Evidence map›Paper›PMID 26733270›Full record

ReviewFrontiers in physiology2015

Cancer Metabolism: A Modeling Perspective.

Pouyan Ghaffari, Adil Mardinoglu, Jens Nielsen

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 76 citations in OpenAlex.

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  8. Modeling blood metabolite homeostatic levels reduces sample heterogeneity across cohorts.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

3 authors at 3 institutions in 2 countries.

Pouyan GhaffariDepartment of Biology and Biological Engineering, Chalmers University of Technology Gothenburg, Sweden.
Adil MardinogluDepartment of Biology and Biological Engineering, Chalmers University of TechnologyGothenburg, Sweden; Science for Life Laboratory, KTH - Royal Institute of TechnologyStockholm, Sweden.
Jens NielsenDepartment of Biology and Biological Engineering, Chalmers University of TechnologyGothenburg, Sweden; Science for Life Laboratory, KTH - Royal Institute of TechnologyStockholm, Sweden; Novo Nordisk Foundation Center for Biosustainability, Technical University of DenmarkHørsholm, Denmark.
Chalmers University of Technology · SENovo Nordisk Foundation · DKScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor cells alter their metabolism to maintain unregulated cellular proliferation and survival, but this transformation leaves them reliant on constant supply of nutrients and energy. In addition to the widely studied dysregulated glucose metabolism to fuel tumor cell growth, accumulating evidences suggest that utilization of amino acids and lipids contributes significantly to cancer cell metabolism. Also recent progresses in our understanding of carcinogenesis have revealed that cancer is a complex disease and cannot be understood through simple investigation of genetic mutations of cancerous cells. Cancer cells present in complex tumor tissues communicate with the surrounding microenvironment and develop traits which promote their growth, survival, and metastasis. Decoding the full scope and targeting dysregulated metabolic pathways that support neoplastic transformations and their preservation requires both the advancement of experimental technologies for more comprehensive measurement of omics as well as the advancement of robust computational methods for accurate analysis of the generated data. Here, we review cancer-associated reprogramming of metabolism and highlight the capability of genome-scale metabolic modeling approaches in perceiving a system-level perspective of cancer metabolism and in detecting novel selective drug targets.

Indexed as

cancer metabolismgenome scale metabolic reconstructionmetabolic modelingmetabolic networks and pathwayssystems biologysystems medicinetumor metabolism

Identifiers

PMID26733270
PMCPMC4679931
OpenAlexW2210463865

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.