Evidence map›Paper›PMID 33638275›Full record

ArticleFEBS open bio2021

Dosage strategies for delaying resistance emergence in heterogeneous tumors.

Vahideh Vakil, Wade Trappe

Abstract read
In one paragraph

Article in FEBS open bio, 2021. 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. Review
  2. Article
  3. Article
  4. 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

2 authors.

Vahideh VakilWireless Information Network Laboratory (WINLAB), Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.ORCID 0000-0003-0761-9570
Wade TrappeWireless Information Network Laboratory (WINLAB), Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance in cancer treatments is a frequent problem that, when it arises, leads to failure in therapeutic efforts. Tumor heterogeneity is the primary reason for resistance emergence and a precise treatment design that takes heterogeneity into account is required to postpone the rise of resistant subpopulations in the tumor environment. In this paper, we present a mathematical framework involving clonal evolution modeling of drug-sensitive and drug-resistant clones. Using our framework, we examine delaying the rise of resistance in heterogeneous tumors during control phase of therapy in a containment treatment approach. We apply pharmacokinetic/pharmacodynamic (PKPD) modeling and show that dosage strategies can be designed to control the resistant subpopulation. Our results show that the drug dosage and schedule determine the relative dynamics of sensitive and resistant clones. We present an optimal control problem that finds the dosing strategy that maximizes the delay in resistance emergence for a given period of containment treatment.

Indexed as

Antineoplastic AgentsBiomarkers, PharmacologicalDrug Dosage CalculationsDrug Resistance, NeoplasmHumansModels, TheoreticalNeoplasmsPhenotypeAntineoplastic AgentsBiomarkers, Pharmacologicalclonal evolutioncontainmentdosage strategydrug resistanceoptimal control

Identifiers

PMID33638275
PMCPMC8091820

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.