Evidence map›Paper›PMID 23071355›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012

Targeting cancer metabolism.

Beverly A Teicher, W Marston Linehan, Lee J Helman

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

90 citing papers in PubMed, 150 citations in OpenAlex.

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  16. Pleotropic effects of statins: the dilemma of wider utilization of statin.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2023
    Review
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30 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Beverly A TeicherMolecular Pharmacology Branch, Developmental Therapeutics Program, National Cancer Institute, Bethesda, Maryland, USA. Beverly.Teicher@nih.gov
W Marston Linehan
Lee J Helman
National Cancer Institute · US

Funding

Molecular Therapeutics of Kidney Cancer: VHL Gene and Fumarate Hydratase GeneZIABC011038 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LINEHAN, WILLIAM MARSTON · 2009 to 2025
$29.8M
Molecular Therapeutics of Kidney Cancer: MET Gene and BHD GeneZIABC011043 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LINEHAN, WILLIAM MARSTON · 2009 to 2025
$20.9M
Clinical Studies of the Molecular Genetic Basis of Kidney CancerZIABC011028 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LINEHAN, WILLIAM MARSTON · 2009 to 2025
$17.9M
Solid TumorsZIASC006891 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI HELMAN, LEE J. · 2009 to 2017
$5.0M
Intramural NIH HHS Z99 CA999999Intramural NIH HHS ZIA BC011028Intramural NIH HHS ZIA BC011038NCI NIH HHS Y99 CA999999
6 · The paper itself

Abstract

The understanding that oncogenes can have profound effects on cellular metabolism and the discovery of mutations and alterations in several metabolism-related enzymes--isocitrate dehydrogenase 1 (IDH1), isocitrate dehydrogenase 2 (IDH2), succinate dehydrogenase (SDH), fumarate hydratase (FH), and pyruvate kinase M2 (PKM2)--has renewed interest in cancer metabolism and renewed hope of taking therapeutic advantage of cancer metabolism. Otto Warburg observed that aerobic glycolysis was a characteristic of cancer cells. More than 50 years later, we understand that aerobic glycolysis and uptake of glutamine and glycine allow cancer cells to produce energy (ATP) and the nucleotides, amino acids, and lipids required for proliferation. Expression of the MYC oncogene drives the increase in cellular biomass facilitating proliferation. PKM2 expression in cancer cells stimulates aerobic glycolysis. Among intermediary metabolism enzymes, mutations in SDH occur in gastointestinal stromal tumors and result in a pseudohypoxic metabolic milieu. FH mutations lead to a characteristic renal cell carcinoma. Isocitrate dehydrogenase (IDH1/2) mutations have been found in leukemias, gliomas, prostate cancer, colon cancer, thyroid cancer, and sarcomas. These recently recognized oncogenic metabolic lesions may be selective targets for new anticancer therapeutics.

Indexed as

Cell ProliferationGlycolysisNeoplasmsFumarate HydrataseHumansIsocitrate DehydrogenaseMolecular Targeted TherapyMutationPyruvate KinaseSuccinate DehydrogenaseFumarate HydrataseIsocitrate DehydrogenasePyruvate KinaseSuccinate Dehydrogenase

Identifiers

PMID23071355
PMCPMC3475613
OpenAlexW2147047620

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.