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This research aims to understand the effects of targeted KRASG12V degradation on lung adenocarcinoma and its resistance mechanisms.

Targeted KRASG12V Degradation in vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis

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This research aims to understand the effects of targeted KRASG12V degradation on lung adenocarcinoma and its resistance mechanisms.
Developed a preclinical LUAD mouse model
Conducted transcriptional, histological, and immunophenotypic analyses
Evaluated the tumor microenvironment remodeling during treatment
Targeted KRAS degradation resulted in significant tumor regression due to cancer cell-autonomous mechanisms.
Disease relapse occurred during prolonged PROTAC treatment primarily from proteolysis machinery dysregulation.
Resistance mechanisms identified were distinct from those associated with traditional KRAS inhibition.

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Preclinical trial demonstrates targeted KRAS degradation triggers tumor regression in lung adenocarcinoma, suggesting new treatment strategies.

Martín et al. (2026) studied this question.

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Preclinical trial demonstrates targeted KRAS degradation triggers tumor regression in lung adenocarcinoma, suggesting new treatment strategies.