Author

A. A. Gudiel

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· 2

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

D. M. Feldser· 2 shared A. C. Gladstein· 1 shared D. C. Brady· 1 shared D. C. Wallace· 1 shared D. M. Walter· 1 shared I. A. Asangani· 1 shared J. M. Posimo· 1 shared J. O. Acosta· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 31 mutual co-author links

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2 shared papersCancer Biology

D. M. Feldser

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2 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

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