Evidence map›Paper›PMID 30048718›Full record

ArticleJournal of theoretical biology2018

Capitalizing on competition: An evolutionary model of competitive release in metastatic castration resistant prostate cancer treatment.

Jeffrey West, Yongqian Ma, Paul K Newton

Abstract read
In one paragraph

Article in Journal of theoretical biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed.

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  15. Tumour Growth Mechanisms Determine Effectiveness of Adaptive Therapy in Glandular Tumours.Interdisciplinary sciences, computational life sciences · 2024
    Article
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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.

Jeffrey WestIntegrated Mathematical Oncology Department, H. Lee Moffitt Cancer Center & Research Institute, 12902 Magnolia Drive, SRB 4 Rm 24000H Tampa, Florida, 33612, USA. Electronic address: jeffrey.west@moffitt.org.
Yongqian MaDepartment of Physics and Astronomy, University of Southern California, Los Angeles, CA, USA. Electronic address: yongqiam@usc.edu.
Paul K NewtonDepartment of Aerospace & Mechanical Engineering and Mathematics, University of Southern California, Los Angeles, CA, 90089-1234, USA; Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90089-1234, USA. Electronic address: newton@usc.edu.

Funding

"Research Supplement to Promote Diversity in Health-Related Research", as part of Moffitt PS-OC, "Cancer as a Complex adaptive System"U54CA193489 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDERSON, ALEXANDER ROBERTSON ALLAN, GATENBY, ROBERT A · 2015 to 2020
$12.5M
NCI NIH HHS U54 CA193489
6 · The paper itself

Abstract

The development of chemotherapeutic resistance resulting in tumor relapse is largely the consequence of the mechanism of competitive release of pre-existing resistant tumor cells selected for regrowth after chemotherapeutic agents attack the previously dominant chemo-sensitive population. We introduce a prisoner's dilemma game theoretic mathematical model based on the replicator of three competing cell populations: healthy (cooperators), sensitive (defectors), and resistant (defectors) cells. The model is shown to recapitulate prostate-specific antigen measurement data from three clinical trials for metastatic castration-resistant prostate cancer patients treated with 1) prednisone, 2) mitoxantrone and prednisone and 3) docetaxel and prednisone. Continuous maximum tolerated dose schedules reduce the sensitive cell population, initially shrinking tumor burden, but subsequently "release" the resistant cells from competition to re-populate and re-grow the tumor in a resistant form. The evolutionary model allows us to quantify responses to conventional (continuous) therapeutic strategies as well as to design adaptive strategies.These novel adaptive strategies are robust to small perturbations in timing and extend simulated time to relapse from continuous therapy administration.

Indexed as

Models, BiologicalProstatic Neoplasms, Castration-ResistantAntineoplastic Combined Chemotherapy ProtocolsDocetaxelHumansMaleMitoxantronePrednisoneDocetaxelMitoxantronePrednisoneAdaptive controlAdaptive therapyChemotherapeutic resistanceCompetitive releaseEvolutionary dynamicsEvolutionary game theoryMetastatic castration-resistant prostate cancerPrisoner’s dilemmaReplicator dynamics

Identifiers

PMID30048718
PMCPMC7519622

What OpenQuestion holds

Textmetadata
LicenceTDM
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.