Macrophages constitute one of the most common components of immune cells, which penetrate tumors and they have a key role in tumor prognosis. Here, we identified an unrecognized macrophage subpopulation, which favors tumorigenesis. These macrophages express programmed cell death protein 1 (PD1) in a constitutive manner and accumulates in esophageal squamous cell carcinoma (ESCC) in advanced stage of the disease and is negatively associated with the survival of ESCC patients. The PD1+ tumor-associated macrophages (PD1+ TAMs) displayed surface pattern and function akin to M2: a substantial enhancement in CD206 and IL-10 expression; a specific reduction in HLA-DR, CD64, and IL-12 expression; and a significant increase in the ability to inhibit CD8+ T-cell proliferation. Triggering of PD1 signal is effective in increasing PD1+ TAM function. Moreover, exosomal HMGB1 obtained from tumors are efficient in triggering differentiation of monocytes into PD1+ TAMs, which display phenotypic and functional properties of M2. Overall, our work is the first finding to confirm that exosomal HMGB1 obtained from ESCC can successfully trigger clonal expansion of PD1+ TAM. Further, as the macrophages exhibit an M2-like surface profile and function, thereby creating conditions for development of ESCC. Thus, effective methods of treatment include combining immunotherapy with targeting PD1+ TAMs and tumor-derived exosomal HMGB1 to resuscitate immune function in individuals suffering from ESCC.

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Adding the removal of RLN LNs might improve OS and DFS with acceptable morbidity for patients with ESCC.

BackgroundThe association between type 2 diabetes mellitus (T2DM) and the risk of esophageal cancer remains unclear. The present study aimed to evaluate the impact of T2DM on short-term outcomes and long-term survival in patients with esophageal squamous cell cancer (ESCC).MethodsThe present retrospective study included 862 patients diagnosed with ESCC between January 2001 and December 2010. Among them, 280 patients had T2DM. A 1:1 propensity score-matched cohort consisting of 280 patients with and 280 without T2DM was selected from the 862 patients. The associations between T2DM and clinicopathologic characteristics were assessed using the χ2 or Fisher’s exact test. Survival of ESCC patients with and without T2DM was calculated by using the Kaplan–Meier method and compared by using the Cox regression model between the two groups.ResultsThe occurrence rate of anastomotic leakage was significantly higher in patients with T2DM than in those without T2DM (P < 0.001). In the subgroup with weight loss rate ≤ 5.05%, ESCC patients with T2DM had a significant longer overall survival than did those without T2DM (P = 0.003), whereas in the subgroup with weight loss rate > 5.05%, the patients without T2DM showed a longer survival (P = 0.001). Univariate and multivariate analysis results showed that T2DM was not an independent prognostic factor for patient survival.ConclusionsType 2 diabetes mellitus is not an independent prognostic factor in patients with ESCC. However, the combination of T2DM with severe weight loss would be a predictor of poor prognosis.

2019) MiR-629-3p-induced downregulation of SFTPC promotes cell proliferation and predicts poor survival in lung adenocarcinoma, Artificial Cells, Nanomedicine, and Biotechnology, 47:1, 3286-3296, ABSTRACTThe long-term prognosis of patients with lung cancer remains poor and thus it is imminent to further elucidate the molecular mechanism for the oncogenesis of lung cancer. In this study, we observed that surfactant protein C (SFTPC) expression was downregulated in human lung adenocarcinoma tissues and cell lines, and low SFTPC expression correlated with poor overall survival of lung adenocarcinoma patients. Moreover, we found that overexpression of SFTPC could inhibit lung cancer cell proliferation in vitro and in vivo, but downregulation of SFTPC showed the opposite results. Besides, it was observed that miR-629-3p expression was upregulated in human lung adenocarcinoma tissues and cell lines. More importantly, we found that miR-629-3p could downregulate SFTPC expression by directly binding to the SFTPC 3'-UTR and inhibit the regulatory effect of SFTPC on lung adenocarcinoma cell proliferation. In conclusion, these data suggested that miR-629-3p-meditated downregulation of SFTPC may promote lung adenocarcinoma progression. ARTICLE HISTORY

The number of resected LNs is an independent prognostic factor for the survival of node-negative ESCC patients. The minimum resection number recommended for accurate staging is 16.

Smoking is well known as a risk factor for esophageal cancer, but controversial as a prognostic factor. Moreover, evidence is scarce that a dose-response relationship exists. We conducted a retrospective study on the effect and dose-response relationship of prediagnostic smoking on the postoperative disease-specific survival of patients with lymph node-negative esophageal squamous cell carcinoma (ESCC). We enrolled 643 patients with lymph node-negative ESCC who had undergone esophagectomy between 1990 and 2005 at the Department of Thoracic Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China. The patients' demographic, pathological, preoperative and cancer outcome data were obtained from medical records. These data were reviewed and analyzed using life table, Kaplan-Meier analysis and multivariate Cox regression. A significant reduction in 3-and 5-year survival rates was observed in smokers with lymph node-negative ESCC compared with those in non-smokers. The 3-and 5-year survival rates were 54% and 46% for smokers, and 67% and 64% for non-drinkers, respectively (P < 0.05). Multivariate Cox analysis revealed that smoking was an independent prognostic factor (P = 0.008, hazard ratio = 1.404). Both log-rank test (P = 0.065) and multivariate analysis (P = 0.091) showed no significant difference between the survival rates of light and heavy smokers. Prediagnostic smoking is an independent prognostic factor for patients with lymph node-negative ESCC, but the dose-response relationship needs further investigation. (Cancer Sci 2012; 103: 1985-1988 E sophageal cancer is the sixth leading cause of cancer mortality worldwide.(1) According to the most recent global estimates, esophagus cancer causes 407 000 deaths annually. (2) In China, it is the fifth most common and fourth most lethal malignant tumor, and squamous cell carcinoma prevails in terms of histology.(3) Despite advances in early diagnosis and surgical treatments, overall prognosis is poor with the 5-year survival rate rarely >20%. It is well known that smoking is damaging public health on a global scale by playing an important role in the development of lung, head, neck and esophageal cancers. Well-conducted population-based studies have reported a significantly increased risk of esophageal squamous cell carcinoma (ESCC) associated with smoking, regardless of dosage.(8-10) However, the correlation between smoking and patient survival is less investigated and more controversial. Some studies reported that smokers had a worse prognosis, (11,12) while others denied the correlation.(13) The present study aimed to determine whether prediagnostic smoking has an independent influence on disease-specific survival (DSS) in patients with lymph node-negative ESCC, and whether a dose-dependent relationship exists. Materials and MethodsWe conducted a large-scale retrospective study by searching the esophageal cancer database of the Department of Thoracic Surgery at Sun Yat-sen University Cancer Center, Guangzhou, China. In total, 643 patients with lymph node-neg...

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