Author

D. M. Feldser

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

Biology Disciplines

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Cancer Biology· 5

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Organism:mouse· 4 Assay:bulk RNA-seq· 3 Research Focus:cancer & tumor microenvironment· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:drug response / drug discovery· 2 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1

Frequent Co-Authors

M. Cicchini· 3 shared A. A. Gudiel· 2 shared A. C. Gladstein· 2 shared K. M. Adler· 2 shared K. R. Doerig· 2 shared A. B. Pierce· 1 shared B. Stanger· 1 shared D. C. Brady· 1 shared

Activity by Year

2019-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersCancer Biology

M. Cicchini

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5 papers

Recent·Most cited

Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 signaling

D. M. Walter, A. C. Gladstein, K. R. Doerig, R. Natesan, S. G. Baskaran, A. A. Gudiel, K. M. Adler, J. O. Acosta, D. C. Wallace, I. A. Asangani, D. M. Feldser

This study shows that SETD2 inactivation in lung adenocarcinoma leads to increased oxidative metabolism and mTORC1 activity, making these tumors sensitive to inhibitors of oxidative respiration and mTORC1.

bioRxiv · Oct 6, 2022 · PreprintCancer Biology

p53 restoration in small cell lung cancer identifies a latent Cyclophilin-dependent necrosis mechanism

J. Acosta, Q. Li, N. F. Freebrug, N. Murali, G. P. Grothusen, M. Cicchini, H. Mai, A. C. Gladstein, K. M. Adler, K. R. Doerig, J. Li, M. Ruiz-Torres, K. L. Manning, B. Stanger, L. Busino, , D. M. Feldser

This study shows that p53 restoration in SCLC can induce necrosis via cyclophilin-dependent mechanisms, revealing subtype-specific responses and potential therapeutic targets.

bioRxiv · Jul 22, 2022Cancer Biology

LKB1 inactivation modulates chromatin accessibility to drive metastatic progression

S. E. Pierce, J. M. Granja, M. R. Corces, J. J. Brady, M. K. Tsai, A. B. Pierce, R. Tang, P. Chu, D. M. Feldser, H. Chang, M. C. Bassik, W. J. Greenleaf, M. M. Winslow

This study shows that LKB1 inactivation alters chromatin accessibility, promoting metastatic progression in lung cancer through SOX17 activation.

bioRxiv · Mar 29, 2021Cancer Biology

Requirement for PKC epsilon in KRAS-driven lung tumorigenesis

R. Garg, M. Cooke, S. Wang, F. Benavides, M. C. Abba, M. Cicchini, D. M. Feldser, M. G. Kazanietz

This study shows PKCε is required for KRAS-driven lung tumorigenesis and identifies it as a potential therapeutic target.

bioRxiv · Jun 26, 2020 · PreprintCancer Biology

Copper is an essential regulator of the autophagic kinases ULK1/2 to drive lung adenocarcinoma

T. Tsang, J. M. Posimo, A. A. Gudiel, M. Cicchini, D. M. Feldser, D. C. Brady

This study identifies copper as a regulator of ULK1/2 kinase activity in lung adenocarcinoma, showing that copper chelation can inhibit autophagy and tumor growth.

bioRxiv · Oct 24, 2019Cancer Biology