Evidence map›Paper›PMID 26835356›Full record

ReviewTranslational pediatrics2015

Energy metabolism in neuroblastoma and Wilms tumor.

Sepideh Aminzadeh, Silvia Vidali, Wolfgang Sperl, Barbara Kofler, René G Feichtinger

Open access · greenAbstract readReview
In one paragraph

Review in Translational pediatrics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  11. Review
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  14. Article
  15. Role of Energy Metabolism in the Progression of Neuroblastoma.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Mitochondrial DNA Haplogroups and Susceptibility to Neuroblastoma.Journal of the National Cancer Institute · 2020
    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 at 1 institution in 1 country.

Sepideh Aminzadeh1 Laura Bassi Centre of Expertise-THERAPEP, Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, 2 Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Silvia Vidali1 Laura Bassi Centre of Expertise-THERAPEP, Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, 2 Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Wolfgang Sperl1 Laura Bassi Centre of Expertise-THERAPEP, Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, 2 Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Barbara Kofler1 Laura Bassi Centre of Expertise-THERAPEP, Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, 2 Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
René G Feichtinger1 Laura Bassi Centre of Expertise-THERAPEP, Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, 2 Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Paracelsus Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To support high proliferation, the majority of cancer cells undergo fundamental metabolic changes such as increasing their glucose uptake and shifting to glycolysis for ATP production at the expense of far more efficient mitochondrial energy production by oxidative phosphorylation (OXPHOS), which at first glance is a paradox. This phenomenon is known as the Warburg effect. However, enhanced glycolysis is necessary to provide building blocks for anabolic growth. Apart from the generation of ATP, intermediates of glycolysis serve as precursors for a variety of biosynthetic pathways essential for cell proliferation. In the last 10-15 years the field of tumor metabolism has experienced an enormous boom in interest. It is now well established that tumor suppressor genes and oncogenes often play a central role in the regulation of cellular metabolism. Therefore, they significantly contribute to the manifestation of the Warburg effect. While much attention has focused on adult solid tumors, so far there has been comparatively little effort directed at elucidation of the mechanism responsible for the Warburg effect in childhood cancers. In this review we focus on metabolic pathways in neuroblastoma (NB) and Wilms tumor (WT), the two most frequent solid tumors in children. Both tumor types show alterations of the OXPHOS system and glycolytic features. Chromosomal alterations and activation of oncogenes like MYC or inactivation of tumor suppressor genes like TP53 can in part explain the changes of energy metabolism in these cancers. The strict dependence of cancer cells on glucose metabolism is a fairly common feature among otherwise biologically diverse types of cancer. Therefore, inhibition of glycolysis or starvation of cancer cells through glucose deprivation via a high-fat low-carbohydrate diet may be a promising avenue for future adjuvant therapeutic strategies.

Indexed as

Cancer metabolismmitochondrianeuroblastoma (NB)oxidative phosphorylation (OXPHOS)Wilms tumor (WT)

Identifiers

PMID26835356
PMCPMC4729069
OpenAlexW2176720195

What OpenQuestion holds

Textmetadata
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.