Evidence map›Paper›PMID 31687086›Full record

ReviewOxidative medicine and cellular longevity2019

Cancer Etiology: A Metabolic Disease Originating from Life's Major Evolutionary Transition?

B Poljsak, V Kovac, R Dahmane, T Levec, A Starc

Abstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2019. 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.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Ancient Diseases in Vertebrates: Tumours through the Ages.Animals : an open access journal from MDPI · 2024
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. SARS-CoV2 Infection and Comorbidities, Role in Oncogenesis.Asian Pacific journal of cancer prevention : APJCP · 2022
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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.

B PoljsakFaculty of Health Sciences, University of Ljubljana, Laboratory of Oxidative Stress Research, Ljubljana, Slovenia.ORCID https://orcid.org/0000-0003-3598-3468
V KovacFaculty of Health Sciences, University of Ljubljana, Laboratory of Oxidative Stress Research, Ljubljana, Slovenia.
R DahmaneFaculty of Health Sciences, University of Ljubljana, Chair of Biomedicine in Health Care, Ljubljana, Slovenia.ORCID https://orcid.org/0000-0002-7657-4057
T LevecFaculty of Health Sciences, University of Ljubljana, Chair of Public Health, Ljubljana, Slovenia.
A StarcFaculty of Health Sciences, University of Ljubljana, Chair of Public Health, Ljubljana, Slovenia.ORCID https://orcid.org/0000-0002-2128-7974

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A clear understanding of the origins of cancer is the basis of successful strategies for effective cancer prevention and management. The origin of cancer at the molecular and cellular levels is not well understood. Is the primary cause of the origin of cancer the genomic instability or impaired energy metabolism? An attempt was made to present cancer etiology originating from life's major evolutionary transition. The first evolutionary transition went from simple to complex cells when eukaryotic cells with glycolytic energy production merged with the oxidative mitochondrion (The Endosymbiosis Theory first proposed by Lynn Margulis in the 1960s). The second transition went from single-celled to multicellular organisms once the cells obtained mitochondria, which enabled them to obtain a higher amount of energy. Evidence will be presented that these two transitions, as well as the decline of NAD+ and ATP levels, are the root of cancer diseases. Restoring redox homeostasis and reactivation of mitochondrial oxidative metabolism are important factors in cancer prevention.

Indexed as

Biological EvolutionAnimalsDrug Resistance, NeoplasmEnergy MetabolismHumansMetabolic DiseasesMitochondriaNeoplasms

Identifiers

PMID31687086
PMCPMC6800902

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.