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Author Correction: An enolase inhibitor for the targeted treatment of ENO1-deleted cancers

Yu-Hsi Lin
Nikunj Satani
Florian L. Muller
Amendments and Corrections18 Dec 2020
Nature Metabolism

Volume: 3, P: 122
An enolase inhibitor for the targeted treatment of ENO1-deleted cancers

Oncogenic transformation can render cancer cells dependent on aberrant expression of glycolytic enzyme isoforms. Lin et al. describe a novel enolase inhibitor, POMHEX, that can selectively kill ENO1-deleted glioblastomas.

Yu-Hsi Lin
Nikunj Satani
Florian L. Muller
Research23 Nov 2020
Nature Metabolism

Volume: 2, P: 1413-1426
Homozygous MTAP deletion in primary human glioblastoma is not associated with elevation of methylthioadenosine

The metabolite methylthioadenosine (MTA) inhibits PRMT5. Therefore, MTA accumulation due to MTA phosphorylase (MTAP) deletion has been proposed as a vulnerability for PRMT5-targeted therapy in cancer. Here, the authors show that MTA does not accumulate in MTAP-deficient cancer cells but is secreted and metabolized by MTAP-intact cells in the tumour microenvironment.

Yasaman Barekatain
Jeffrey J. Ackroyd
Florian L. Muller
ResearchOpen Access09 Jul 2021
Nature Communications

Volume: 12, P: 1-13
An inhibitor of oxidative phosphorylation exploits cancer vulnerability

A new inhibitor targeting the mitochondrial complex I shows antitumor activity in preclinical models of acute myeloid leukemia and glioblastoma relying on oxidative phosphorylation.

Jennifer R. Molina
Yuting Sun
Joseph R. Marszalek
Research11 Jun 2018
Nature Medicine

Volume: 24, P: 1036-1046
SF2312 is a natural phosphonate inhibitor of enolase

SF2312, a phosphonate antibiotic, directly binds and inhibits the activity of the glycolytic enzyme enolase and is selectively toxic to ENO1-deleted glioma cells through inhibition of glycolysis and depletion of ATP.

Paul G Leonard
Nikunj Satani
Florian L Muller
Research10 Oct 2016
Nature Chemical Biology

Volume: 12, P: 1053-1058
Author Correction: Mutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer

Yonathan Lissanu Deribe
Yuting Sun
P. Andrew Futreal
Amendments and Corrections13 Aug 2018
Nature Medicine

Volume: 24, P: 1627
Mutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer

SMARCA4 loss in non-small-cell lung cancer creates a metabolic dependency on oxidative phosphorylation that can be targeted using a new small-molecule inhibitor.

Yonathan Lissanu Deribe
Yuting Sun
P. Andrew Futreal
Research11 Jun 2018
Nature Medicine

Volume: 24, P: 1047-1057
Association between endometriosis and risk of systemic lupus erythematosus

Yu-Hsi Fan
Pui-Ying Leong
James Cheng-Chung Wei
ResearchOpen Access12 Jan 2021
Scientific Reports

Volume: 11, P: 1-9

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Author Correction: An enolase inhibitor for the targeted treatment of ENO1-deleted cancers

An enolase inhibitor for the targeted treatment of ENO1-deleted cancers

Homozygous MTAP deletion in primary human glioblastoma is not associated with elevation of methylthioadenosine

An inhibitor of oxidative phosphorylation exploits cancer vulnerability

SF2312 is a natural phosphonate inhibitor of enolase

Author Correction: Mutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer

Mutations in the SWI/SNF complex induce a targetable dependence on oxidative phosphorylation in lung cancer

Association between endometriosis and risk of systemic lupus erythematosus

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