Several studies have shown the interaction between OPN and VEGF in the metastatic process and the existing/acquired resistance to CTs.11,12,15 Researchers reported a potential relationship between proliferation, tumorigenicity and level of OPN expression in cell line studies.4 In our study, we also found positive OPN expression in all patients tissue samples. Similar to the literature reports, strong OPN expression was identified in 25/30 (83.4%) of the cases. Although an important role has been shown for OPN in regulating chemotherapeutic drug resistance through increased drug transporter expression, no relationship was observed between OPN and response to treatment in our study. Long-term treatment with cytotoxic drugs may further upregulate OPN release from tumor cells. Therefore, researchers suggested that OPN could be a therapeutic target for cancer treatment and avoid drug resistance. In recent studies, OPN knockdown has been shown to increase the activity of CT drugs and inhibit p-glycoprotein expression. The researchers also found that the levels of OPN could be increased, which were antagonized by the addition of various chemical agents in PI3K/AKT pathway, during endogenous secretion of OPN in the prostate cancer cells line.4,16,17 Most of the studies which have demonstrated findings associated with resistance to CTs are mainly cell culture studies rather than definitive clinical studies. Hence, we focused on the OPN expression level as a possible marker of drug resistance. However, our results indicate no relationship between OPN and response to TBR while a statistically significant difference is seen in terms of increased OPN overexpression with low GS in contrast to the findings of some previous studies.18