cancer development

A. M. Zhang, J. Magrill, T. J. J. de Winter, X. Hu, S. Skovso, D. F. Schaeffer, J. L. Kopp, J. D. Johnson

This study shows that reducing endogenous insulin production decreases pancreatic cancer precursors in mice, suggesting insulin hypersecretion contributes to pancreatic cancer development.

bioRxiv · Jan 24, 2019 · PreprintCancer Biology