Background: The development of minimally invasive surgery has initiated many changes in the surgical treatment of esophageal cancer (EC) patients. The aim of this study was to compare the short-term outcomes of robotic-assisted minimally invasive esophagectomy (RAMIE), video-assisted minimally invasive esophagectomy (VAMIE), and open esophagectomy (OE). Methods: Our study included patients who had undergone McKeown esophagectomy at Tianjin Medical University Cancer Institute and Hospital between January 2016 and December 2018. We analyzed clinical baseline data, as well as perioperative and pathological outcomes. Results: A total of 312 cases met the inclusion criteria (OE: 77, VAMIE: 144, RAMIE: 91). The OE group had a greater number of late-stage patients as well as those who received the neo-adjuvant therapy, compared with the other two groups (P=0.001). The procedure time in the OE group was also shorter by approximately 20 minutes (P=0.021). Total blood loss was significantly lower in the two MIE groups (P=0.004) than in the OE group. There were no differences in the total number of dissected lymph nodes between the three groups (OE: 24.09±10.77, VAMIE: 23.07±10.18, RAMIE: 22.84±8.37, P=0.680). Both the lymph node number (P=0.155) and achievement rate (P=0.190) in the right recurrent laryngeal nerve (RLN) area were comparable between the three groups. However, in the left RLN area, minimally invasive approaches resulted in a higher number of harvested lymph nodes (P=0.032) and greater achievement rate (P=0.018).Neither MIE procedure increased the incidence of postoperative complications. Conclusions: Minimally invasive surgery could guarantee the quality of bilateral RLN lymphadenectomy without increasing postoperative complications, especially in RAMIE patients. The rational choice of different surgical approaches would improve both safety and oncological outcomes for patients.

Primary adenosquamous carcinoma (ASC) of the esophagus is a rare kind of malignancy characterized by mixed glandular and squamous differentiation as well as a propensity for aggressive clinical behavior. Data on the evaluation of the clinicopathological features and the prognosis of patients suffering from this malignancy are few because of the rarity of this disease. We conducted a retrospective review of 24 patients with primary esophageal ASC among 6546 esophageal cancer patients who underwent transthoracic esophagectomy in our hospital. The clinicopathological presentation, diagnosis, treatment, and prognostic factors of the patients were respectively investigated. The Kaplan-Meier method and the log rank test were used to calculate and compare overall survival (OS). The Cox proportional hazards model was employed to identify independent prognostic factors. There were 18 males and 6 females with a median age of 60 years (range: 40-78 years). The clinical symptoms, macroscopic type, as well as the radiological and endoscopic features of esophageal ASC were similar to those of esophageal squamous cell carcinoma. Sixteen (88.9%) of the 18 cases who underwent preoperative esophagoscopic biopsy were misdiagnosed as adenocarcinoma or squamous cell carcinoma. The overall median follow-up period was 36 months, and the median survival time was 32 months. The 1, 3, 5-year OS rates were 75.0%, 48.5%, and 19.4%, respectively. Univariate analysis showed that gender (P=0.047), lymph node metastasis (P=0.007), and TNM stage (P=0.037) were important factors associated with OS of the 22 patients who underwent radical resection. Multivariate analysis showed that the pathological N stage was the only independent prognostic factor (P=0.031, hazard ratio [HR], 5.369, 95% confidence interval [CI], 1.167-24.700). These results suggest that esophageal ASC is an uncommon disease prone to be misdiagnosed by endoscopic biopsy. Surgical resection is the primary treatment, but the prognosis of ASC is usually poorer than conventional squamous cell carcinoma. Lymph node metastasis is an independent prognostic factor after radical resection.

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Impact statementFor a long time, the development of peripheral cytopenias as a complication to cirrhotic portal hypertension has been attributed to hypersplenism; however, this has never been fully demonstrated. Dameshek summarized that hypersplenism should be diagnosed by the presence of four conditions: (a) mono-or multi-lineage peripheral cytopenias; (b) compensatory hyperplasia of bone marrow; (c) splenomegaly; and (d) correction of cytopenias after splenectomy. We retrospectively analyzed the clinical data from 183 surgical patients, and found that 80.5% of peripheral cytopenias was caused by hypersplenism, 16% by a combination of factors, and 3.5% by other factors unrelated to hypersplenism. As the first quantitative findings in this field, our results verify that hypersplenism is a major, but not exclusive, cause of peripheral cytopenias, and provides important clinical evidence for investigating the cause of peripheral cytopenias. AbstractThe clinical data of 183 patients with hepatitic cirrhosis and portal hypertensive splenomegaly complicated by peripheral cytopenia were retrospectively analyzed to investigate the causes of peripheral cytopenia, as well as the proportion of the causes in these patients. All patients underwent splenectomy. Before operation, these patients had one or more types of peripheral cytopenia (cumulative cytopenia: 390 patient-times). After splenectomy, blood counts in 79.2% (309/390) returned to normal, while in 15.9% (62/390) they increased but failed to reach to normal levels, and in 4.9% (19/390) they became lower than before the operations. For the last group of patients (n ¼ 19), long-term follow-up showed that blood counts returned to normal in five patients. In other words, in 80.5% [(309 þ 5)/390 or 314/ 390] of patient-times, the peripheral cytopenia was due to hypersplenism, in 15.9% it was due to a combination of factors, and in 3.6% [14/390] it had nothing to do with the hypersplenism. Thus, hypersplenism is a major cause, but not the only cause, of peripheral cytopenia in patients with hepatic cirrhosis and portal hypertensive splenomegaly, and splenectormy is an effective treatment for these patients.

Lymph node involvement in thymic malignancies is more common than previously recognized, especially in tumors with aggressive histology and advanced T category. Intentional lymph node dissection increases the detection of nodal involvement and improves accuracy of staging. In selected high-risk patients, systemic dissection of both N1and N2 nodes should be considered for accurate tumor staging.

miR-497 plays an important role in inhibiting the proliferation of NSCLC by targeting YAP1. Our results suggest that miR-497 is a potential therapeutic target in treating patients with NSCLC.

Bcl-2/adenovirus E1B 19-kDa interacting protein (BNIP3), a pro-apoptosis protein regulated by the methylation status of its promoter, has been implicated in inducing autophagy. However, the roles of BNIP3 and BNIP3-induced autophagy under hypoxia remain uncertain in esophageal squamous cell carcinoma (ESCC). Two esophageal squamous cancer cell lines, CAES17 and KYSE140, were selected on the basis of the expression and methylation status of BNIP3 to investigate the features of BNIP3 under hypoxia. Hypoxia increased cell death and the expression of BNIP3, whose promoter status was lower methylation, in a time-dependent manner. BNIP3 knockdown by RNA interference downregulated cell death. These studies demonstrated that the exposure of ESCC cells to hypoxia increased the autophagic punctate distribution of MDC staining and GFP-LC3 and that autophagy rate could be inhibited by BNIP3-siRNA. In addition, under hypoxia, cells transfected with BNIP3-siRNA exhibited a lower apoptosis rate than the control, and the apoptosis induced by BNIP3 exhibited a caspase-independent manner. Furthermore, the administration of the autophagic inhibitor 3-methyladenine (3-MA) could augment BNIP3-induced cell apoptosis and death, suggesting that autophagy plays a protective role under hypoxia. Together, our studies indicated that BNIP3 exerts prodeath effects through the induction of caspase-independent apoptosis under hypoxia in ESCC, though BNIP3-induced autophagy acting as a survival mechanism.

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