Evidence map›Paper›PMID 26621573›Full record

ReviewMedical science monitor : international medical journal of experimental and clinical research2015

Cancer: Mitochondrial Origins.

George B Stefano, Richard M Kream

Open access · hybridAbstract readReview
In one paragraph

Review in Medical science monitor : international medical journal of experimental and clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Microbiome and Health: Ramifications of Intelligent Deception.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Aging Reversal and Healthy Longevity is in Reach: Dependence on Mitochondrial DNA Heteroplasmy as a Key Molecular Target.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Review
  13. Antibiotics May Trigger Mitochondrial Dysfunction Inducing Psychiatric Disorders.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Review
  14. Review
  15. Glycolytic Coupling to Mitochondrial Energy Production Ensures Survival in an Oxygen Rich Environment.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Review
  16. 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

2 authors.

George B StefanoMitoGenetics, LLC, Farmingdale, NY, USA.
Richard M KreamMitoGenetics, LLC, Farmingdale, NY, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The primacy of glucose derived from photosynthesis as an existential source of chemical energy across plant and animal phyla is universally accepted as a core principle in the biological sciences. In mammalian cells, initial processing of glucose to triose phosphate intermediates takes place within the cytosolic glycolytic pathway and terminates with temporal transport of reducing equivalents derived from pyruvate metabolism by membrane-associated respiratory complexes in the mitochondrial matrix. The intra-mitochondrial availability of molecular oxygen as the ultimate electron acceptor drives the evolutionary fashioned chemiosmotic production of ATP as a high-efficiency biological process. The mechanistic bases of carcinogenesis have demonstrated profound alteration of normative mitochondrial function, notably dysregulated respiratory processes. Accordingly, the classic Warburg effect functionally links aerobic glycolysis, aberrant production and release of lactate, and metabolic down-regulation of mitochondrial oxidative processes with the carcinogenetic phenotype. We surmise, however, that aerobic fermentation by cancer cells may also represent a developmental re-emergence of an evolutionarily conserved early phenotype, which was "sidelined" with the emergence of mitochondrial oxidative phosphorylation as a primary mechanism for ATP production in normal cells. Regardless of state-dependent physiological status in mixed populations of cancer cells, it has been established that mitochondria are functionally linked to the initiation of cancer and its progression. Biochemical, molecular, and physiological differences in cancer cell mitochondria, notably mtDNA heteroplasmy and allele-specific expression of selected nuclear genes, may represent major focal points for novel targeting and elimination of cancer cells in metastatic disease afflicting human populations. To date, and despite considerable research efforts, the practical realization of advanced mitochondrial targeted therapies has not been forthcoming.

Indexed as

Adenosine TriphosphateDNA, MitochondrialEnergy MetabolismGlucoseGlycolysisHumansMitochondriaNeoplasmsAdenosine TriphosphateDNA, MitochondrialGlucose

Identifiers

PMID26621573
PMCPMC4671449
OpenAlexW2218098835

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.