Evidence map›Paper›PMID 33540679›Full record

ReviewCells2021

Mapping the Metabolic Networks of Tumor Cells and Cancer-Associated Fibroblasts.

Jessica Karta, Ysaline Bossicard, Konstantinos Kotzamanis, Helmut Dolznig, Elisabeth Letellier

Abstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

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  20. Metabolomic Biomarkers in Blood Samples Identify Cancers in a Mixed Population of Patients with Nonspecific Symptoms.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    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

5 authors.

Jessica KartaMolecular Disease Mechanisms Group, Department of Life Sciences and Medicine, Faculty of Science, Technology and Medicine, University of Luxembourg, 6 avenue du Swing, L-4367 Belval, Luxembourg.
Ysaline BossicardMolecular Disease Mechanisms Group, Department of Life Sciences and Medicine, Faculty of Science, Technology and Medicine, University of Luxembourg, 6 avenue du Swing, L-4367 Belval, Luxembourg.
Konstantinos KotzamanisMolecular Disease Mechanisms Group, Department of Life Sciences and Medicine, Faculty of Science, Technology and Medicine, University of Luxembourg, 6 avenue du Swing, L-4367 Belval, Luxembourg.
Helmut DolznigTumor Stroma Interaction Group, Institute of Medical Genetics, Medical University of Vienna, Währinger Strasse 10, 1090 Vienna, Austria.
Elisabeth LetellierMolecular Disease Mechanisms Group, Department of Life Sciences and Medicine, Faculty of Science, Technology and Medicine, University of Luxembourg, 6 avenue du Swing, L-4367 Belval, Luxembourg.ORCID 0000-0001-8242-9393

Funding

European Commission SECRET-ITN-859962Fondation du Pélican de Mie and Pierre Hippert-Faber E-AGR-0023-10-ZFondation Gustave et Simone Prévot R-AGR-0807-52Fondation Marie-Jeanne et Edmond Schumacher R-AGR-0807-51Fonds National de la Recherche Luxembourg CORE/C16/BM/11282028Fonds National de la Recherche Luxembourg PoC/18/12554295Niederösterreichische Forschungs- und Bildungsges.m.bH. NFB, LSC18-017
6 · The paper itself

Abstract

Metabolism is considered to be the core of all cellular activity. Thus, extensive studies of metabolic processes are ongoing in various fields of biology, including cancer research. Cancer cells are known to adapt their metabolism to sustain high proliferation rates and survive in unfavorable environments with low oxygen and nutrient concentrations. Hence, targeting cancer cell metabolism is a promising therapeutic strategy in cancer research. However, cancers consist not only of genetically altered tumor cells but are interwoven with endothelial cells, immune cells and fibroblasts, which together with the extracellular matrix (ECM) constitute the tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs), which are linked to poor prognosis in different cancer types, are one important component of the TME. CAFs play a significant role in reprogramming the metabolic landscape of tumor cells, but how, and in what manner, this interaction takes place remains rather unclear. This review aims to highlight the metabolic landscape of tumor cells and CAFs, including their recently identified subtypes, in different tumor types. In addition, we discuss various in vitro and in vivo metabolic techniques as well as different in silico computational tools that can be used to identify and characterize CAF-tumor cell interactions. Finally, we provide our view on how mapping the complex metabolic networks of stromal-tumor metabolism will help in finding novel metabolic targets for cancer treatment.

Indexed as

Cancer-Associated FibroblastsCell CountHumansTumor Cells, CulturedTumor MicroenvironmentCAF-tumor cross-talkcancercancer-associated fibroblasts (CAFs)in silico modelingmetabolomics’ measurement techniquespersonalized metabolic drugstumor metabolism

Identifiers

PMID33540679
PMCPMC7912987

What OpenQuestion holds

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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.