Evidence map›Paper›PMID 36832301›Full record

ArticleDiagnostics (Basel, Switzerland)2023

From Pathogens to Cancer: Are Cancer Cells Evolved Mitochondrial Super Cells?

Mario G Balzanelli, Pietro Distratis, Rita Lazzaro, Van Hung Pham, Raffaele Del Prete, Adriana Mosca, Francesco Inchingolo, Sergey K Aityan, Luigi Santacroce, Kieu C D Nguyen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Diagnostics (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Bidirectional Association between Periodontitis and Thyroid Disease: A Scoping Review.International journal of environmental research and public health · 2024
    Article
  4. 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

11 authors at 3 institutions in 2 countries.

Mario G BalzanelliSET-118, Department of Pre-Hospital and Emergency, SG Giuseppe Moscati Hospital, 74120 Taranto, Italy.
Pietro DistratisSET-118, Department of Pre-Hospital and Emergency, SG Giuseppe Moscati Hospital, 74120 Taranto, Italy.
Rita LazzaroSET-118, Department of Pre-Hospital and Emergency, SG Giuseppe Moscati Hospital, 74120 Taranto, Italy.
Van Hung PhamInternational Research Institute of Genetics and Immunology, Ho Chi Minh City 70000, Vietnam.
Raffaele Del PreteDepartment of Interdisciplinary Medicine, Microbiology and Virology Unit, School of Medicine, University of Bari "Aldo Moro", 70124 Bari, Italy.
Adriana MoscaDepartment of Interdisciplinary Medicine, School of Medicine, University of Bari "Aldo Moro", 70124 Bari, Italy.
Francesco InchingoloDepartment of Interdisciplinary Medicine, School of Medicine, University of Bari "Aldo Moro", 70124 Bari, Italy.ORCID 0000-0003-3797-5883
Sergey K AityanDepartment of Multidisciplinary Research Center, Lincoln University, Oakland, CA 94612, USA.
Luigi SantacroceDepartment of Interdisciplinary Medicine, School of Medicine, University of Bari "Aldo Moro", 70124 Bari, Italy.ORCID 0000-0001-5671-8124
Kieu C D NguyenDepartment of Interdisciplinary Medicine, School of Medicine, University of Bari "Aldo Moro", 70124 Bari, Italy.
Ciro Gargiulo IsaccoSET-118, Department of Pre-Hospital and Emergency, SG Giuseppe Moscati Hospital, 74120 Taranto, Italy.
University of Bari Aldo Moro · ITAzienda Ospedaliera S.Giuseppe Moscati · ITLincoln University - California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Life is based on a highly specific combination of atoms, metabolism, and genetics which eventually reflects the chemistry of the Universe which is composed of hydrogen, oxygen, nitrogen, sulfur, phosphorus, and carbon. The interaction of atomic, metabolic, and genetic cycles results in the organization and de-organization of chemical information of that which we consider as living entities, including cancer cells. In order to approach the problem of the origin of cancer it is therefore reasonable to start from the assumption that the sub-molecular level, the atomic structure, should be the considered starting point on which metabolism, genetics, and external insults eventually emanate. Second, it is crucial to characterize which of the entities and parts composing human cells may live a separate life; certainly, this theoretical standpoint would consider mitochondria, an organelle of "bacteria" origin embedded in conditions favorable for the onset of both. This organelle has not only been tolerated by immunity but has also been placed as a central regulator of cell defense. Virus, bacteria, and mitochondria are also similar in the light of genetic and metabolic elements; they share not only equivalent DNA and RNA features but also many basic biological activities. Thus, it is important to finalize that once the cellular integrity has been constantly broken down, the mitochondria like any other virus or bacteria return to their original autonomy to simply survive. The Warburg's law that states the ability of cancers to ferment glucose in the presence of oxygen, indicates mitochondria respiration abnormalities may be the underlying cause of this transformation towards super cancer cells. Though genetic events play a key part in altering biochemical metabolism, inducing aerobic glycolysis, this is not enough to impair mitochondrial function since mitochondrial biogenesis and quality control are constantly upregulated in cancers. While some cancers have mutations in the nuclear-encoded mitochondrial tricarboxylic acid (TCA) cycle, enzymes that produce oncogenic metabolites, there is also a bio-physic pathway for pathogenic mitochondrial genome mutations. The atomic level of all biological activities can be considered the very beginning, marked by the electron abnormal behavior that consequently affects DNA of both cells and mitochondria. Whilst the cell's nucleus DNA after a certain number of errors and defection tends to gradually switch off, the mitochondria DNA starts adopting several escape strategies, switching-on a few important genes that belong back at their original roots as independent beings. The ability to adopt this survival trick, by becoming completely immune to current life-threatening events, is probably the beginning of a differentiation process towards a "super-power cell", the cancer cells that remind many pathogens, including virus, bacteria, and fungi. Thus, here, we present a hypothesis regarding those changes that first begin at the mitochondria atomic level to steadily involve molecular, tissue and organ levels in response to the virus or bacteria constant insults that drive a mitochondria itself to become an "immortal cancer cell". Improved insights into this interplay between these pathogens and mitochondria progression may disclose newly epistemological paradigms as well as innovative procedures in targeting cancer cell progressive invasion.

Indexed as

cancerDNAelectronsmitochondriareactive oxygen species (ROS)RNAsuperoxide anion (O2−, hydroxyl radical OH)

Identifiers

PMID36832301
PMCPMC9954806
OpenAlexW4321459862

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.