What question did this study set out to answer?

Evaluate the impact of KRASG12D inhibition on immune checkpoint expression in lung cancer and its implications for treatment.

Abstract B029: Immune checkpoint mediated resistance to KRASG12D inhibition

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Demonstrates reshaping of the tumor microenvironment in KRASG12D-driven lung cancer, indicating therapeutic strategies to enhance cancer treatment.

Evaluate the impact of KRASG12D inhibition on immune checkpoint expression in lung cancer and its implications for treatment.
Used KRASG12D genetically engineered mouse model.
Administered pan-RAS inhibitor RMC-7977 for 5 days.
Conducted single-cell RNA sequencing to assess immune cell changes.
Tested co-targeted therapy with RMC-7977 and anti-PD-L1.
RMC-7977 increased PD-L1 expression in neutrophils by 36% without affecting abundance.
Co-targeted therapy showed reduced neutrophil abundance but no PD-L1 percentage change.
Genetic inhibition combined with anti-PD-L1 significantly extended survival.
Pharmacological inhibition did not show similar survival benefits, indicating distinct resistance mechanisms.

Khairkhah et al. (2026) studied this question.

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Demonstrates reshaping of the tumor microenvironment in KRASG12D-driven lung cancer, indicating therapeutic strategies to enhance cancer treatment.