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
Summary
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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