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Corrigendum Free access | 10.1172/JCI179917

PHGDH is required for germinal center formation and is a therapeutic target in MYC-driven lymphoma

Annalisa D’Avola, Nathalie Legrave, Mylène Tajan, Probir Chakravarty, Ryan L. Shearer, Hamish W. King, Katarina Kluckova, Eric C. Cheung, Andrew J. Clear, Arief S. Gunawan, Lingling Zhang, Louisa K. James, James I. MacRae, John G. Gribben, Dinis P. Calado, Karen H. Vousden, and John C. Riches

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Published February 15, 2024 - More info

Published in Volume 134, Issue 4 on February 15, 2024
J Clin Invest. 2024;134(4):e179917. https://doi.org/10.1172/JCI179917.
© 2024 The American Society for Clinical Investigation
Published February 15, 2024 - Version history
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Related article:

PHGDH is required for germinal center formation and is a therapeutic target in MYC-driven lymphoma
Annalisa D’Avola, … , Karen H. Vousden, John C. Riches
Annalisa D’Avola, … , Karen H. Vousden, John C. Riches
Research Article Immunology Metabolism Article has an altmetric score of 6

PHGDH is required for germinal center formation and is a therapeutic target in MYC-driven lymphoma

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Abstract

The synthesis of serine from glucose is a key metabolic pathway supporting cellular proliferation in healthy and malignant cells. Despite this, the role that this aspect of metabolism plays in germinal center biology and pathology is not known. Here, we performed a comprehensive characterization of the role of the serine synthesis pathway in germinal center B cells and lymphomas derived from these cells. We demonstrate that upregulation of a functional serine synthesis pathway is a metabolic hallmark of B cell activation and the germinal center reaction. Inhibition of phosphoglycerate dehydrogenase (PHGDH), the first and rate-limiting enzyme in this pathway, led to defective germinal formation and impaired high-affinity antibody production. In addition, overexpression of enzymes involved in serine synthesis was a characteristic of germinal center B cell–derived lymphomas, with high levels of expression being predictive of reduced overall survival in diffuse large B cell lymphoma. Inhibition of PHGDH induced apoptosis in lymphoma cells, reducing disease progression. These findings establish PHGDH as a critical player in humoral immunity and a clinically relevant target in lymphoma.

Authors

Annalisa D’Avola, Nathalie Legrave, Mylène Tajan, Probir Chakravarty, Ryan L. Shearer, Hamish W. King, Katarina Kluckova, Eric C. Cheung, Andrew J. Clear, Arief S. Gunawan, Lingling Zhang, Louisa K. James, James I. MacRae, John G. Gribben, Dinis P. Calado, Karen H. Vousden, John C. Riches

×

Original citation: J Clin Invest. 2022;132(9):e153436. https://doi.org/10.1172/JCI153436

Citation for this corrigendum: J Clin Invest. 2024;134(4):e179917. https://doi.org/10.1172/JCI179917

In Figure 6A, the label for the SUDHL4 cell line was incorrect. In Figure 7G, the photographs for the 7- and 14-day time points were switched. The correct figure parts are below.

The authors regret the errors.

Footnotes

See the related article at PHGDH is required for germinal center formation and is a therapeutic target in MYC-driven lymphoma.

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