Evidence map›Paper›PMID 38289469›Full record

ArticleTheory in biosciences = Theorie in den Biowissenschaften2024

Modeling stress-induced responses: plasticity in continuous state space and gradual clonal evolution.

Anuraag Bukkuri

Abstract read
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In one paragraph

Article in Theory in biosciences = Theorie in den Biowissenschaften, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. 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

1 author.

Anuraag BukkuriCancer Biology and Evolution Program and Department of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, USA. anuraag.bukkuri@moffitt.org.

Funding

Crafoordska Stiftelsen 20220633National Science Foundation Graduate Research Fellowship Program 1746051Royal Swedish Academy of Sciences Stiftelsen GS Magnusons fond MG2022-0019Stiftelsen Längmanska Kulturfonden BA22-0753
6 · The paper itself

Abstract

Mathematical models of cancer and bacterial evolution have generally stemmed from a gene-centric framework, assuming clonal evolution via acquisition of resistance-conferring mutations and selection of their corresponding subpopulations. More recently, the role of phenotypic plasticity has been recognized and models accounting for phenotypic switching between discrete cell states (e.g., epithelial and mesenchymal) have been developed. However, seldom do models incorporate both plasticity and mutationally driven resistance, particularly when the state space is continuous and resistance evolves in a continuous fashion. In this paper, we develop a framework to model plastic and mutational mechanisms of acquiring resistance in a continuous gradual fashion. We use this framework to examine ways in which cancer and bacterial populations can respond to stress and consider implications for therapeutic strategies. Although we primarily discuss our framework in the context of cancer and bacteria, it applies broadly to any system capable of evolving via plasticity and genetic evolution.

Indexed as

NeoplasmsAdaptation, PhysiologicalBiological EvolutionClonal EvolutionEvolution, MolecularHumansMutationPhenotypeBacterial evolutionCancer evolutionEco-evolutionary dynamicsPlasticityTherapeutic resistance

Identifiers

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.