Evidence map›Paper›PMID 26195751›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Preventing clonal evolutionary processes in cancer: Insights from mathematical models.

Ignacio A Rodriguez-Brenes, Dominik Wodarz

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Cancer Stem Cells: Current Challenges and Future Perspectives.Methods in molecular biology (Clifton, N.J.) · 2024
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  9. A population genetics perspective on the determinants of intra-tumor heterogeneity.Biochimica et biophysica acta. Reviews on cancer · 2017
    Review
  10. Article
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  12. In the light of evolution IX: Clonal reproduction: Alternatives to sex.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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.

Ignacio A Rodriguez-BrenesDepartment of Ecology and Evolutionary Biology, Ayala School of Biological Sciences, University of California, Irvine, CA 92697; Department of Mathematics, University of California, Irvine, CA 92697.
Dominik WodarzDepartment of Ecology and Evolutionary Biology, Ayala School of Biological Sciences, University of California, Irvine, CA 92697; Department of Mathematics, University of California, Irvine, CA 92697 dwodarz@uci.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clonal evolutionary processes can drive pathogenesis in human diseases, with cancer being a prominent example. To prevent or treat cancer, mechanisms that can potentially interfere with clonal evolutionary processes need to be understood better. Mathematical modeling is an important research tool that plays an ever-increasing role in cancer research. This paper discusses how mathematical models can be useful to gain insights into mechanisms that can prevent disease initiation, help analyze treatment responses, and aid in the design of treatment strategies to combat the emergence of drug-resistant cells. The discussion will be done in the context of specific examples. Among defense mechanisms, we explore how replicative limits and cellular senescence induced by telomere shortening can influence the emergence and evolution of tumors. Among treatment approaches, we consider the targeted treatment of chronic lymphocytic leukemia (CLL) with tyrosine kinase inhibitors. We illustrate how basic evolutionary mathematical models have the potential to make patient-specific predictions about disease and treatment outcome, and argue that evolutionary models could become important clinical tools in the field of personalized medicine.

Indexed as

Clonal EvolutionModels, BiologicalCell LineageCellular SenescenceHumansMutationNeoplasmsPrecancerous ConditionsStem CellsStochastic Processescancerclonal evolutionmathematical modelstargeted therapytelomeres

Identifiers

PMID26195751
PMCPMC4517241

What OpenQuestion holds

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Registered trials

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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.