Evidence map›Paper›PMID 26149467›Full record

ArticleScientific reports2015

Quantitative constraint-based computational model of tumor-to-stroma coupling via lactate shuttle.

Fabrizio Capuani, Daniele De Martino, Enzo Marinari, Andrea De Martino

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Review
  5. Review
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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

4 authors at 2 institutions in 1 country.

Fabrizio CapuaniDipartimento di Fisica, Sapienza Università di Roma, Piazzale A. Moro 5, Rome (Italy).
Daniele De Martino1] Dipartimento di Fisica, Sapienza Università di Roma, Piazzale A. Moro 5, Rome (Italy) [2] Center for Life Nano Science@Sapienza, Istituto Italiano di Tecnologia, Viale Regina Elena 291, Rome (Italy).
Enzo Marinari1] Dipartimento di Fisica, Sapienza Università di Roma, Piazzale A. Moro 5, Rome (Italy) [2] INFN Sezione di Roma 1, Piazzale A. Moro 5, Rome (Italy).
Andrea De Martino1] Dipartimento di Fisica, Sapienza Università di Roma, Piazzale A. Moro 5, Rome (Italy) [2] Center for Life Nano Science@Sapienza, Istituto Italiano di Tecnologia, Viale Regina Elena 291, Rome (Italy) [3] Soft and Living Matter Laboratory, Istituto di Nanotecnologia (CNR/NANOTEC), Consiglio Nazionale delle Ricerche, Rome (Italy).
Sapienza University of Rome · ITNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells utilize large amounts of ATP to sustain growth, relying primarily on non-oxidative, fermentative pathways for its production. In many types of cancers this leads, even in the presence of oxygen, to the secretion of carbon equivalents (usually in the form of lactate) in the cell's surroundings, a feature known as the Warburg effect. While the molecular basis of this phenomenon are still to be elucidated, it is clear that the spilling of energy resources contributes to creating a peculiar microenvironment for tumors, possibly characterized by a degree of toxicity. This suggests that mechanisms for recycling the fermentation products (e.g. a lactate shuttle) may be active, effectively inducing a mutually beneficial metabolic coupling between aberrant and non-aberrant cells. Here we analyze this scenario through a large-scale in silico metabolic model of interacting human cells. By going beyond the cell-autonomous description, we show that elementary physico-chemical constraints indeed favor the establishment of such a coupling under very broad conditions. The characterization we obtained by tuning the aberrant cell's demand for ATP, amino-acids and fatty acids and/or the imbalance in nutrient partitioning provides quantitative support to the idea that synergistic multi-cell effects play a central role in cancer sustainment.

Indexed as

Models, BiologicalAdenosine TriphosphateGlucoseHumansLactic AcidL-Lactate DehydrogenaseMetabolic Flux AnalysisNeoplasmsOxidative PhosphorylationStromal CellsAdenosine TriphosphateGlucoseLactic AcidL-Lactate Dehydrogenase

Identifiers

PMID26149467
PMCPMC4493718
OpenAlexW2273015459

What OpenQuestion holds

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LicenceCC BY
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.