Background: Epidermal growth factor receptor (EGFR), c-Met, and human epidermal growth factor receptor 2 (HER2) are overexpressed in a variety of human cancers, and may serve as biomarkers for disease prognosis. We examined whether high expression of these molecular markers correlates with poor disease prognosis in esophageal squamous cell cancer (ESCC). Materials and Methods: Expression of EGFR, c-Met, and HER2 protein was detected by immunohistochemistry (IHC) in 180 paraffin-embedded tissue samples from stage IIB-IIIC ESCC patients. The overall survival (OS) rates were calculated according to the Kaplan-Meier method, and the log-rank test was used to evaluate differences between survival curves. The Cox proportional hazards model was used for univariate and multivariate analyses. Results: The median survival of all patients was 46 months. There was no significant difference in OS in terms of HER2 and EGFR status (P = 0.177 and P=0.061, respectively). However, there was a significant difference in OS between c-Met high expression patients and c-Met low expression or negative patients (median: 41.9 months vs. 56.7 months; P = 0.001). Multivariate analysis also showed that, of the covariates analyzed, c-Met high expression was the only prognostic factor for OS (HR: 0.459 [95 % confidence interval: 0.287-0.733]; P = 0.001). Patients with ESCC that had concurrent overexpression of EGFR and c-Met had significantly worse survival than ESCC that displayed overexpression of either EGFR or c-Met individually or that did not have overexpression of either protein (P=0.000). Conclusions: Overexpression of HER2 and EGFR individually is not significantly associated with poor prognosis in ESCC. High expression of c-Met may be indicative of a poorer prognosis in ESCC. In order to promote efficient and rapid development of therapeutic methods in ESCC, further studies are necessary to explore the role of c-Met.

Abstract. Cisplatin (CDDP) is a commonly used drug for gallbladder cancer (GBC) chemotherapy. However, resistance to CDDP treatment results in relapse. Therefore, there is a need for the development of more effective treatment strategies to overcome chemoresistance. Dual-specificity phosphatase 1 (DUSP1) was reported to be involved in the resistance of a number of chemotherapeutic agents and was revealed to be highly expressed in CDDP-resistant GBC cells and CDDP-treated tumor types compared with normal cells or tissues in the present study. DUSP1 was revealed to inhibit the cytotoxicity of CDDP in two GBC cell lines, SGC996 and GBC-SD. P38 mitogen-activated protein kinases may be involved in the mechanism of chemoresistance. Furthermore, the number of DNA double-strand breaks in SGC996 OE cells was reduced compared with SGC996 vector cells indicating DUSP1 may attenuate the chemotherapeutic efficiency. Due to its potency against CDDP treatment, DUSP1 may be a promising target to overcome chemoresistance in GBC therapy. IntroductionGallbladder cancer (GBC) has a high occurrence among populations in the Andean area, Native Americans and Mexican Americans (1). GBC is often diagnosed at a late stage due to its unapparent symptoms at the early stage (2). Surgery is currently the primary option for GBC treatment alongside a combination of 5-fluorouracil (5-FU) and cisplatin (CDDP), which is a common choice for advanced GBC (3,4). Although chemotherapy exerts a therapeutic effect in a number of patients, chemoresistance eventually occurs in patients that receive chemotherapy (5).CDDP is one of the most widely used cytotoxic anticancer drugs (6-9). CDDP mainly reacts with the N7-position of guanine, forming inter-and intra-strand DNA cross-links and blocks replication and transcription, and may result in replication-mediated double-strand breaks (DSBs) (10,11). However, resistance to these drugs undermines their curative potential. The resistance to CDDP and numerous other chemotherapeutic agents is partially due to a wide range of genetic and epigenetic alterations which result in abnormal cell survival (12)(13)(14). In the present study, the expression of a number of chemotherapy resistance-associated genes (DUSP1, HIF-1α, MDR1, MRP1) was compared between CDDP-resistant SGC996 and GBC-SD cells and normal SGC996 and GBC-SD cells. Notably, one gene (dual-specificity phosphatase 1 (DUSP1)) expression was markedly increased in the established CDDP-resistant cells compared with the normal cells. Using an in vivo assay, DUSP1 expression in subcutaneous tumors was also elevated following CDDP treatment.DUSP1 is one member of the DUSP family, which consists of a total of 25 members. The expression of DUSP1 is cancer-dependent (15). In a range of epithelial tumor types including pancreatic ductal adenocarcinoma (PDAC), non-small-cell lung cancer, breast, ovarian, gastric and early-stage prostate cancer, DUSP1 was revealed to be overexpressed, however it was decreased in hepatocellular carcinoma (16)(17)(18)(19). The DUSP fami...

Prophylactic use of GSF reduced hospitalization rate and the rate of intravenous application of antibiotics.

BACKGROUND In recent years, neoadjuvant chemoradiotherapy (NCRT) combined with surgery has been gradually applied in patients with locally advanced thoracic esophageal cancer, but its effectiveness and safety remains unclear. In this clinical trial, we prospectively investigated the efficacy and safety of NCRT plus surgery in the treatment of thoracic esophageal squamous cell carcinoma (TESCC). AIM To investigate the efficacy and safety of NCRT combined with surgery in the treatment of potentially resectable TESCC. METHODS Thirty patients with advanced TESCC hospitalized in our hospital from July 2016 to June 2019 were prospectively studied. All patients received NCRT, which included intensity modulated conformal radiotherapy (40-44 Gy/20-22f, 2 Gy/f) and chemotherapy (paclitaxel 150-175 mg/m 2 d1, 22 + lobaplatin 25-30 mg/m 2 d2, 23 for two cycles). Surgery was performed after radiotherapy and chemotherapy. The effectiveness and safety of these treatments were observed. RESULTS Among these 30 patients, complete response was achieved in two cases (6.7%) and partial response in 26 cases (86.7%), yielding an objective response rate of 100%. All patients underwent radical surgery successfully. The R0 resection rate was 100%, and the pathologic complete response rate was 33.3%. The incidence of grade III- IV granulocytopenia was 10% during the NCRT, and anastomotic leakage occurred in one patient after surgery. CONCLUSION For patients with potentially resectable TESCC, NCRT can effectively reduce the tumor size, increase R0 resection rate, and achieve obvious pathological degradation, with mild adverse reactions. Thus, it is worthy of wider clinical application.

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