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Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids

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Treatment with Imatinib in NSCLC is associated with decrease of phosphorylated PDGFR-beta and VEGF expression,

G Vlahovic¹, Z N Rabbani, J E Herndon

¹Duke University Medical Center, P.O. Box 3335, Durham, NC 27710, USA. vlaho001@mc.duke.edu

British Journal of Cancer

|September 28, 2006

Summary

Imatinib treatment significantly reduced intratumoral interstitial fluid pressure (IFP) and tumor hypoxia by inhibiting phosphorylated platelet-derived growth factor receptor-beta (p-PDGFR-beta). This approach improves tumor oxygenation and may enhance treatment response in cancer patients.

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Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia

Published on: September 18, 2013

Area of Science:

Oncology
Pharmacology
Biomedical Engineering

Background:

Elevated intratumoral interstitial fluid pressure (IFP) and tumor hypoxia are linked to poor patient survival and treatment outcomes.
The precise relationship between IFP and tumor hypoxia remains unclear.
Preclinical data suggest that reducing IFP can enhance responses to cytotoxic therapies.

Purpose of the Study:

To investigate the effect of Imatinib, a p-PDGFR-beta inhibitor, on IFP and tumor hypoxia.
To determine if Imatinib downregulates VEGF expression and improves tumor oxygenation.
To establish a link between p-PDGFR-beta inhibition, IFP reduction, and improved tumor oxygenation.

Main Methods:

A549 human lung adenocarcinoma xenografts overexpressing PDGFR-beta were used in nude mice.
Animals were randomized to control or Imatinib treatment groups (50 mg kg(-1) for 4 days).
IFP was measured pre- and post-treatment. Tumor hypoxia was assessed using EF5 staining, and p-PDGFR-beta and VEGF levels were quantified via immunohistochemistry and image analysis.

Main Results:

Imatinib treatment significantly reduced p-PDGFR-beta, VEGF expression, and IFP in tumors.
Tumor oxygenation was significantly improved following Imatinib administration.
This study provides the first evidence that Imatinib improves tumor oxygenation and downregulates VEGF in p-PDGFR-beta-overexpressing tumors.

Conclusions:

Imatinib effectively reduces IFP in p-PDGFR-beta-overexpressing tumors.
Imatinib treatment enhances tumor oxygenation and downregulates VEGF.
Targeting p-PDGFR-beta with Imatinib presents a promising strategy for improving cancer treatment outcomes by addressing both IFP and hypoxia.