CD133 mRNA data was expressed as means ± SD, and statistical analysis was carried out using Student’s t test. Relative evaluations of CD133 mRNA level with several clinicopathological data were made by Spearman’s rho analysis. The Kaplan-Meier method was used to estimate survival as a function of time, and survival differences were analyzed

by Log-rank test. The Cox regression model was used for multivariate analysis of prognostic factors. In all of the tests, a P value less than 0.05 was considered to be statistically significant. Results CD133 protein expression in primary lesion Particles sharing brown color indicated to CD133 protein expression occurred in some parts of gland parietes, cellular membrane surface of some tumor cells and some epithelium in primary lesion, in which CD133 positive particles mainly located in some parts of tumor cells in the mucosa and the submucosa

layers Androgen Receptor activity inhibition (Figure 1C and 1D). Some CD133 positive cells were identified in the wall of crypts and in the cancerous emboli in vessel-like structures in primary lesion (Figure 1E and 1F). No positive staining was seen in NCGT as control subgroup (Figure 1B), which positivity rate of CD133 (0%) was significantly lower than that in cancerous find more subgroup (29.3%, 29 cases/99 cases, P = 0.000). Figure 1 Morphological observation on the tumor cells with CD133 protein and Ki-67 immunostainings in primary lesion. Note: A showed HE staining for GC tissue (×200). B showed CD133 immunostaining for NCGT (×200). C (×200) and D (×400) showed CD133 immunostaining for GC tissue. E (×200) and F (×400) showed tumor cells with CD133 positivity in the cancerous emboli in vessel-like structure. G (×200) and H (×200) showed the higher positive and the lower positive expressions of Ki-67 immunostaining (×200) respectively. Selleckchem PRIMA-1MET Correlation of CD133 protein expression with clinicopathological parameters CD133 expression was significantly correlated with tumor

diameter of > 5 cm (P = 0.041), severer lymph node metastasis (P = 0.017), later TNM stage (P = 0.044), occurrences of lymphatic vessel infiltration (P = 0.000) and vascular infiltration (P = 0.000) (Table 1). Furthermore, with the increase of invasion depth of tumor, the Baf-A1 clinical trial expressive rate of CD133 raised obviously, but no statistical significance. However, further stratified analysis revealed that the expressive rate of CD133 in subgroup of T3-T4 (6.06%, 6 cases/99 cases) was significantly higher than that in subgroup of T1-T2 (23.23%, 23 cases/99 cases, P = 0.038). The multivariate evaluation by Logistic analysis demonstrated that invasion depth (P = 0.011), lymph node metastasis (P = 0.043) and TNM stage (P = 0.049) were the independent risk factors for CD133 protein expression respectively (Table 2).