Evidence map›Paper›PMID 23825115›Full record

ArticleJournal of the Royal Society, Interface2013

Minimizing the risk of cancer: tissue architecture and cellular replication limits.

Ignacio A Rodriguez-Brenes, Dominik Wodarz, Natalia L Komarova

Abstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
  2. Review
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  4. Differentiation of leukemic blasts is not completely blocked in acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Toward an evolutionary model of cancer: Considering the mechanisms that govern the fate of somatic mutations.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Preventing clonal evolutionary processes in cancer: Insights from mathematical models.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. Article
  19. 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

3 authors.

Ignacio A Rodriguez-BrenesDepartment of Mathematics, University of California Irvine, Irvine, CA, USA. iarodrig@uci.edu
Dominik Wodarz
Natalia L Komarova

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Normal somatic cells are capable of only a limited number of divisions, which prevents unlimited cell proliferation and the onset of tumours. Cancer cells find ways to circumvent this obstacle, typically by expressing the enzyme telomerase and less often by alternative recombination strategies. Given this fundamental link between cellular replication limits and cancer, it is important to understand how a tissue's architecture affects the replicative capacity of a cell population. We define this as the average number of remaining divisions at equilibrium. The lower the replication capacity, the lower the chances to escape the replication limit during abnormal growth when a tumour develops. In this paper, we examine how the replication capacity is influenced by defining characteristics of cell lineages, such as the number of intermediate cell compartments, self-renewal capability of cells and division rates. We describe an optimal tissue architecture that minimizes the replication capacity of dividing cells and thus the risk of cancer. Interestingly, some of the features that define an optimal tissue architecture have been documented in a variety of tissues, suggesting that they may have evolved as a cancer-protecting strategy in multicellular organisms.

Indexed as

Cell DivisionGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticModels, BiologicalAnimalsHumansNeoplasm ProteinsNeoplasmsRisk FactorsTelomeraseNeoplasm ProteinsTelomerasecancercell lineagestelomeres

Identifiers

PMID23825115
PMCPMC3730689

What OpenQuestion holds

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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.