Abstract

INTRODUCTION. Most anticancer drugs kill tumor cells by inducing apoptotic cell death [1]. Enhancement of this apoptosis-inducing activity or overcoming tumor's resistance to apoptosis induction by anticancer drugs could bring a significant improvement in cancer therapy. Cytokines and tissue-specific factors mediate communication between tumor cells and surrounding stromal cells [2,3]. These agents are believed also to modulate tumor cells' response to anti-cancer drugs. This phenomenon is predominantly acute in metastatic prostate cancer, where most patients with metastatic disease survive less than 3 years. The purpose of this study was to examine the impact of stromal cells (fibroblast and endothelial cells)-induced cytokines on the response of tumor cells to anticancer drugs.

Highlights

  • Most anticancer drugs kill tumor cells by inducing apoptotic cell death [1]

  • Cytotoxicity of taxol was least affected compared to COL-3

  • Cytotoxicity and druginduced apoptosis was higher in the presence of 3T3 cells, human lung and skin fibroblast cocultures but was unaffected in prostate stromal cells and microvessel endothelial cells

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Summary

Introduction

Most anticancer drugs kill tumor cells by inducing apoptotic cell death [1]. Enhancement of this apoptosis-inducing activity or overcoming tumor's resistance to apoptosis induction by anticancer drugs could bring a significant improvement in cancer therapy. Cytokines and tissue-specific factors mediate communication between tumor cells and surrounding stromal cells [2,3]. These agents are believed to modulate tumor cells' response to anti-cancer drugs. This phenomenon is predominantly acute in metastatic prostate cancer, where most patients with metastatic disease survive less than 3 years. The purpose of this study was to examine the impact of stromal cells (fibroblast and endothelial cells)-induced cytokines on the response of tumor cells to anticancer drugs

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