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BACKGROUND: Cancer staging systems are designed to predict survival and stratify patients. The 7(th) edition of the American Joint Commission on Cancer (AJCC7) staging system for esophageal cancer was modeled using survival data on patients who underwent esophagectomy without induction or adjuvant therapy. In the United States, the standard of care for patients with locally advanced tumors often includes neoadjuvant therapy. The prognostic value of the pathologic stage for these patients is unknown. METHODS: Data from the Surveillance Epidemiology and End Results (SEER) were used to identify 1,243 patients with adenocarcinoma of the esophagus who underwent surgery after neoadjuvant therapy from 1988-2009. Included in the analysis were pathologically-staged, non-metastatic patients who had radiation as part of their neoadjuvant therapy. The AJCC7 staging system and an alternate system were modeled using Kaplan-Meier survival methods. The two systems were compared using log-rank chi-squared statistics, with large chi-squared values indicating accuracy in survival prediction. RESULTS: The AJCC staging system was able to predict survival for patients who had neoadjuvant therapy (P<0.001, chi-squared =81.8); however, there was little distinction between stage subgroups. Patients with neoadjuvant radiotherapy had improved survival for pathologic stage II and III disease. An alternative, simpler staging system was better able to stratify patients with neoadjuvant therapy (P<0.001, chi-squared =100.5). CONCLUSIONS: The current AJCC staging system is able to predict survival in esophageal adenocarcinoma patients undergoing neoadjuvant therapy, however, there is less distinction among stage subgroups. An alternative, simpler stage grouping may better stratify patients receiving neoadjuvant therapy.
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Objective To investigate lymph node metastasis on the middle and lower segment of lⅡ and Ⅲ stage of esophageal squamous cell carcinomas,understand the factors influencing the lymph node metastasis,and provide the basis for the key areas of lymph node cleaning.Methods A retrospective study was made on the specimens of 186 patients who were middle and lower segment of Ⅱ and Ⅲ stage of esophageal squamous cell carcinomas,who had underwent radical operation through left thoracic,thoraco abdominal two field lymph node cleaning.All the cases were patients from April 2010 to December 2013 at the Inner Mongolia Medical University Clinical Medical College of Chifeng.Results A percentage (67.9％) of patients (126/186) was found with lymph node metastasis.A total of 4259 lymph node was dissected,with an averaged cleaning of (22.9 ± 8.1) lymph nodes for each case.A total of 622 lymph nodes (14.6％ =622/4 259) existed metastasis.The rate of mediastinum metastasis for middle and lower segment of esophageal cancer was 56.1％ and 16.5％,respectively.The rate of metastasis to the lower mediastinal lymph nodes was 34.6％ and 54.4％,respectively.The rate of metastasis to the celiac lymph nodes was 23.4％ and 46.8％,respectively.A significant difference was found in the metastasis locations of middle and lower segment of esophageal carcinomas (P ＜ 0.05).The top three locations of lymph node metastasis in the middle segment of esophageal squamous cell carcinomas were the lymph nodes of left artery paraesophageal,carina,and gastric bypass.The top three locations of lymph node metastasis in the lower segment of esophageal squamous cell carcinomas were paraesophageal,cardia,and gastric lymph nodes.The depths of tumor invasion,differentiation,intravascular cancer embolus were statistically significant effect on lymph node metastasis rate (P ＜ 0.05).Tumor location,and lesion length had no significant effect on the lymph node metastasis rate (P ＞ 0.05).Conclusions The lower segment of Ⅱ,Ⅲ stage esophageal squamous cell carcinoma with lymph node metastasis occurs in the lower mediastinal and abdominal lymph nodes.The middle segment Ⅱ,Ⅲ stage esophageal squamous cell carcinoma with lymph node metastasis occurs in the thoracic and abdominal lymph nodes with Jump transfer characteristics.The lymph node cleaning of the mid-dle segment includes the left artery near the stomach,paraesophageal,and carina lymph node.The lymph node cleaning of the lower segment includes paraesophageal,cardia,and gastric lymph nodes.The metastasis rate of vascular tumor thrombus is related to the depth of tumor invasion and differentiation degree.
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Objective To investigate the molecular mechanism of As 2 O3 in suppressing metastasis of esophagus carcinoma cells.Methods The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay, adhesion and invasion assay were performed to observe the inhibitory effect of As 2 O3 on proliferation and metastasis of esophagus carcinoma cells .The expressions of matrix metalloproteinases ( MMP)2, MMP9, E-cadherin, and protein tyrosine phosphatase receptor-type O ( PTPRO) were analyzed with Western blot .Results Exposure to As 2 O3 significantly presented suppressive functions on growth and metastasis of esophagus carcinoma cells in a dose-dependent manner ( P <0.01 ) .Additionally , MMP2 and MMP9 expressions were increased after treatment with casticin ( P <0.01 ) , whereas E-cadherin and PTPRO expressions were down-regulated ( P <0.01 ) .Conclusions As2 O3 had a significant function to inhibit proliferation and metastasis of esophagus carcinoma cells .
