Evidence map›Paper›PMID 39669240›Full record

ReviewGenetics in medicine open2023

The evolutionary cancer genome theory and its reasoning.

Vladimir F Niculescu

Abstract readReview
In one paragraph

Review in Genetics in medicine open, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Special Issue "Advances in Genome Regulation in Cancer".International journal of molecular sciences · 2023
    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

1 author.

Vladimir F NiculescuKirschenweg 1, Diedorf, Bavaria, 86420, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncogenesis and the origin of cancer are still not fully understood despite the efforts of histologists, pathologists, and molecular geneticists to determine how cancer develops. Previous embryogenic and gene- and genome-based hypotheses have attempted to solve this enigma. Each of them has its kernel of truth, but a unifying, universally accepted theory is still missing. Fortunately, a unicellular cell system has been found in amoebozoans, which exhibits all the basic characteristics of the cancer life cycle and demonstrates that cancer is not a biological aberration but a consequence of molecular and cellular evolution. The impressive systemic similarities between the life cycle of Entamoeba and the life cycle of cancer demonstrate the deep homology of cancer to the amoebozoans, metazoans, and fungi ancestor that branched into the clades of Amoebozoa, Metazoa, and Fungi (AMF) and shows that the roots of oncogenesis and tumorigenesis lie in an ancient gene network, which is conserved in the genome of all metazoans and humans. This evolutionary gene network theory of cancer (evolutionary cancer genome theory) integrates previous findings and hypotheses and is one step further along the road to a universal cancer cell theory. It supports genetic cancer medicine and recommends soma-to-germ transitions-referred to as epithelial-to-mesenchymal transition in cancer-and cancer germline as potential targets. According to the evolutionary cancer genome theory, cancer exploits an ancient gene network module of premetazoan origin.

Indexed as

CancerEntamoebaGenome damage and reconstructionPGCCsStemness

Identifiers

PMID39669240
PMCPMC11613669

What OpenQuestion holds

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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.