Evidence map›Paper›PMID 31331093›Full record

ReviewGenes2019

When Three Isn't a Crowd: A Digyny Concept for Treatment-Resistant, Near-Triploid Human Cancers.

Kristine Salmina, Bogdan I Gerashchenko, Michael Hausmann, Ninel M Vainshelbaum, Pawel Zayakin, Juris Erenpreiss, Talivaldis Freivalds, Mark S Cragg, Jekaterina Erenpreisa

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
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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

9 authors at 6 institutions in 4 countries.

Kristine SalminaLatvian Biomedical Research and Study Centre, LV-1067 Riga, Latvia.
Bogdan I GerashchenkoR.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology, National Academy of Sciences of Ukraine, 03022 Kyiv, Ukraine.
Michael HausmannKirchhoff Institute for Physics, Heidelberg University, D-69120 Heidelberg, Germany.
Ninel M VainshelbaumLatvian Biomedical Research and Study Centre, LV-1067 Riga, Latvia.
Pawel ZayakinLatvian Biomedical Research and Study Centre, LV-1067 Riga, Latvia.
Juris ErenpreissRiga Stradins University, LV-1007 Riga, Latvia.
Talivaldis FreivaldsInstitute of Cardiology and Regenerative Medicine, University of Latvia, LV-1004 Riga, Latvia.
Mark S CraggCentre for Cancer Immunology, University of Southampton, Southampton SO16 6YD, UK.
Jekaterina ErenpreisaLatvian Biomedical Research and Study Centre, LV-1067 Riga, Latvia. katrina@biomed.lu.lv.
Latvian Biomedical Research and Study Centre · LVHeidelberg University · DENational Academy of Sciences of Ukraine · UARiga Stradiņš University · LVUniversity of Latvia · LVUniversity of Southampton · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Near-triploid human tumors are frequently resistant to radio/chemotherapy through mechanisms that are unclear. We recently reported a tight association of male tumor triploidy with XXY karyotypes based on a meta-analysis of 15 tumor cohorts extracted from the Mitelman database. Here we provide a conceptual framework of the digyny-like origin of this karyotype based on the germline features of malignant tumors and adaptive capacity of digyny, which supports survival in adverse conditions. Studying how the recombinatorial reproduction via diploidy can be executed in primary cancer samples and HeLa cells after DNA damage, we report the first evidence that diploid and triploid cell sub-populations constitutively coexist and inter-change genomes via endoreduplicated polyploid cells generated through genotoxic challenge. We show that irradiated triploid HeLa cells can enter tripolar mitosis producing three diploid sub-subnuclei by segregation and pairwise fusions of whole genomes. Considering the upregulation of meiotic genes in tumors, we propose that the reconstructed diploid sub-cells can initiate pseudo-meiosis producing two "gametes" (diploid "maternal" and haploid "paternal") followed by digynic-like reconstitution of a triploid stemline that returns to mitotic cycling. This process ensures tumor survival and growth by (1) DNA repair and genetic variation, (2) protection against recessive lethal mutations using the third genome.

Indexed as

Chromosomes, Human, XChromosomes, Human, YKaryotypeNeoplastic Stem CellsTriploidyGerm CellsHeLa CellsHumansMaleMeiosisModels, GeneticNeoplasmsSpindle ApparatusTumor Cells, Culturedchemoresistancedigynynear-triploid cancerpedogamypolynuclear cancer cellsradioresistancereprogrammingtripolar mitosistumor blastomeres

Identifiers

PMID31331093
PMCPMC6678365
OpenAlexW2962677080

What Socratic 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 Socratic graph.