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September 10, 2025Zeitschrift für GastroenterologieOpen Access

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

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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.

Implication

Blocking RAS-pathway in pancreatic cancer may enhance mitochondrial changes, suggesting new therapy options.

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.

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Cite This Study

Hafner et al. (2025) studied this question.

synapsesocial.com/papers/68c193fb9b7b07f3a061847e https://doi.org/10.1055/s-0045-1810960

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Implication

Blocking RAS-pathway in pancreatic cancer may enhance mitochondrial changes, suggesting new therapy options.

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

Key Points

Implication

Abstract

Discussion

Cite This Study

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

Key Points

Implication

Abstract

Discussion

Cite This Study

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