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Purpose To analyze the correlations between PD-L1 expression and clinicopathological factors and their prognostic values in esophageal squamous cell carcinoma (ESCC) patients.Methods PD-L1 expression in the primary tumors from 253 patients with ESCC was evaluated using tissue microarray and immunohistochemistry (IHC).PD-L1 positivity was defined as positive staining of 1％ and 5％ tumor cells.Survival curves were constructed by using the Kaplan-Meier method.Univariate and multivariate Cox proportional hazard regression models were performed to identify associations with outcome variables.Results Overall,tumoral PD-L1 expression was potentially associated with favorable DFS and OS.When the patients were stratified into stage Ⅰ + Ⅱ (60.9％,154/253) and stage Ⅲ + Ⅳa (39.1％,99/253),the prognostic role was not consistent.In patients with stage Ⅰ + Ⅱ disease,tumoral PD-L1 expression was associated with better DFS and OS upon multivariate analysis (1％ as the cutoff:P =0.046 and 0.021,5％ as the cutoff:P=0.011 and0.004).However,PD-L1 expression was not correlated with prognosis in patients with stage Ⅲ + Ⅳa disease (1％ as the cutoff:P =0.586 and 0.682,5％ as the cutoff:P =0.807 and 0.620).Conclusion The prognostic role of tumoral PDL expression is variable in different stages of ESCC,and tumoral PDL expression is an independent favorable predictor in ESCC patients with Stage Ⅰ-Ⅱ disease,but not in stage Ⅲ-Ⅳa or lymph node metastasis.
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To explore the status of HER-2 gene amplification and protein expression in Chinese esophageal squamous cell carcinoma patients and its relationship with the clinicopathological parameters.Methods The HER-2 gene amplification was detected by FISH and protein expression by IHC in 96 patients with esophageal squamous cell carcinoma that would be followed up for 3 years.Results Three cases presented with 3 +,15 cases with 2 +,11 cases with 1 +,and 67 with negative by HER-2 immunohistochemical staining;2 of 3 cases presented with HER-2 amplification in in 3 +,1 case presented with over 6 HER-2 copy numbers.HER-2 amplification and HER-2 overexpression had significant correlation (P ＜ 0.000 1).HER2 amplification or overexpression was associated with clinicopathological parameters,such as,carcinomas without necrosis (P =0.012) and lower stage (P =0.040).There was better DFS or OS trend in patients with HER-2 overexpression or amplification,but the significant difference did not reached.Conclusion This research has demonstrated the correspondence between gene amplification and protein overexpression of HER-2 in ESCC.HER-2 gene overexpression or amplification is a potential better predictive parameter in ESCC,but needs further study.
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To investigate the clinicopathological features as well as prognosis of early esophageal squamous cell neoplasm (ESCN) treated with endoscopic resection (ER).Methods 368 patients were collected from 2007 to 2013.Clinicopathological features including invasion depth and margin were evaluated.Survival curves were constructed by using the Kaplan-Meier method.Univariate and multivariate Cox proportional hazard regression models were performed to identify associations with outcome variables.Results There were 252 males and 116 females with a median age of 61 (16-84) years.Patient numbers of hyperplasia,low grade intraepithelial neoplasia,high grade intraepithelial neoplasia,m1,m2,m3,sm1 and sm2 were 47(12.8％),61 (16.6％),61 (16.6％),54(14.7％),38(10.3％),63(17.1％),12(3.3％) and 32(8.7％),respectively.The cumulative overall 1-year,3-year,and 5-year rates of survival in the metachronous esophageal lesions were 4.1％,12.9％ and 32.6％,respectively.The incidence of lymph node/distant metastasis was 1.54％ in m3,6.25％ in sm2,and 0 in other subgroups.The overall 1-year,3-year,and 5-year survival rates were 99.5％,97.3％,and 87.5％,respectively.Significant difference was identified between sm2 and non-sm2 patients in metastatic rate (P =0.021),however,no significant difference existed between m3 patients and sm2 patients (P =0.252).Metachronous esophageal lesion and survival between sm2 and non-sm2 patients demonstrated no statistical difference (P =0.401 and P =0.634).Conclusion ER is an effective and relatively safe treatment for superficial ESCN.The procedure is still appropriate in selecting sin2 patients.It is necessary to monitor the second primary cancer in sm2 patients during follow-up.
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Objective To investigate the changes of osteopontin (OPN) expression in murine colitis induced by dextran sodium sulfate (DSS) and its role in inflammatory bowel disease (IBD).MethodsThirty-two male BALB/C mice were randomly assigned into 4 groups: control group (group A), DSS-induced murine colitis model group (group B), salazosulfapyridine treatment group (group C) and infliximab treatment group (group D). Plasma OPN concentration was measured by enzyme linked immunosorbent assay (ELISA). OPN mRNA level was detect by using reverse transcriptase polymerase chain reaction (RT-PCR) and protein expression in colonic tissues was analyzed by using Western blotting. The location expression of OPN in colonic tissues was determined by immunohistochemical staining. ResultsIn group A, B,C and D, the plasma concentrations of OPN were (5.26±1.93) ng/ml, (10.21±2.37) ng/ml, (4.58±1.83) ng/ml and (4.82±1.83) ng/ml,respectively: the mRNA levels of OPN in colonic tissues were (0.36±0.16), (0.71±0.17),(0.32±0.07) and (0. 34±0. 08), respectively; the protein levels of OPN in colonic tissues were (0.44±0.10), (0.85±0.04), (0.61±0.11) and (0.58±0.17), respectively. The OPN-positive cell numbers in lamina propria mononuclear were (46.6±10.9), (155.5±43.8), (73.1±6.8) and (70.6±8.3), respectively. The expression of OPN in group B was significantly higher than that in group A (P<0.05). Compared with group B, the expressions of OPN in group C and D were significantly decreased (all P valus <0. 05). No significant difference was detected between group C and D. Conclusions The study shows that the expression of OPN significantly increased in DSS-induced murine colitis and decreased after treated with drugs. OPN-mediated immune response contributes to DSS-induced murine colitis.