Evidence map›Paper›PMID 42658196›Full record

ArticleeLife2026

Systematic analysis of network-driven adaptive resistance to CDK4/6 and oestrogen receptor inhibition using meta-dynamic network modelling.

Anthony Hart, Sung-Young Shin, Lan K Nguyen

Abstract read
In one paragraph

Article in eLife, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

3 authors.

Anthony HartDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Australia.ORCID https://orcid.org/0000-0003-1557-6515
Sung-Young ShinDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Australia.
Lan K NguyenDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Australia.ORCID https://orcid.org/0000-0003-4040-7705

Funding

Australian Government Research Training ProgramAustralian Research Council CE230100001Australian Research Council DP210103074National Breast Cancer Foundation IIRS-20-094Victorian Cancer Agency MCRF18026
6 · The paper itself

Abstract

Drug resistance inevitably emerges during the treatment of cancer by targeted therapy. Adaptive resistance is a major form of drug resistance, wherein the rewiring of protein signalling networks in response to drug perturbation allows drug-targeted protein activity to recover. This can occur in the continuous presence of the drug and enables cells to survive/grow. Simultaneously, molecular heterogeneity enables the selection of drug-resistant cancer clones that can survive an initial drug insult, proliferate, and eventually cause disease relapse. Despite their importance, the link between heterogeneity and adaptive resistance, specifically how heterogeneity influences protein signalling dynamics to drive adaptive resistance, remains poorly understood. Here, we have explored the relationship between heterogeneity, protein signalling dynamics, and adaptive resistance through the development of a novel modelling technique coined Meta Dynamic Network (MDN) modelling. We use MDN modelling to characterise how heterogeneity influences the drug-response signalling dynamics of the proteins that regulate early cell cycle progression and demonstrate that heterogeneity can robustly facilitate adaptive resistance associated dynamics for key cell cycle regulators. We determined the influence of heterogeneity at the level of both reaction coefficients and protein abundance and show that reaction coefficients are a much stronger driver of adaptive resistance. Owing to the mechanistic nature of the underpinning ordinary differential equation framework, we then identified a full spectrum of subnetworks capable of driving adaptive resistance dynamics in the key early cell cycle regulators. Finally, we show that single-cell dynamic data supports the validity of our MDN modelling technique and a comparison between our predicted resistance mechanisms and known CDK4/6 and oestrogen receptor inhibitor resistance mechanisms suggests MDN modelling can be deployed to robustly predict network-level resistance mechanisms for novel drugs and additional protein signalling networks.

Indexed as

Antineoplastic AgentsCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Drug Resistance, NeoplasmReceptors, EstrogenHumansModels, BiologicalSignal TransductionAntineoplastic AgentsCDK4 protein, humanCDK6 protein, humanCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Receptors, Estrogenadaptive resistancecancer biologyCDK4/6 inhibitioncomputational biologycomputational modellingheterogeneityhumanprotein signallingsystems biology

Identifiers

PMID42658196
PMCPMC13521565

What Socratic holds

Textmetadata
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 Socratic graph.