Evidence map›Paper›PMID 41076489›Full record

ArticleBritish journal of cancer2026

Modeling response to the KRAS-G12C inhibitor AZD4625 in KRAS

Joshua C Rosen, Pinjiang Cao, Nhu-An Pham, Matthew Waas, Quan Li, Katrina Hueniken, Mutian Wang, Roya Navab, Leanne Wybenga-Groot, Nikolina Radulovich and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 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

16 authors.

Joshua C RosenPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Pinjiang CaoPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Nhu-An PhamPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Matthew WaasPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Quan LiPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Katrina HuenikenPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Mutian WangPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Roya NavabPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Leanne Wybenga-GrootThe Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Nikolina RadulovichPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Michael NiedbalaAstraZeneca, Waltham, MA, USA.
Alex KoersAstraZeneca, Cambridge, UK.
Sarah RossAstraZeneca, Cambridge, UK.
Michael F MoranThe Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Adrian SacherPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada. Adrian.Sacher@uhn.ca.ORCID http://orcid.org/0000-0001-7865-2701
Ming-Sound TsaoPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada. ming.tsao@uhn.ca.ORCID http://orcid.org/0000-0002-9160-5405

Funding

Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada) FDN-148395Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada) The Canada Graduate Research Scholarship - Master's
6 · The paper itself

Abstract

backgroundKRAS

methodsWe studied short-term changes in signaling and mechanisms of primary resistance to AZD4625 in twelve KRAS

resultsSustained tumor regression in four (33%) PDXs was observed while the remaining eight models were intrinsically resistant to AZD4625. Organoid responses to AZD4625 were concordant with their derived PDXs. Acute AZD4625 exposure significantly decreased gene expression of the ERK1/2 negative regulator, DUSP6, in all models while protein MAPK and AKT/mTOR signals were downregulated more frequently in the AZD4625-sensitive than AZD4625-resistant cohorts. Analyzing PDX transcriptomes and proteomes identified mTOR signaling as a putative mechanism of primary resistance to AZD4625.

conclusionsOur findings confirm AZD4625 as a highly active KRAS

Indexed as

Adenocarcinoma of LungCarcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmLung NeoplasmsProto-Oncogene Proteins p21(ras)AnimalsCell Line, TumorFemaleHumansMiceMutationSignal TransductionXenograft Model Antitumor AssaysKRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID41076489
PMCPMC12765001

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.