Evidence map›Paper›PMID 26703575›Full record

ReviewInternational journal of molecular sciences2015

Tissue Regeneration in the Chronically Inflamed Tumor Environment: Implications for Cell Fusion Driven Tumor Progression and Therapy Resistant Tumor Hybrid Cells.

Thomas Dittmar, Kurt S Zänker

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. The authors respond to feedback onFrontiers in oncology · 2026
    Article
  2. Article
  3. Review
  4. Mapping cell-cell fusion at single-cell resolution.bioRxiv : the preprint server for biology · 2025
    Article
  5. Review
  6. Intrinsic signalling factors associated with cancer cell-cell fusion.Cell communication and signaling : CCS · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Kinins in Glioblastoma Microenvironment.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2019
    Article
  15. Article
  16. Review
  17. Tumor Microenvironment and Cell Fusion.BioMed research international · 2019
    Review
  18. Circulating Hybrid Cells Join the Fray of Circulating Cellular Biomarkers.Cellular and molecular gastroenterology and hepatology · 2019
    Review
  19. Article
  20. 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 at 1 institution in 1 country.

Thomas DittmarInstitute of Immunology & Experimental Oncology, Center for Biomedical Education and Research (ZBAF), University of Witten/Herdecke, Witten 58453, Germany. thomas.dittmar@uni-wh.de.
Kurt S ZänkerInstitute of Immunology & Experimental Oncology, Center for Biomedical Education and Research (ZBAF), University of Witten/Herdecke, Witten 58453, Germany. kurt.zaenker@uni-wh.de.
Witten/Herdecke University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biological phenomenon of cell fusion in a cancer context is still a matter of controversial debates. Even though a plethora of in vitro and in vivo data have been published in the past decades the ultimate proof that tumor hybrid cells could originate in (human) cancers and could contribute to the progression of the disease is still missing, suggesting that the cell fusion hypothesis is rather fiction than fact. However, is the lack of this ultimate proof a valid argument against this hypothesis, particularly if one has to consider that appropriate markers do not (yet) exist, thus making it virtually impossible to identify a human tumor cell clearly as a tumor hybrid cell. In the present review, we will summarize the evidence supporting the cell fusion in cancer concept. Moreover, we will refine the cell fusion hypothesis by providing evidence that cell fusion is a potent inducer of aneuploidy, genomic instability and, most likely, even chromothripsis, suggesting that cell fusion, like mutations and aneuploidy, might be an inducer of a mutator phenotype. Finally, we will show that "accidental" tissue repair processes during cancer therapy could lead to the origin of therapy resistant cancer hybrid stem cells.

Indexed as

Clonal EvolutionTumor MicroenvironmentAnimalsCell FusionGenomic InstabilityHumansHybrid CellsNeoplasmsRegenerationaneuploidycancercell fusionchromothripsisgenomic instabilitymutationsmutator phenotypetissue regeneration

Identifiers

PMID26703575
PMCPMC4691180
OpenAlexW2201530851

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.