KRAS Inhibitor-Induced Cancer Cell Death Enhances Sensitivity to Immune-Mediated Bystander Killing of Drug-Resistant Subclones.

doi:10.1158/0008-5472.CAN-25-5693

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Article

KRAS Inhibitor-Induced Cancer Cell Death Enhances Sensitivity to Immune-Mediated Bystander Killing of Drug-Resistant Subclones.

Cancer research - 2 Sept 2026

Tomaschko Mona, Ng KangBo, Moore Christopher, Pillsbury Claire E, Rana Sareena, Campbell James, Mukherjee Saptaparna, Mikolajczak Anna, Anastasiou Panayiotis, de Castro Andrea, Alonso de la Vega Alicia, de Carné Trécesson Sophie, Goehring Nathan W, Molina-Arcas Miriam, Downward Julian

Abstract excerpt

The clinical benefit of therapies targeting the KRAS G12C mutation is substantially limited by the development of resistance through multiple mechanisms. Therefore, to achieve lasting benefit with these therapies, effective strategies to tackle the evolution of drug resistance are required. To investigate this, we developed a preclinical model that mimics the development of resistance to KRAS G12C inhibitors...

Read the complete abstract on PubMed

Topics

Drug Resistance, Neoplasm
Animals
Humans
Proto-Oncogene Proteins p21(ras)

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Mice

Cell Line, Tumor

Bystander Effect

Cell Death

Neoplasms

Protein Tyrosine Phosphatase, Non-Receptor Type 11

Immune Checkpoint Inhibitors

Xenograft Model Antitumor Assays

Programmed Cell Death 1 Receptor

Mutation

Oncogene Protein p21(ras)

Source

Open in PubMed Open full text

Identifiers

PMID: 42258763
DOI: 10.1158/0008-5472.CAN-25-5693
PMCID: PMC13535323

Genes

KRAS

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 24 Oct 2026.

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