Evidence map›Paper›PMID 31811141›Full record

ArticleNature communications2019

Reactive metabolite production is a targetable liability of glycolytic metabolism in lung cancer.

Alba Luengo, Keene L Abbott, Shawn M Davidson, Aaron M Hosios, Brandon Faubert, Sze Ham Chan, Elizaveta Freinkman, Lauren G Zacharias, Thomas P Mathews, Clary B Clish and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The chemical language of protein glycation.Nature chemical biology · 2025
    Review
  12. Review
  13. Article
  14. Dual roles of methylglyoxal in cancer.Frontiers in oncology · 2025
    Review
  15. Article
  16. Role of microRNA-363 during tumor progression and invasion.Journal of physiology and biochemistry · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 1 country.

Alba LuengoKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.ORCID http://orcid.org/0000-0002-4236-0229
Keene L AbbottKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.ORCID http://orcid.org/0000-0002-6166-704X
Shawn M DavidsonKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Aaron M HosiosKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Brandon FaubertChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0002-2886-886X
Sze Ham ChanWhitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, MA, 02142, USA.
Elizaveta FreinkmanWhitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, MA, 02142, USA.
Lauren G ZachariasChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Thomas P MathewsChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Clary B ClishBroad Institute of MIT and Harvard University, Cambridge, MA, 02142, USA.ORCID http://orcid.org/0000-0001-8259-9245
Ralph J DeBerardinisChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Caroline A LewisWhitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, MA, 02142, USA.ORCID http://orcid.org/0000-0003-1787-5084
Matthew G Vander HeidenKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. mvh@mit.edu.ORCID http://orcid.org/0000-0002-6702-4192
Children's Medical Center · USBroad Institute · USMassachusetts Institute of Technology · USWhitehead Institute for Biomedical Research · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Paula T Hammond · 1985 to 2026
$93.9M
PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
Metabolic Regulators of Tumor Growth and ProgressionR35CA220449 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI RALPH J DEBERARDINIS · 2017 to 2026
$9.4M
Understanding the role of metabolism in cancerR35CA242379 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI VANDER HEIDEN, MATTHEW G. · 2019 to 2025
$5.8M
Analysis of cancer cell metabolism in diverse environmental conditionsR01CA201276 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI VANDER HEIDEN, MATTHEW G., VITKUP, DENNIS · 2016 to 2020
$3.0M
Regulation of glucose metabolism to allow tumor initiation and growthR01CA168653 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI VANDER HEIDEN, MATTHEW G. · 2013 to 2019
$1.9M
NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA168653NCI NIH HHS R01 CA201276NCI NIH HHS R35 CA220449NCI NIH HHS R35 CA242379NIGMS NIH HHS T32 GM007287
6 · The paper itself

Abstract

Increased glucose uptake and metabolism is a prominent phenotype of most cancers, but efforts to clinically target this metabolic alteration have been challenging. Here, we present evidence that lactoylglutathione (LGSH), a byproduct of methylglyoxal detoxification, is elevated in both human and murine non-small cell lung cancers (NSCLC). Methylglyoxal is a reactive metabolite byproduct of glycolysis that reacts non-enzymatically with nucleophiles in cells, including basic amino acids, and reduces cellular fitness. Detoxification of methylglyoxal requires reduced glutathione (GSH), which accumulates to high levels in NSCLC relative to normal lung. Ablation of the methylglyoxal detoxification enzyme glyoxalase I (Glo1) potentiates methylglyoxal sensitivity and reduces tumor growth in mice, arguing that targeting pathways involved in detoxification of reactive metabolites is an approach to exploit the consequences of increased glucose metabolism in cancer.

Indexed as

GlycolysisAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorGlucoseGlutathioneHumansInactivation, MetabolicLactoylglutathione LyaseLungLung NeoplasmsMaleMetabolomicsMiceMice, Inbred C57BLPyruvaldehydeGlucoseGlutathioneLactoylglutathione LyasePyruvaldehyde

Identifiers

PMID31811141
PMCPMC6898239
OpenAlexW2993665124

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.