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The Ras Gene02:38

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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
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Mutant KRAS promotes malignant pleural effusion formation.

Theodora Agalioti1, Anastasios D Giannou1, Anthi C Krontira1

  • 1Laboratory for Molecular Respiratory Carcinogenesis, Department of Physiology, Faculty of Medicine, University of Patras, 26504 Rio, Greece.

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|May 17, 2017
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Mutant KRAS drives malignant pleural effusion (MPE) by releasing CCL2, mobilizing myeloid cells. Targeting KRAS or CCL2 shows promise for treating MPE.

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Malignant pleural effusion (MPE) is a severe complication of metastatic cancer with poorly understood mechanisms.
  • KRAS mutations are implicated in various cancers, but their role in MPE pathogenesis is unclear.

Purpose of the Study:

  • To elucidate the mechanisms underlying MPE development.
  • To investigate the role of mutant KRAS in MPE induction.
  • To explore potential therapeutic strategies targeting KRAS or CCL2.

Main Methods:

  • Utilized a mouse model of MPE with pleural disseminated, mutant KRAS-bearing tumor cells.
  • Conducted splenectomy and splenocyte restoration experiments to assess myeloid cell mobilization.
  • Analyzed human MPE samples and cell lines for KRAS mutations using Sanger sequencing.
  • Evaluated the efficacy of a KRAS inhibitor (deltarasin) and anti-CCL2 antibody in the mouse model.

Main Results:

  • Mutant KRAS-bearing tumor cells upregulate and release CCL2, mobilizing myeloid cells from bone marrow to the pleural space via the spleen.
  • Splenectomy reduced MPE formation, while splenocyte restoration reversed this effect.
  • KRAS mutations were frequently detected in human MPE samples, though sometimes lost during automated sequencing analysis.
  • Both deltarasin and the anti-CCL2 antibody effectively reduced MPE in the experimental mouse model.

Conclusions:

  • Mutant KRAS is a key driver of MPE development through CCL2-mediated myeloid cell recruitment.
  • KRAS mutations are relevant in human MPE, necessitating careful sequencing analysis.
  • Targeting the KRAS-CCL2 axis offers a promising therapeutic avenue for malignant pleural effusion.