Evidence map›Paper›PMID 23549172›Full record

ArticleCell cycle (Georgetown, Tex.)2013

The Warburg effect version 2.0: metabolic reprogramming of cancer stem cells.

Javier A Menendez, Jorge Joven, Sílvia Cufí, Bruna Corominas-Faja, Cristina Oliveras-Ferraros, Elisabet Cuyàs, Begoña Martin-Castillo, Eugeni López-Bonet, Tomás Alarcón, Alejandro Vazquez-Martin

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.

  1. Pooled it
  2. Diabetes and cancer: glucose control impact on survival and tumor outcomes.Reviews in endocrine & metabolic disorders · 2026
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  15. Role of p53 suppression in the pathogenesis of hepatocellular carcinoma.World journal of gastrointestinal pathophysiology · 2023
    Review
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  17. Observational
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36 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

10 authors at 6 institutions in 3 countries.

Javier A MenendezMetabolism & Cancer Group, Translational Research Laboratory, Catalan Institute of Oncology-Girona (ICO-Girona), Girona, Spain. jmenendez@iconcologia.net
Jorge Joven
Sílvia Cufí
Bruna Corominas-Faja
Cristina Oliveras-Ferraros
Elisabet Cuyàs
Begoña Martin-Castillo
Eugeni López-Bonet
Tomás Alarcón
Alejandro Vazquez-Martin
Molecular Oncology (United States) · USInstitut Català d'Oncologia · ESInstitut d'Investigació Biomèdica de Girona · ESCentre de Recerca Matemàtica · ESCentro de Investigación Biomédica en Red · ESTranslational Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

When fighting cancer, knowledge on metabolism has always been important. Today, it matters more than ever. The restricted cataloging of cancer genomes is quite unlikely to achieve the task of curing cancer, unless it is integrated into metabolic networks that respond to and influence the constantly evolving cancer stem cell (CSC) cellular states. Once the genomic era of carcinogenesis had pushed the 1920s Otto Warburg's metabolic cancer hypothesis into obscurity for decades, the most recent studies begin to support a new developing paradigm, in which the molecular logic behind the conversion of non-CSCs into CSCs can be better understood in terms of the "metabolic facilitators" and "metabolic impediments" that operate as proximate openings and roadblocks, respectively, for the transcriptional events and signal transduction programs that ultimately orchestrate the intrinsic and/or microenvironmental paths to CSC cellular states. Here we propose that a profound understanding of how human carcinomas install a proper "Warburg effect version 2.0" allowing them to "run" the CSCs' "software" programs should guide a new era of metabolo-genomic-personalized cancer medicine. By viewing metabolic reprogramming of CSCs as an essential characteristic that allows dynamic, multidimensional and evolving cancer populations to compete successfully for their expansion on the organism, we now argue that CSCs bioenergetics might be another cancer hallmark. A definitive understanding of metabolic reprogramming in CSCs may complement or to some extent replace, the 30-y-old paradigm of targeting oncogenes to treat human carcinomas, because it can be possible to metabolically create non-permissive or "hostile" metabotypes to prevent the occurrence of CSC cellular states with tumor- and metastasis-initiating capacity.

Indexed as

Models, BiologicalCell RespirationCell Transformation, NeoplasticDrug DiscoveryEnergy MetabolismGlycolysisHumansMedical OncologyMetabolic Networks and PathwaysNeoplastic Stem Cellscancer stem cellsmetabolismpluripotencyreprogrammingstemnessWarburg effect

Identifiers

PMID23549172
PMCPMC3674082
OpenAlexW2041094651

What OpenQuestion holds

Textmetadata
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.