Evidence map›Paper›PMID 24511375›Full record

ArticleInterface focus2013

Mathematical models of immune-induced cancer dormancy and the emergence of immune evasion.

Kathleen P Wilkie, Philip Hahnfeldt

Abstract read
In one paragraph

Article in Interface focus, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Gaming the cancer-immunity cycle by synchronizing the dose schedules.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Mathematical modeling of tumor-immune cell interactions.Journal of theoretical biology · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Modeling putative therapeutic implications of exosome exchange between tumor and immune cells.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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.

Kathleen P WilkieCenter of Cancer Systems Biology, GRI, Saint Elizabeth's Medical Center , Tufts University School of Medicine , 736 Cambridge Street, CBR1, Boston, MA 02135 USA.
Philip HahnfeldtCenter of Cancer Systems Biology, GRI, Saint Elizabeth's Medical Center , Tufts University School of Medicine , 736 Cambridge Street, CBR1, Boston, MA 02135 USA.

Funding

Project 5 UC BerkleyU54CA149233 · NCI · STEWARD ST. ELIZABETH'S MEDICAL CENTER · PI HLATKY, LYNN · 2010 to 2014
$7.3M
NCI NIH HHS U54 CA149233
6 · The paper itself

Abstract

Cancer dormancy, a state in which cancer cells persist in a host without significant growth, is a natural forestallment of progression to manifest disease and is thus of great clinical interest. Experimental work in mice suggests that in immune-induced dormancy, the longer a cancer remains dormant in a host, the more resistant the cancer cells become to cytotoxic T-cell-mediated killing. In this work, mathematical models are used to analyse the possible causative mechanisms of cancer escape from immune-induced dormancy. Using a data-driven approach, both decaying efficacy in immune predation and immune recruitment are analysed with results suggesting that decline in recruitment is a stronger determinant of escape than increased resistance to predation. Using a mechanistic approach, the existence of an immune-resistant cancer cell subpopulation is considered, and the effects on cancer dormancy and potential immunoediting mechanisms of cancer escape are analysed and discussed. The immunoediting mechanism assumes that the immune system selectively prunes the cancer of immune-sensitive cells, which is shown to cause an initially heterogeneous population to become a more homogeneous, and more resistant, population. The fact that this selection may result in the appearance of decreasing efficacy in T-cell cytotoxic effect with time in dormancy is also demonstrated. This work suggests that through actions that temporarily delay cancer growth through the targeted removal of immune-sensitive subpopulations, the immune response may actually progress the cancer to a more aggressive state.

Indexed as

cancer dormancyimmunoeditingmathematical model

Identifiers

PMID24511375
PMCPMC3915830

What OpenQuestion holds

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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.