Evidence map›Paper›PMID 28040803›Full record

ReviewOncotarget2016

Oncogenic regulation of tumor metabolic reprogramming.

Míriam Tarrado-Castellarnau, Pedro de Atauri, Marta Cascante

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

92 citing papers in PubMed, 156 citations in OpenAlex.

  1. Trial
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  13. Mechanisms of resistance to NAMPT inhibitors in cancer.Cancer drug resistance (Alhambra, Calif.) · 2025
    Review
  14. Understanding Metabolic Pathway Rewiring by Oncogenic Gamma Herpesvirus.Journal of microbiology and biotechnology · 2024
    Review
  15. Review
  16. Review
  17. Review
  18. Emerging roles of the chromatin remodeler MORC2 in cancer metabolism.Medical oncology (Northwood, London, England) · 2024
    Review
  19. Review
  20. Article

32 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

3 authors at 1 institution in 1 country.

Míriam Tarrado-CastellarnauDepartment of Biochemistry and Molecular Biomedicine, Universitat de Barcelona, Institute of Biomedicine of Universitat de Barcelona (IBUB) and CSIC-Associated Unit, Barcelona, Spain.
Pedro de AtauriDepartment of Biochemistry and Molecular Biomedicine, Universitat de Barcelona, Institute of Biomedicine of Universitat de Barcelona (IBUB) and CSIC-Associated Unit, Barcelona, Spain.
Marta CascanteDepartment of Biochemistry and Molecular Biomedicine, Universitat de Barcelona, Institute of Biomedicine of Universitat de Barcelona (IBUB) and CSIC-Associated Unit, Barcelona, Spain.
Universitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Development of malignancy is accompanied by a complete metabolic reprogramming closely related to the acquisition of most of cancer hallmarks. In fact, key oncogenic pathways converge to adapt the metabolism of carbohydrates, proteins, lipids and nucleic acids to the dynamic tumor microenvironment, conferring a selective advantage to cancer cells. Therefore, metabolic properties of tumor cells are significantly different from those of non-transformed cells. In addition, tumor metabolic reprogramming is linked to drug resistance in cancer treatment. Accordingly, metabolic adaptations are specific vulnerabilities that can be used in different therapeutic approaches for cancer therapy. In this review, we discuss the dysregulation of the main metabolic pathways that enable cell transformation and its association with oncogenic signaling pathways, focusing on the effects of c-MYC, hypoxia inducible factor 1 (HIF1), phosphoinositide-3-kinase (PI3K), and the mechanistic target of rapamycin (mTOR) on cancer cell metabolism. Elucidating these connections is of crucial importance to identify new targets and develop selective cancer treatments that improve response to therapy and overcome the emerging resistance to chemotherapeutics.

Indexed as

Gene Expression Regulation, NeoplasticOncogenesTumor MicroenvironmentAmino AcidsAnimalsBiomarkers, TumorCarcinogenesisCell CycleCell Transformation, NeoplasticGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitLipid MetabolismLipidsMitochondriaNeoplasmsAmino AcidsBiomarkers, TumorHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitLipidsMTOR protein, humanOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-mycTOR Serine-Threonine KinasesHIFmetabolic reprogrammingmTORMYCPI3K

Identifiers

PMID28040803
PMCPMC5308762
OpenAlexW2479507898

What Socratic 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 Socratic graph.