Evidence map›Paper›PMID 34572839›Full record

ReviewCancers2021

Genome Scale Modeling to Study the Metabolic Competition between Cells in the Tumor Microenvironment.

Itziar Frades, Carles Foguet, Marta Cascante, Marcos J Araúzo-Bravo

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The Need for a Systems Biology Approach in Cancer Explained.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Article
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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 3 institutions in 2 countries.

Itziar FradesComputational Biology and Systems Biomedicine Group, Biodonostia Health Research Institute, 20009 San Sebastian, Spain.
Carles FoguetDepartment of Biochemistry and Molecular Biomedicine, Institute of Biomedicine of University of Barcelona, Faculty of Biology, Universitat de Barcelona, Av. Diagonal 643, 08028 Barcelona, Spain.ORCID 0000-0001-8494-9595
Marta CascanteDepartment of Biochemistry and Molecular Biomedicine, Institute of Biomedicine of University of Barcelona, Faculty of Biology, Universitat de Barcelona, Av. Diagonal 643, 08028 Barcelona, Spain.ORCID 0000-0002-2062-4633
Marcos J Araúzo-BravoComputational Biology and Systems Biomedicine Group, Biodonostia Health Research Institute, 20009 San Sebastian, Spain.ORCID 0000-0002-3264-464X
Instituto de Salud Carlos III · ESBiogipuzkoa Health Research Institute · ESIkerbasque · ES

Funding

European Regional Development Fund ERA-Net program ERACoSysMed/H2020 JTC-2 2017, Grant Agreement No. 643271Horizon 2020 H2020-FETOPEN, Project 899417Institució Catalana de Recerca i Estudis Avançats PID2020-115051RB-I00Instituto de Salud Carlos III AC17/00012Instituto de Salud Carlos III CIBEREHD, CB17/04/00023Ministerio de Economía, Industria y Competitividad, Gobierno de España BFU2016-77987-P
6 · The paper itself

Abstract

The tumor's physiology emerges from the dynamic interplay of numerous cell types, such as cancer cells, immune cells and stromal cells, within the tumor microenvironment. Immune and cancer cells compete for nutrients within the tumor microenvironment, leading to a metabolic battle between these cell populations. Tumor cells can reprogram their metabolism to meet the high demand of building blocks and ATP for proliferation, and to gain an advantage over the action of immune cells. The study of the metabolic reprogramming mechanisms underlying cancer requires the quantification of metabolic fluxes which can be estimated at the genome-scale with constraint-based or kinetic modeling. Constraint-based models use a set of linear constraints to simulate steady-state metabolic fluxes, whereas kinetic models can simulate both the transient behavior and steady-state values of cellular fluxes and concentrations. The integration of cell- or tissue-specific data enables the construction of context-specific models that reflect cell-type- or tissue-specific metabolic properties. While the available modeling frameworks enable limited modeling of the metabolic crosstalk between tumor and immune cells in the tumor stroma, future developments will likely involve new hybrid kinetic/stoichiometric formulations.

Indexed as

constraint-based modelinggenome-scale metabolic modelsimmune systemkinetic metabolic modelsmetabolic crosstalkmetabolic reprogramming in cancerstoichiometric models

Identifiers

PMID34572839
PMCPMC8470216
OpenAlexW3200553802

What OpenQuestion holds

Textmetadata
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.