Evidence map›Paper›PMID 28432052›Full record

ReviewCancer research2017

Genomic Instability in Cancer: Teetering on the Limit of Tolerance.

Noemi Andor, Carlo C Maley, Hanlee P Ji

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

145 citing papers in PubMed, 244 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Assessment of the Type and Degree of Genomic Instability in Gliomas.International journal of molecular sciences · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Role of PLK4 inhibition in cancer therapy.Cancer metastasis reviews · 2025
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

85 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 2 countries.

Noemi AndorDivision of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, California.
Carlo C MaleyBiodesign Center for Personalized Diagnostics and School of Life Sciences, Arizona State University, Tempe, Arizona.
Hanlee P JiDivision of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, California. genomics_ji@stanford.edu.
Cancer Research UK · GBPalo Alto University · USStanford Medicine · US

Funding

WHOLE YEAST GENOME TRANSCRIPTIONAL AND FUNCTIONAL GENE MAPS--A FEASIBILITY STUDYP01HG000205 · NHGRI · STANFORD UNIVERSITY · PI DAVIS, RONALD WAYNE, HOWE, ROGER THOMAS · 1990 to 2016
$120.9M
PHYLOGENIES of Barrett's Esophagus LineagesP01CA091955 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GRADY, WILLIAM MALLORY · 2002 to 2019
$35.9M
Modeling Neoplastic Progression in Barrett's Esophagus - Renewal -2R01CA140657 · NCI · WISTAR INSTITUTE · PI Carlo Maley · 2009 to 2026
$5.0M
Stem Cells, Differentiation and Therapeutic Resistance in AMLR01CA149566 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CARROLL, MARTIN · 2011 to 2015
$3.0M
Application of Evolutionary Principles to Maintain Cancer Control (PQ21)R01CA170595 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI GATENBY, ROBERT A · 2012 to 2015
$2.1M
(PQC3) Genomic Diversity and Microenvironment as Drivers of Metastasis in DCISR01CA185138 · NCI · DUKE UNIVERSITY · PI HWANG, E.SHELLEY, MALEY, CARLO · 2014 to 2017
$2.0M
A clone's genomic stability as biomarker of its DNA-damage resilienceK99CA215256 · NCI · STANFORD UNIVERSITY · PI ANDOR, NOEMI · 2017 to 2018
$333k
NCI NIH HHS K99 CA215256NCI NIH HHS P01 CA091955NCI NIH HHS R01 CA140657NCI NIH HHS R01 CA149566NCI NIH HHS R01 CA170595NCI NIH HHS R01 CA185138NHGRI NIH HHS P01 HG000205
6 · The paper itself

Abstract

Cancer genomic instability contributes to the phenomenon of intratumoral genetic heterogeneity, provides the genetic diversity required for natural selection, and enables the extensive phenotypic diversity that is frequently observed among patients. Genomic instability has previously been associated with poor prognosis. However, we have evidence that for solid tumors of epithelial origin, extreme levels of genomic instability, where more than 75% of the genome is subject to somatic copy number alterations, are associated with a potentially better prognosis compared with intermediate levels under this threshold. This has been observed in clonal subpopulations of larger size, especially when genomic instability is shared among a limited number of clones. We hypothesize that cancers with extreme levels of genomic instability may be teetering on the brink of a threshold where so much of their genome is adversely altered that cells rarely replicate successfully. Another possibility is that tumors with high levels of genomic instability are more immunogenic than other cancers with a less extensive burden of genetic aberrations. Regardless of the exact mechanism, but hinging on our ability to quantify how a tumor's burden of genetic aberrations is distributed among coexisting clones, genomic instability has important therapeutic implications. Herein, we explore the possibility that a high genomic instability could be the basis for a tumor's sensitivity to DNA-damaging therapies. We primarily focus on studies of epithelial-derived solid tumors.

Indexed as

Genetic HeterogeneityGenome, HumanDNA Copy Number VariationsDNA DamageGenomic InstabilityHumansNeoplasmsPrognosis

Identifiers

PMID28432052
PMCPMC5413432
OpenAlexW2606156013

What OpenQuestion holds

Textmetadata
LicenceTDM
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.