BackgroundOpen esophagectomy (OE) is associated with significant morbidity and mortality. Minimally invasive oesophagectomy (MIO) reduces complications in resectable esophageal cancer. The aim of this study is to explore the superiority of MIO in reducing complications and in-hospital mortality than OE.MethodsMEDLINE, Embase, Science Citation Index, Wanfang, and Wiley Online Library were thoroughly searched. Odds ratio (OR)/weighted mean difference (WMD) with a 95% confidence interval (CI) was used to assess the strength of association.ResultsFifty-seven studies containing 15,790 cases of resectable esophageal cancer were included. MIO had less intraoperative blood loss, short hospital stay, and high operative time (P < 0.05) than OE. MIO also had reduced incidence of total complications; (OR = 0.700, 95% CI = 0.626 ~ 0.781, P V < 0.05), pulmonary complications (OR = 0.527, 95% CI = 0431 ~ 0.645, P V < 0.05), cardiovascular complications (OR = 0.770, 95% CI = 0.681 ~ 0.872, P V < 0.05), and surgical technology related (STR) complications (OR = 0.639, 95% CI = 0.522 ~ 0.781, P V < 0.05), as well as lower in-hospital mortality (OR = 0.668, 95% CI = 0.539 ~ 0.827, P V < 0.05). However, the number of harvested lymph nodes, intensive care unit (ICU) stay, gastrointestinal complications, anastomotic leak (AL), and recurrent laryngeal nerve palsy (RLNP) had no significant difference.ConclusionsMIO is superior to OE in terms of perioperative complications and in-hospital mortality.
The present study analyzed the expression of the histone deacetylase (HDAC) 1, 2 and 3 in primary esophageal squamous cell carcinoma (ESCC) samples and how their levels correlate with clinicopathological parameters. ESCC patients (n=88) in the present study had received no previous treatment before undergoing surgical excision. The mRNA expression of HDAC1,-2 and-3 were detected by semi-quantified PCR in ESCC samples and distal normal samples. The relationship of HDAC1,-2 and-3 expression with clinicopathological parameters was analyzed by χ 2 test. The correlation among these HDACs was analyzed by Pearson's correlation test. Compared with distal normal tissues, ESCC samples had higher expression of HDAC1, but not HDAC2 or HDAC3 (P<0.05). The expression of HDACs was different between Kazak and Han ethnicities. The expression of HDAC2 was correlated with invasion depth (P<0.05), but not with sex, age, metastasis, or the degree of tumor differentiation (P>0.05). There was no association between HDAC1 or HDAC3 and clinicopathological parameters (P>0.05). For the Kazak and Han ethnicities, HDAC1 expression was present in male patients, patients with well/moderate differentiated ESCC and T3 and T4 ESCC (P<0.01). HDAC1 in patients aged <60 was associated with ethnicity (P<0.05). HDAC2 expression was different in positive LN metastasis, well/moderate differentiation and T3 and T4 ESCC (P<0.01). HDAC3 expression in male patients, patients with negative LN metastasis and well/moderate differentiation ESCC was associated with ethnicity (P<0.05). Additionally, the expression levels of HDAC1,-2 and-3 did not correlate with each other. Thus, HDAC1 expression may be used as a risk factor for ESCC and HDAC2 levels may be used to predict invasion depth. The expression of HDAC1,-2 and-3 has ethnic differences.
Esophageal cancer (EC) is the eighth most prevalent cancer and the sixth leading cause of cancer-related mortality worldwide. As an antiapoptotic and a proapoptotic protein, respectively, survivin and Bad play an important role in carcinogenesis of the most human cancers including EC. However, the regulatory relationships between them remain unclear. We sought to investigate the effects of survivin knockdown and overexpression on the expression of Bad gene, cell cycle progression, and apoptosis of esophageal carcinoma cell. The mRNA expression levels of survivin and Bad were determined in EC tissue samples. The knockdown and overexpression experiments were performed in ECA109 and KYSE450 cells via transfection with survivin overexpression and shRNA plasmids. A Bad overexpression experiment was conducted to confirm the biological effect on knockdown of survivin via modulating Bad expression. RT-qPCR and Western blot analysis were used to detect mRNA and protein expression, respectively. Cell cycle and apoptosis were analyzed by flow cytometry. The chromatin immunoprecipitation (ChIP) was conducted to determine the binding sites of survivin on the promoter of Bad gene. By analyzing the mRNA expression of survivin and Bad in 40 ESCC patient specimens, we found that the positive expression rate of survivin in tumor tissues (88%, 35/40) was remarkably high, compared with the distal nontumor tissues (48%, 19/40, p < 0.01). On the other hand, the positive expression rate of Bad in tumor tissues (70%, 28/40) was remarkably low, compared with the distal nontumor tissues (95%, 38/40, p < 0.01). Overexpression of survivin decreases Bad mRNA and protein expression and promotes transformation of cell cycle to S phase. Conversely, knockdown of survivin increases Bad mRNA and protein expression and induces cell cycle arrest and apoptosis. Bad overexpression inducing apoptosis of esophageal carcinoma cell shows the similar apoptotic effect with survivin knockdown. ChIP assays indicate that survivin directly binds to the Bad promoter region, diminishing the transcriptional activity of Bad. In conclusion, the result suggested that survivin regulates Bad gene expression by binding to its promoter and modulates cell cycle and apoptosis in esophageal carcinoma cell.
