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September 10, 2025Open Access

Vertical RAS-pathway inhibition in pancreatic cancer drives therapeutically exploitable mitochondrial alterations

Key Points

Therapeutically exploitable mitochondrial alterations arise from RAS-pathway inhibition in pancreatic cancer.
Inhibition of KRAS can alter metabolic rewiring, and dual targeting of SHP2 and MAPK may prove beneficial.
The approach involves targeting metabolic adaptations that drive resistance to current therapies in PDAC.
These findings highlight the need for further exploration into SHP2/MAPK inhibition's impact on cancer resistance.

Abstract

Oncogenic KRAS mutations drive metabolic rewiring in pancreatic ductal adenocarcinoma (PDAC). Src-homology 2 domain-containing phosphatase 2 (SHP2) is essential for full KRAS activity and promising dual SHP2/mitogen-activated protein kinase (MAPK) inhibition is currently being tested in clinical trials. Exploitable metabolic adaptations may contribute to an invariably evolving resistance.

Vertical RAS-pathway inhibition in pancreatic cancer drives therapeutically exploitable mitochondrial alterations

Key Points

Abstract

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