Author

B. S. Nelson

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Cancer Biology· 5

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Assay:metabolomics· 3 Approach:statistical model· 3 Assay:bulk RNA-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Research Focus:differential expression· 2 Organism:mouse· 2

Frequent Co-Authors

C. A. Lyssiotis· 5 shared C. J. Halbrook· 5 shared H. C. Crawford· 4 shared G. Thurston· 3 shared J. Ramos· 3 shared L. Lin· 3 shared L. Zhang· 3 shared M. Pasca di Magliano· 3 shared

Activity by Year

2019-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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5 shared papersCancer Biology

C. A. Lyssiotis

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5 papers

Recent·Most cited

Glucose-6-phosphate dehydrogenase deficiency accelerates pancreatic acinar-to-ductal metaplasia

M. D. Radyk, B. S. Nelson, C. J. Halbrook, A. Wood, B. Lavoie, L. Salvatore, G. Corfas, J. Colacino, Y. M. Shah, H. C. Crawford, C. A. Lyssiotis

This study shows that G6PD deficiency accelerates pancreatic acinar-to-ductal metaplasia by enhancing NADPH production for ROS management, highlighting a metabolic role in early tumorigenesis.

bioRxiv · Nov 6, 2023 · PreprintCancer Biology

The Pancreatic Tumor Microenvironment Compensates for Loss of GOT2

S. A. Kerk, L. Lin, A. L. Myers, Y. Zhang, J. A. Jimenez, P. Sajjakulnukit, B. S. Nelson, B. Chen, A. Robinson, G. Thurston, S. B. Kemp, N. G. Steele, M. T. Hoffman, H.-J. Wen, D. Long, , C. A. Lyssiotis

This study shows that the pancreatic tumor microenvironment compensates for loss of GOT2 by providing pyruvate, maintaining redox homeostasis and tumor growth in vivo.

bioRxiv · Aug 7, 2020Cancer Biology

Clonal Heterogeneity Supports Mitochondrial Metabolism in Pancreatic Cancer

C. J. Halbrook, G. Thurston, A. McCarthy, B. S. Nelson, P. Sajjakulnukit, A. S. Krall, P. J. Mullen, L. Zhang, S. Batra, A. Viale, B. Z. Stanger, H. R. Cristofk, J. Zhang, M. Pasca di Magliano, C. Jorgensen, C. A. Lyssiotis

The paper identifies two metabolic subclasses in pancreatic cancer cells and shows asparagine's role in supporting proliferation under mitochondrial stress, suggesting a new therapeutic strategy.

bioRxiv · May 15, 2020 · PreprintCancer Biology

GOT1 Inhibition Primes Pancreatic Cancer for Ferroptosis through the Autophagic Release of Labile Iron

D. M. Kremer, B. S. Nelson, L. Lin, E. Yarosz, C. J. Halbrook, S. A. Kerk, P. Sajjakulnukit, A. Myers, G. Thurston, S. Hou, E. S. Carpenter, A. Andren, Z. Nwosu, N. Cusmano, S. Wisner, , C. A. Lyssiotis

This study shows that inhibiting GOT1 in pancreatic cancer primes cells for ferroptosis by promoting autophagy-mediated release of labile iron.

bioRxiv · Feb 28, 2020 · PreprintCancer Biology

Tissue of Origin Dictates GOT1 Dependence and Confers Synthetic Lethality to Radiotherapy

B. S. Nelson, L. Lin, D. M. Kremer, C. M. Sousa, C. Cotta-Ramusino, A. Myers, J. Ramos, T. Gao, I. Kovalenko, K. Wilder-Romans, J. Dresser, M. Davis, H.-J. Lee, Z. C. Nwosu, S. Campit, , C. A. Lyssiotis

The paper shows that pancreatic ductal adenocarcinoma (PDA) is more dependent on GOT1 than colorectal cancer (CRC) and that GOT1 inhibition synergizes with radiotherapy to inhibit PDA growth.

bioRxiv · Jul 25, 2019Cancer Biology