Glutamine blockade induces divergent metabolic programs to overcome tumor immune evasion-Reference-Cited by-同舟云学术

Glutamine blockade induces divergent metabolic programs to overcome tumor immune evasion

Published:2019-11-22 Issue:6468 Volume:366 Page:1013-1021
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Leone Robert D.¹^ORCID,Zhao Liang¹^ORCID,Englert Judson M.¹^ORCID,Sun Im-Meng¹,Oh Min-Hee¹^ORCID,Sun Im-Hong¹,Arwood Matthew L.¹^ORCID,Bettencourt Ian A.¹^ORCID,Patel Chirag H.¹,Wen Jiayu¹,Tam Ada¹,Blosser Richard L.¹,Prchalova Eva²,Alt Jesse²,Rais Rana²^ORCID,Slusher Barbara S.²^ORCID,Powell Jonathan D.¹^ORCID

Affiliation:

1. The Bloomberg-Kimmel Institute for Cancer Immunotherapy at Johns Hopkins, Baltimore, MD 21287, USA.

2. Johns Hopkins Drug Discovery, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.

Abstract

A fresh look at glutamine targeting Glutamine is essential for tumor growth and has long been an attractive therapeutic target for cancer researchers. Some attempts at blocking glutamine metabolism in cancer patients resulted in toxicity, prompting Leone et al. to develop an innovative approach to reduce general side effects. They designed a prodrug form (JHU083) of the glutamine antagonist 6-diazo-5-oxo- l -norleucine (DON), which is administered in an inert state but then preferentially activated by enzymes enriched in the tumor microenvironment. JHU083 simultaneously shut down glycolysis and oxidative phosphorylation in mouse cancer cells while enhancing T cell oxidative phosphorylation and anticancer immune responses. Science , this issue p. 1013

Funder

NIH Office of the Director

The Bloomberg∼Kimmel Institute for Cancer Immunotherapy.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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