crossing96/oncoscreening huggingface dataset:
Hypermethylation-modulated down-regulation of CDH1 expression contributes to the progression of esophageal cancer.	CDH1, a cell adhesion molecule, which plays a key role in maintaining the epithelial phenotype, is regarded as an invasion-suppressor gene in light of accumulating evidence from in vitro experiments and clinical observations. In an attempt to clarify the mechanism responsible for inactivation of this gene in carcinomas, we investigated the methylation status of the CDH1 gene 5'-CpG islands and its regulatory mechanism in the progression of esophageal squamous cell carcinoma. Real-time methylation-specific polymerase chain reaction (qMSP) and treatment with the demethylating agent 5-aza-2'-deoxycytidine (5-Aza-CdR) were conducted to analyze the methylation status at the CDH1 promoter region in the human esophageal carcinoma cell lines, EC1 and EC9706. A total of 235 invasive esophageal squamous cell carcinomas (ESCC) at stages I-IV and their corresponding normal tissue samples, were included in an immunohistochemistry study and methylation analysis of CDH1. The results demonstrate that in EC1 and EC9706 cells, the CDH1 promoter is methylated and treatment with 5-Aza-CdR restored CDH1 expression. Enhanced CDH1 expression decreased cell migration, invasion ability and increased adhesion ability. Decreased CDH1 expression was detected in 59.6% of ESCC tissues, compared with their adjacent non-neoplastic epithelia, which had a close correlation with the primary tumor status, lymph node status, distant metatasis and clinicopathologic stage. Hypermethylation at the CDH1 promoter was detected in 97.9% of 140 cases of ESCC with low CDH1 expression. The methylation of CDH1 promoters (P=0.929) was closely correlated with the lack of expression of their corresponding proteins. The Cox regression model for survival analysis showed that increases in CDH1 methylation had a greater impact on the prognosis than tumor clinical stage. These findings suggest that CDH1 gene silencing by promoter hypermethylation and the resultant reduction of CDH1 expression may play an important role in the progression of ESCC. CDH1 methylation was a significant predictor of survival in ESCC patients after surgery.	esophagus
Endoscopic dissection of large endogenous myogenic tumors in the esophagus and stomach is safe and feasible: a report of 42 cases.	OBJECTIVE: Submucosal myogenic tumors, including leiomyoma and stromal tumors, are currently treated primarily by open surgery or laparoscopic excision. The aim of this retrospective study was to evaluate the feasibility of endoscopic dissection (ED) for resecting endogenous esophageal leiomyoma (EL) and gastric stromal tumors (GSTs) with diameters of 5 cm. METHODS: We enrolled 42 patients with endogenous EL and GST who had undergone endoscopic surgery (endoscopic group). These cases were compared retrospectively with 22 patients who had undergone thoracotomy or laparotomy (control group). Endoscopic group (n = 42) received ED for EL and GST resection, including circumferential removal of superficial mucosa of targeted tumor. Control group (n = 22) received thoracotomy or laparotomy for resection of esophageal and gastric myogenic tumors. Main outcome measures were operative time, intraoperative bleeding and perforation, postoperative complications, and hospital stays and costs were compared between groups. RESULTS: Endogenous EL and GST were successfully removed from all patients. Bleeding and perforation occurred in seven and five EL and GST patients, respectively. Bleeding was corrected with argon plasma coagulation (APC). Perforation was endoscopically repaired with clips. Mean operative time was 49 min for endoscopic EL and 55 min for GST resection. No major bleeding or perforation occurred postoperatively. Endoscopic treatment had shorter length of stay and lower hospital costs than conventional procedures. CONCLUSIONS: ED is safe and feasible for resection of endogenous EL and GST in selected cases.	esophagus
Update: modern approaches to the treatment of localized esophageal cancer.	The optimal treatment strategy for esophageal cancer continues to be a topic of debate. Improvements in chemotherapy drugs, surgical techniques, and radiotherapy planning and delivery have led to the design of treatment approaches that are specific to both the stage of the tumor and the overall performance status of the patient. Surgery continues to be the standard treatment option for localized disease, but multimodality treatments that include radiation and chemotherapy with surgery are increasingly used. The next few years will continue to see improvements in radiation techniques, especially proton beam treatment; the development of additional minimally invasive surgical approaches to minimize postoperative side effects; and the discovery of molecular biomarkers to help specifically target treatment of esophageal cancer in individual patients.	esophagus
Downregulation of stathmin is involved in malignant phenotype reversion and cell apoptosis in esophageal squamous cell carcinoma.	BACKGROUND AND OBJECTIVES: Stathmin plays a critical role in the regulation of mitosis and mediates the development of malignant tumors. Here, we investigated the potential role of stathmin in cell cycle and apoptosis in esophageal squamous cell carcinoma (ESCC). METHODS: A stathmin short hairpin RNA (shRNA) plasmid was employed to downregulate stathmin expression in the ESCC cell line EC9706 cells. Cell proliferation was measured by cell counting, MTT, and colony formation assay. Cell migration was measured by Boyden chamber. Western blot was used to analyze the expressions of stathmin, survivin, and apoptosis-related proteins in transfected cells. Cell cycle and apoptosis were determined by flow cytometry and DNA ladder. Oncogenicity assay in nude mice was utilized to analyze phenotypic changes of transfected cells in vivo. RESULTS: After transfection with stathmin shRNA plasmid, stathmin expression markedly decreased in EC9706 cells. Stathmin downregulation significantly inhibited cell proliferation, cell migration in vitro, and tumorigenicity in vivo, meanwhile arrested cell cycle in the G2/M phase and induced cell apoptosis. Further, stathmin downregulation resulted in downregulation of Bcl-2 and survivin proteins, activation of Caspase-3. CONCLUSIONS: These findings demonstrate that stathmin may play an essential role in carcinogenesis of ESCC, which will lay a foundation for target therapy of ESCC.	esophagus
