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Updated: May 6, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
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Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

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Killing tumors by keeping ras and PI3' kinase apart

Tina L Yuan1, Frank McCormick

  • 1Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94158, USA.

Cancer Cell
|November 16, 2013
PubMed

Insights

KRAS-driven lung cancers depend on the interaction between Ras proteins and p110 catalytic subunits for full Phosphoinositide 3-kinase (PI3K) activation and tumor growth. This interaction is crucial for maintaining cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Ras proteins are key regulators of cell signaling pathways, including Phosphoinositide 3-kinase (PI3K) activation.
  • The precise timing and location of Ras-mediated PI3K activation remain incompletely understood.
  • KRAS mutations are common drivers in various cancers, particularly lung cancer.

Purpose of the Study:

  • To investigate the specific role of the Ras-p110 interaction in KRAS-driven lung cancer.
  • To determine when and where this interaction is essential for tumor maintenance and PI3K pathway activation.

Main Methods:

  • The study likely employed molecular biology techniques to assess protein-protein interactions.
  • Investigated the impact of disrupting the Ras-p110 interaction on cancer cell signaling and tumor growth in preclinical models.

Main Results:

  • Castellano and colleagues identified a critical requirement for the Ras-p110α interaction in KRAS-driven lung cancers.
  • This interaction is essential for the full activation of the PI3K pathway.
  • Disruption of this interaction led to impaired tumor maintenance.

Conclusions:

  • The Ras-p110α interaction is a key event for sustaining KRAS-driven lung tumorigenesis.
  • Targeting this specific interaction could represent a novel therapeutic strategy for KRAS-mutant lung cancers.

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