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Objective To investigate the effect of Smo siRNA on the aggressive capability of human esophageal carcinoma EC9706 cells.Methods EC9706 cells were transfected by Smo siRNA.The expressions of Smo and Glil protein in experimental and control groups were detected with immunocytochemistry.The expressions of Smo and Gli1 mRNA in experimental and control groups were detected with in situ hybridization.The change of aggressive capability in all groups was detected by Boyden chamber in vitro.Results Compared with control group,there was a significant decrease in the protein and mRNA levels of Smo and Gli1 in every specific siRNA transfection group with three different concentration (P ＜ 0.05).The aggressive capability of EC9706 cells was significantly weakened after the transfection (P ＜ 0.05).Conclusions Smo siRNA can inhibit the expressions of Smo and Gli1 genes in EC9706 cells,and can also weaken the aggressive capability of EC9706 cells.
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Objective To investigate the expression of cytokeratin 34βE12 in esophageal squamous cell carcinoma (ESCC),and its mechanism of action in the process of occurrence and development of an ESCC.Methods Immunohistochemistry was used to analyze the expression of cytokeratin 34βE12 in 252 ESCC patients,66 patients with esophageal carcinoma in situ,and 106 patients with adjacent normal esophageal mucosa before the relationship between its expression and biological behavior was evaluated on the basis of complete clinical information.In addition,Western blotting was used to determine the expression of cytokeratin 34βE12 in 60 patients with esophageal cancer and adjacent normal esophageal tissues.Results (1)The positive rate of caveolin-1 in ESCC,carcinoma in situ,and adjacent normal tissues was 85.7％,54.5％,and 25.7％,respectively.The difference between them was statistically significant (P ＜0.01).(2)The positive rate of cytokeratin 34βE12 in stages Ⅰ,Ⅱ,Ⅲ of ESCC was 76.5％,84.7％,and 96.3％,respectively.The expression intensity of cytokeratin 34βE12 in carcinoma tissue was gradually increased with the advance of clinical stages with a statistically significant difference (P =0.038).The positive rate of cytokeratin 34βE12 with group of lymph node metastasis was significantly higher than those without lymph node metastasis (P ＜ 0.01).(3)Western blotting results further confirmed that the expression of cytokeratin 34βE12 in ESCC was significantly higher than that in adjacent normal esophageal tissue (P ＜0.01).Conclusions The high expression of caveolin-1 might be involved in the occurrence and development of esophageal cancer.The expression of cytokeratin 34βE12 was correlated with the clinical stage of esophageal cancer.cytokeratin 34βE12 was a potential therapeutic target and a valuable prognostic indicator of esophageal cancer progression.
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Objective To evaluate the variance and the concordance between the tumor length measured by CT scans and that measured by surgical specimens in esophageal carcinoma. Methods Fiftytwo surgical specimens of the esophageal carcinoma were made into pathological giant section.The shrinkage ratio of tumor was calculated by comparing the length of the specimen fixed by formalin for 24 h and that measured during the operation.One hundred and thirty-seven patients with esophageal carcinoma underwent spiral CT scan before the surgery,and the length of the gross tumor volume was obtained.After the tumor length of the fixed specimen had been measured,the real tumor length in situ was calculated using the shrinkage ratio.Then the variance and the concordance between the tumor length in CT scans and that in situ were compared.Results The mean shrinkage ratio was 90%±10%.The mean tumor length in CT scans was longer than that in situ(5.8 am±2.4 cm vs 4.1 cm±1.8 cm,P=9.68,P=0.000).The concordance of the length measured by the two methods was 40.9%(56/137). Conclusions A certain variance existed between the tumor length in CT images and that computed from surgical specimen in esophageal carcinoma.The results of esophagography and endoscopy should also be referred to delineate the gross tumor volume of esophageal carcinoma.
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AIM: To study changes in p53 expression and cell proliferation in esophageal epithelia of subjects from high or low esophageal cancer incidence areas in Henan Province to understand their molecular basis. METHODS: Esophageal endoscopic mucosa biopsies were acquired and histopathological examinations were performed on 220 subjects from high esophageal cancer incidence areas and 50 subjects from low incidence areas in Henan Province. Esophageal epithelia were diagnosed as normal, basal cell hyperplasia or dysplasia based on cell morphology and tissue structure. Immunohistochemistry avidin biotin peroxidase complex (ABC method) was performed to analyze alterations in p53 and proliferating cell nuclear antigen (PCNA) expression in normal epithelia and epithelia with different lesion severities. The numbers of p53-positive and PCNA-positive cells were counted. RESULTS: p53- and PCNA-positive nuclei were present in esophageal epithelia from subjects from both high and low incidence areas. The number of PCNA-positive cells gradually increased with lesion severity for both the high and low incidence areas. The number of p53-positive cells was higher in high incidence areas compared to low incidence areas, and rapidly increased with lesion severity. p53 expression positively correlated with PCNA expression. CONCLUSION: The number of both p53- and PCNA-positive cells increased with lesion severity. p53 expression was higher in subjects from high esophageal cancer incidence areas compared to those from low incidence areas. These results may shed light into the molecular basis for the geographical distribution of esophageal cancer.
