Evidence map›Paper›PMID 33577569›Full record

ArticlePLoS computational biology2021

The impact of phenotypic heterogeneity of tumour cells on treatment and relapse dynamics.

Michael Raatz, Saumil Shah, Guranda Chitadze, Monika Brüggemann, Arne Traulsen

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. [Explainable artificial intelligence in pathology].Pathologie (Heidelberg, Germany) · 2024
    Review
  7. Article
  8. Article
  9. 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

5 authors at 3 institutions in 2 countries.

Michael RaatzDepartment of Evolutionary Theory, Max Planck Institute for Evolutionary Biology, Plön, Germany.ORCID 0000-0002-6968-6560
Saumil ShahDepartment of Evolutionary Theory, Max Planck Institute for Evolutionary Biology, Plön, Germany.ORCID 0000-0003-1642-4687
Guranda ChitadzeDepartment of Hematology, University Hospital Schleswig-Holstein, Kiel, Germany.
Monika BrüggemannDepartment of Hematology, University Hospital Schleswig-Holstein, Kiel, Germany.
Arne TraulsenDepartment of Evolutionary Theory, Max Planck Institute for Evolutionary Biology, Plön, Germany.ORCID 0000-0002-0669-5267
Max Planck Institute for Evolutionary Biology · DEUniversity Hospital Schleswig-Holstein · DEIndian Institute of Science Education and Research Pune · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intratumour heterogeneity is increasingly recognized as a frequent problem for cancer treatment as it allows for the evolution of resistance against treatment. While cancer genotyping becomes more and more established and allows to determine the genetic heterogeneity, less is known about the phenotypic heterogeneity among cancer cells. We investigate how phenotypic differences can impact the efficiency of therapy options that select on this diversity, compared to therapy options that are independent of the phenotype. We employ the ecological concept of trait distributions and characterize the cancer cell population as a collection of subpopulations that differ in their growth rate. We show in a deterministic model that growth rate-dependent treatment types alter the trait distribution of the cell population, resulting in a delayed relapse compared to a growth rate-independent treatment. Whether the cancer cell population goes extinct or relapse occurs is determined by stochastic dynamics, which we investigate using a stochastic model. Again, we find that relapse is delayed for the growth rate-dependent treatment type, albeit an increased relapse probability, suggesting that slowly growing subpopulations are shielded from extinction. Sequential application of growth rate-dependent and growth rate-independent treatment types can largely increase treatment efficiency and delay relapse. Interestingly, even longer intervals between decisions to change the treatment type may achieve close-to-optimal efficiencies and relapse times. Monitoring patients at regular check-ups may thus provide the temporally resolved guidance to tailor treatments to the changing cancer cell trait distribution and allow clinicians to cope with this dynamic heterogeneity.

Indexed as

Neoplasm Recurrence, LocalAlgorithmsCell ProliferationComputer SimulationHumansImmunotherapyModels, GeneticModels, StatisticalNeoplasmsPhenotypePopulation DynamicsStochastic ProcessesTreatment Outcome

Identifiers

PMID33577569
PMCPMC7906468
OpenAlexW3128451090

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.