Author

James T. Hagen

East Carolina UniversityORCID 0000-0002-0587-5370Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

Click to filter author papers

Cancer Biology· 2 Physiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Assay:bulk RNA-seq· 3 Approach:experimental assay· 3 Assay:ATAC-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:drug response / drug discovery· 2 Organism:human· 2 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

Kelsey H. Fisher‐WellmaniD· 3 shared McLane M. MontgomeryiD· 3 shared Raphael Taiwo ArulebaiD· 3 shared Brett R. ChrestiD· 2 shared Charles Edward ChalfantiD· 2 shared David J. FeithiD· 2 shared Joseph M. McClungiD· 2 shared Myles C. Cabot· 2 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 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

3 shared papersCancer Biology

Kelsey H. Fisher‐WellmanORCID

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

PhysiologyScience AdvancesPeer-reviewedJul 10, 2026

The MEK inhibitor trametinib incurs mitochondrial injury and induces innate immune responses in the mouse heart

Kelsey H. Fisher‐Wellman, Richard D. Lutze, Logan G. Kirkland…·Brian C. Jensen

This study shows trametinib causes mitochondrial injury and innate immune activation in mouse hearts, leading to cardiomyopathy and heart failure.

DOI 10.1126/sciadv.aeb2695

Cancer BiologybioRxivPreprintJun 6, 2025

Acid ceramidase inhibition enhances BCL-2 targeting in venetoclax-resistant acute myeloid leukemia via a cytotoxic integrated stress response

Johnson Ung, Su‐Fern Tan, Jeremy J.P. Shaw…·Thomas P. Loughran

This study shows that inhibiting acid ceramidase (AC) enhances venetoclax's effectiveness in venetoclax-resistant AML by inducing a cytotoxic integrated stress response.

DOI 10.1101/2025.06.06.657881

humanbulk RNA-seq

Cancer BiologyScience AdvancesPeer-reviewedApr 9, 2025

Acute myeloid leukemia mitochondria hydrolyze ATP to resist chemotherapy

James T. Hagen, McLane M. Montgomery, Raphael Taiwo Aruleba…·Kelsey H. Fisher‐Wellman

This study identifies a bioenergetic mechanism in AML cells where mitochondria consume ATP to resist chemotherapy, offering a target for improving treatment.

30 citationstop 2%