More byproducts of oxidative stress in tumor cells and slower tumor progression. Similar prognostic role of GSTT1 active genotype has also been found in osteosarcoma. The question arises whether any of the drugs used in the therapy of TCC patients represents a GSTT1 substrate. 
Diedrich et al. showed that GSTT1 may be considered as a relevant factor for chemotherapy of glioblastomas. Although, there are no data on the role of GSTT1 in the inactivation of drugs in MVAC and GC/Cis protocols, at least two of them exert their mechanism of action through reactive oxygen species generation as well as apoptotic pathway activation. In our study further stratification of patients according to chemotherapy treatment did not show significant effect of GSTT1 polymorphism on survival rate. Therefore, it may be concluded that GSTT1 genotype has more influence on tumor progression by altering its redox balance then influencing the metabolism of free radicals produced by anticancer drugs. The role of GSTP1 polymorphism in chemotherapy resistance has been unambiguously documented in vast majority of both in vivo and in vitro studies. Cisplatin and doxorubicin are proven substrates for GSTP1, with GSTP1 Ile as a variant with more affinity. OSCC metastasizes primarily via the lymphatic system. In patients with OSCC, the presence of lymph node metastases is widely accepted as a major prognostic factor and is associated with higher recurrence rates and an approximately 50% reduction in overall survival.However, the mechanisms by which OSCC metastasizes to lymph nodes have been studied only very recently. Previous study reported that overexpression of angiopoietin-2, which has been implicated in lymphatic vessel development, was closely associated with angiogenesis and lymph node metastasis in OSCC. Vascular endothelial growth factor receptor-3 is one of the first lymphatic endothelialcell-specific cell surface molecules involved in regulation of lymphangiogenesis, and might have crucial roles in amplification of pathological AbMole BI-9564 lymphangiogenesis and angiogenesis. However, whether altered expression of Ang-2 and VEGFR-3 affects lymphangiogenesis and survival of OSCC is not known. To better understand the functional contribution of Ang-2 and VEGFR-3 to lymphangiogenesis and progress of OSCC, we used a double-labeling immunohistochemical staining of CD-34/D2-40 in blood vessels and lymphatic vessels of tumor specimens for determination of microvessel density and lymphatic vessel density among 112 cases. Moreover, in these tumor specimens, we also performed immunohistochemical staining of VEGFR-3, a major regulator of lymphangiogenesis, to investigate the correlations between Ang-2 and VEGFR-3 expression and tumor lymphangiogenesis and progress and thereby reveal the role of Ang-2 and VEGFR-3 in lymphatic metastasis and clinical survival in OSCC patients. The current study showed that high expression of Ang-2 individually, or in combination with VEGFR-3, was significantly associated with survival or increased risk for overall death of OSCC patients. The study is the first to demonstrate that expression of Ang-2 and VEGFR-3 could serve as prognostic markers for survival of OSCC patients. Such a biomarker might potentially be used to optimize OSCC patient stratification for personalized treatment and improved survival. However, how the overexpression of these two genes contributes to cancer progression/prognosis is not fully clear. Several mechanisms have been postulated. Lymphangiogenesis in tumor probably is mainly AbMole Neosperidin-dihydrochalcone responsible for such prognosis since both genes play important roles in regulation of lymphangiogenesis.