The methylation and expression of RECK, P53 and RUNX genes in patients with esophageal cancer was investigated. In order to achieve this aim, a sample of 58 patients with esophageal cancer, treated between February 2013 and February 2014, were considered as the observation group. Additionally, a sample of 42 healthy individuals was selected as the control group. Methylation status of RECK, P53 and RUNX genes from the observation and control groups were detected by MSP. Reverse transcriptase-quantitative PCR (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), western blot and immunohistochemistry were used to detect the mRNA and protein levels of RECK, P53 and RUNX in both the observation and the control groups. Results showed that the methylation rates of RECK, P53 and RUNX genes in patients with esophageal cancer were 72.4% (42/58), 1.7% (1/58) and 3.4% (2/58), respectively, which were significantly different from those in the control group [7.1% (3/42), 90.5 (38/42), and 83.3% (35/42), respectively]. The mRNA expression level of RECK is only equal to the 2.3% of that in the control group, while the mRNA expression levels of P53 and RUNX were 65.1 and 47.2 times higher than those in the control group, respectively (p<0.05). ELISA showed that RECK protein level in the observation group (0.12±0.05) µg/l, was significantly lower than the control group (3.46±0.08) µg/l (p<0.05), while, P53 and RUNX protein levels in observation group were significantly higher than that in healthy people (6.43±0.12 µg/l vs. 0.64±0.06 µg/l and 4.32±0.14 µg/l vs. 0.53±0.09 µg/l, respectively), and the results were similar to western blot. The data of immunohistochemistry showed that the proportion of RECK protein positive cells in the observation group was significantly lower than that in the control group (9.5 vs. 82.3%, P<0.05), while the proportions of P53 and RUNX protein positive cell in the observation group were significantly higher than those in the control group (78.4 vs. 11.1% and 87.3 vs. 9.06%), respectively, (P<0.05). This study concluded that, in patients with esophageal cancer, the methylation of RECK gene is increased and the expression of RECK gene is inhibited, while methylation of RUNX gene decreased and their expression was increased. This change in methylation of these genes may promote the occurrence and development of esophageal cancer.
Rationale: It is often difficult to perform transthoracic esophagectomy (TTE) in patients with chest deformities, as these patients may be lost to surgery for non-oncological reasons. Patient concerns: In this case, we had a patient with esophageal squamous cell carcinoma (ESCC) who was not suitable for TTE because of extensive thoracic adhesions caused by the left pneumonectomy 8 years ago. Diagnoses: ESCC. Interventions: Based on Professor Fujiwara’s surgical method, we further improved it by proposing a single-port inflatable mediastinoscopy combined with laparoscopic-assisted esophagectomy. Outcomes: At the time of this writing, computed tomography and gastroscopy revealed no stenosis of anastomosis, and no evidence of disease recurrence. Lessons: To the best of our knowledge, the present case is the first single-port inflatable mediastinoscopic esophagectomy performed on a patient undergoing pneumonectomy.
Synchronous multiple nodules in the lungs, such as peripheral ground-glass opacities (GGOs) and solid small nodules, are common, but only lesions suspected of being malignant should be surgically removed. The surgical strategy is anatomical sub-lobectomy in early stage of non-small cell lung cancer synchronously or asynchronously to decrease the impact of lung resection on the lung function. Here, we report a case of a 56-year-old man, who was a pack-a-day smoker, with endobronchial hamartomas the medial basal bronchus (B7). The patient underwent sleeve resection of the medial basal segment in the right lower lobe, followed by S 1+2 and S 3 segmentectomy because of early-stage lung adenocarcinoma (T1a), which presented as mixed GGOs located in the left upper lobe. The performance of S 7 sleeve segmentectomy of the RLL is very rare. The main concern is stenosis of the anastomosis and the major technical striking point is the caliber discrepancy between proximal and distal bronchi. In our experiences, we used high-tech methods as three-dimensional reconstruction to provide a basis for our surgical planning and proper patient selection and a series of preventing measures taken for anastomotic stenosis, successfully avoided complications. This case provides a new strategy for the treatment of patient with multiple early-stage lung cancer and benign endobronchial tumors, simultaneously.
Esophageal cancer (EC) is the eighth most prevalent cancer and the sixth leading cause of cancer-related mortality worldwide. As an anti-apoptotic and a pro-apoptotic protein respectively, survivin and Bad play important role in carcinogenesis of the most human cancers including EC. However the regulatory relationships between them remain unclear. We sought to investigate the effects of survivin knockdown and overexpression on the expression of Bad gene, cell cycle progression and apoptosis of esophageal carcinoma cell. The mRNA expression levels of survivin and Bad were determined in EC tissue samples. The knockdown and overexpression experiments were performed in ECA109 and KYSE450 cells via transfection with survivin overexpression and shRNA plasmids. RT-qPCR and Western blot analysis were used to detect mRNA and protein expression respectively. Cell cycle and apoptosis were analyzed by flow cytometry. The chromatin immunoprecipitation (ChIP) was conducted to determine the binding sites of survivin on the promoter of Bad gene. By analyzing the mRNA expression of survivin and Bad in 40 ESCC patient specimens, we found that the positive expression rate of survivin in tumor tissues(88%, 35/40) was remarkably high, compared with the distal non-tumor tissues (48%, 19/40, p<0.01). On the other hand, the positive expression rate of Bad in tumor tissues (70%, 28/40) was remarkably low, compared with the distal non-tumor tissues (95%, 38/40, p<0.01). Overxpression of survivin decreases Bad mRNA and protein expression, and promotes transformation of cell cycle to S phase. Conversely, knockdown of survivin increases Bad mRNA and protein expression, and induces cell cycle arrest and apoptosis. ChIP assays indicate that survivin directly binds to the Bad promoter region, diminishing the transcriptional activity of Bad. In conclusion, the result suggested that survivin regulates Bad gene expression by binding to its promoter and modulates cell cycle and apoptosis in esophageal carcinoma cell.
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