Author

Thomas J. Rogers

Van Andel Institute

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· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:metabolomics· 2

Frequent Co-Authors

Althea N. Waldhart· 2 shared Amy JohnsoniD· 2 shared Cameron J. Lee· 2 shared Evan C. LieniD· 2 shared Kelly H SokoliD· 2 shared Rachel J. HouseiD· 2 shared Ryan D. SheldoniD· 2 shared Samuel R. DanielsiD· 2 shared

Activity by Year

2024-2025 · peak 1/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

2 shared papersCancer Biology

Althea N. Waldhart

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

An alternative route for β-hydroxybutyrate metabolism supports fatty acid synthesis in cancer cells

Faith C Kaluba, Thomas J. Rogers, Yu‐Jin Jeong, Rachel J. House, Althea N. Waldhart, Kelly H Sokol, Samuel R. Daniels, Cameron J. Lee, Joseph Longo, Amy Johnson, Vincent J Sartori, Ryan D. Sheldon, Russell G. Jones, Evan C. Lien

This study identifies a non-canonical metabolic pathway in cancer cells that uses β-hydroxybutyrate for fatty acid synthesis, supporting tumor growth under lipid-limited conditions.

Nature Metabolism · Sep 8, 2025Peer-reviewedCancer Biology

Lipid availability influences ferroptosis sensitivity in cancer cells by regulating polyunsaturated fatty acid trafficking

Kelly H Sokol, Cameron J. Lee, Thomas J. Rogers, Althea N. Waldhart, Abigail E. Ellis, Sahithi Madireddy, Samuel R. Daniels, Rachel J. House, Xinyu Ye, Mary Olesnavich, Amy Johnson, Benjamin R. Furness, Ryan D. Sheldon, Evan C. Lien

The paper shows lipid-starved cancer cells are more sensitive to ferroptosis due to increased PUFA trafficking into phospholipids, challenging the assumption that PUFA levels directly determine ferroptosis susceptibility.

Cell chemical biology · Oct 22, 2024Peer-reviewedCancer Biology