Evidence map›Paper›PMID 33008067›Full record

ArticleGenes2020

Origins and Consequences of Chromosomal Instability: From Cellular Adaptation to Genome Chaos-Mediated System Survival.

Christine J Ye, Zachary Sharpe, Henry H Heng

Abstract read
In one paragraph

Article in Genes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Review
  2. Article
  3. Chromoplexy: A Pathway to Genomic Complexity and Cancer Development.International journal of molecular sciences · 2025
    Review
  4. Chromoplexy.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  5. Chromoanagenesis and Beyond: Catastrophic Events Shaping the Genome.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  6. The New Era of Cancer Cytogenetics and Cytogenomics.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  7. Tracking Karyotype Changes in Treatment-Induced Drug-Resistant Evolution.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Somatic mosaicism in the diseased brain.Molecular cytogenetics · 2022
    Review
  15. Review
  16. Article
  17. Life Entrapped in a Network of Atavistic Attractors: How to Find a Rescue.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Review
  20. Review
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

3 authors.

Christine J YeThe Division of Hematology/Oncology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Zachary SharpeCenter for Molecular Medicine and Genomics, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Henry H HengCenter for Molecular Medicine and Genomics, Wayne State University School of Medicine, Detroit, MI 48201, USA.ORCID 0000-0003-1475-9547

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

When discussing chromosomal instability, most of the literature focuses on the characterization of individual molecular mechanisms. These studies search for genomic and environmental causes and consequences of chromosomal instability in cancer, aiming to identify key triggering factors useful to control chromosomal instability and apply this knowledge in the clinic. Since cancer is a phenomenon of new system emergence from normal tissue driven by somatic evolution, such studies should be done in the context of new genome system emergence during evolution. In this perspective, both the origin and key outcome of chromosomal instability are examined using the genome theory of cancer evolution. Specifically, chromosomal instability was linked to a spectrum of genomic and non-genomic variants, from epigenetic alterations to drastic genome chaos. These highly diverse factors were then unified by the evolutionary mechanism of cancer. Following identification of the hidden link between cellular adaptation (positive and essential) and its trade-off (unavoidable and negative) of chromosomal instability, why chromosomal instability is the main player in the macro-cellular evolution of cancer is briefly discussed. Finally, new research directions are suggested, including searching for a common mechanism of evolutionary phase transition, establishing chromosomal instability as an evolutionary biomarker, validating the new two-phase evolutionary model of cancer, and applying such a model to improve clinical outcomes and to understand the genome-defined mechanism of organismal evolution.

Indexed as

Adaptation, PhysiologicalChromosomal InstabilityEvolution, MolecularGenomeAnimalsGenomic InstabilityGenomicsHumansNeoplasmschromosome instability (CIN)fuzzy inheritancegenome theorykaryotype codingtwo phases of cancer evolution

Identifiers

PMID33008067
PMCPMC7601827

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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.