ArticleInternational journal of stem cells2012
Evolution of energy metabolism, stem cells and cancer stem cells: how the warburg and barker hypotheses might be linked.
Article in International journal of stem cells, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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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.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- The Concept of "Cancer Stem Cells" in the Context of Classic Carcinogenesis Hypotheses and Experimental Findings.Life (Basel, Switzerland) · 2021Article
- Differential Kat3 Usage Orchestrates the Integration of Cellular Metabolism with Differentiation.Cancers · 2021Article
- Taking the road less traveled - the therapeutic potential of CBP/β-catenin antagonists.Expert opinion on therapeutic targets · 2021Review
- p300 Serine 89: A Critical Signaling Integrator and Its Effects on Intestinal Homeostasis and Repair.Cancers · 2021Article
- Article
- Cancer Prevention and Therapy of Two Types of Gap Junctional Intercellular Communication⁻Deficient "Cancer Stem Cell".Cancers · 2019Article
- Enhanced Kat3A/Catenin transcription: a common mechanism of therapeutic resistance.Cancer drug resistance (Alhambra, Calif.) · 2019Article
- Nuclear receptor/Wnt beta-catenin interactions are regulated via differential CBP/p300 coactivator usage.PloS one · 2018Article
- CBP/Catenin antagonists: Targeting LSCs' Achilles heel.Experimental hematology · 2017Review
- What roles do colon stem cells and gap junctions play in the left and right location of origin of colorectal cancers?Journal of cell communication and signaling · 2017Article
- Targeting Cancer Stem Cells-A Renewed Therapeutic Paradigm.Oncology & hematology review · 2017Article
- Article
- Biologic relativity: Who is the observer and what is observed?Progress in biophysics and molecular biology · 2016Review
- Kat3 coactivators in somatic stem cells and cancer stem cells: biological roles, evolution, and pharmacologic manipulation.Cell biology and toxicology · 2016Review
- Breastmilk is a novel source of stem cells with multilineage differentiation potential.Stem cells (Dayton, Ohio) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The evolutionary transition from single cells to the metazoan forced the appearance of adult stem cells and a hypoxic niche, when oxygenation of the environment forced the appearance of oxidative phosphorylation from that of glycolysis. The prevailing paradigm in the cancer field is that cancers start from the "immortalization" or "re-programming" of a normal, differentiated cell with many mitochondria, that metabolize via oxidative phosphorylation. This paradigm has been challenged with one that assumes that the target cell for carcinogenesis is the normal, immortal adult stem cell, with few mitochondria. This adult organ-specific stem cell is blocked from "mortalizing" or from "programming" to be terminally differentiated. Two hypotheses have been offered to explain cancers, namely, the "stem cell theory" and the "de-differentiation" or "re-programming" theory. This Commentary postulates that the paleochemistry of the oceans, which, initially, provided conditions for life' s energy to arise via glycolysis, changed to oxidative phosphorylation for life' s processes. In doing so, stem cells evolved, within hypoxic niches, to protect the species germinal and somatic genomes. This Commentary provides support for the "stem cell theory", in that cancer cells, which, unlike differentiated cells, have few mitochondria and metabolize via glycolysis. The major argument against the "de-differentiation theory" is that, if re-programming of a differentiated cell to an "induced pluri-potent stem cell" happened in an adult, teratomas, rather than carcinomas, should be the result.
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Registered trials
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.