One-lung ventilation in a patient with stenting for tracheobronchial stenosis caused by esophageal cancer.	We have provided general anesthesia for a 53-year-old man scheduled to undergo lymph node removal for right mediastinal lymph node metastases caused by esophageal cancer. One year prior, acute respiratory failure occurred because of stenosis of the carinal bifurcation resulting from advanced esophageal cancer with tracheal invasion. The patient underwent placement of tracheobronchial stents (Spiral Z Stent) in two locations (left main bronchus and trachea/right main bronchus), followed by radiotherapy and chemotherapy. In the present case, after an 8.5-mm-ID tracheal tube was placed under bronchoscopic guidance, a 7.0 Fr. bronchial blocker (Arndt Endobronchial Blocker; Cook, Bloomington, IN, USA) was carefully inserted into the stent in the right main bronchus. Next, 3 ml air was injected into the blocker cuff, and left-sided one-lung ventilation was performed. After surgery was completed, the bronchial blocker was removed under bronchoscopic guidance. We confirmed there was no tracheobronchial injury nor stent displacement or deformation, then removed the tracheal tube. Even in patients with tracheobronchial stent placement, one-lung ventilation can be safely and reliably performed by selecting an appropriate bronchial blocker, along with careful insertion into the stent and frequent checking of the blocker position.	esophagus
Endoscopic mucosal resection using a cap-fitted panendoscope and endoscopic submucosal dissection as optimal endoscopic procedures for superficial esophageal carcinoma.	BACKGROUND: Endoscopic mucosal resection using a cap-fitted panendoscope (EMRC) and an endoscopic submucosal dissection (ESD) are increasingly performed to treat superficial esophageal carcinoma (SEC). As an endoscopic procedure appropriate for en bloc complete resection, ESD requires a much higher level of skill and experience than EMRC. METHODS: This retrospective study reviewed 127 SECs in 112 patients treated by EMRC or ESD from January 1997 to September 2009. RESULTS: For lesions 10 mm in diameter or smaller, EMRC and ESD had equivalent en bloc resection rates with tumor-free margins (en bloc + R0 resection rates). For lesions 11 mm in diameter or larger, however, the rate was significantly higher in the ESD group than in the EMRC group (p < 0.01). The mean procedure time was significantly longer in the ESD group than in the EMRC group (p < 0.01) regardless of lesion size. No significant difference was found in esophageal perforation rate between the EMRC and ESD groups. Severe esophageal stricture developed after EMRC of eight lesions (14.3%) and after ESD of six lesions (8.5%). For patients with a mucosal defect involving more than three-fourths of the esophageal circumference, the incidence of severe esophageal stricture after procedure was significantly higher in the EMRC group than in the ESD group (p < 0.05). The overall local recurrence rate was 3.1% (4/127) during an average follow-up period of 39 months (range, 8-123 months). All local recurrences were detected as superficial cancers after EMRC and then treated endoscopically. CONCLUSIONS: For lesions 10 mm in diameter or smaller, EMRC was found to be optimal. For lesions 11 mm in diameter or larger, however, ESD was superior to EMRC in efficacy as assessed by the en bloc + R0 resection rate. Furthermore, ESD was advantageous in preventing stricture formation. The operating endoscopist should carefully select EMRC or ESD according to lesion size.	esophagus
Association of CD8+ T cell infiltration in oesophageal carcinoma lesions with human leucocyte antigen (HLA) class I antigen expression and survival.	Oesophageal cancer is one of the most aggressive tumours with a poor prognosis. However, little is known about the immune response in the tumour microenvironment. To investigate the role of immunosurveillance in the clinical course of oesophageal squamous cell carcinoma, 98 formalin-fixed, paraffin-embedded primary tumours were analysed using immunohistochemical methods for human leucocyte antigen (HLA) class I heavy chain and β2-microglobulin expression and for CD4-, CD8- and CD57-positive cell infiltration. HLA class I expression of tumour cells was correlated positively with infiltration of CD8(+) T cells into the cancer nest, but not with the clinical course of disease. However, CD8(+) and CD4(+) T cell infiltration was correlated with prognosis. These results suggest that tumour antigen-specific cellular immune response plays a role in the clinical course of the disease and that HLA class I antigen expressed on tumour cells contribute to this association most probably by mediating the interactions between tumour cells and CD8(+) T cells.	esophagus
DNA repair gene and MTHFR gene polymorphisms as prognostic markers in locally advanced adenocarcinoma of the esophagus or stomach treated with cisplatin and 5-fluorouracil-based neoadjuvant chemotherapy.	BACKGROUND: DNA repair plays an important role in chemoresistance to platinum-based therapy, and therefore polymorphisms in the genes may modulate therapeutic response. We assessed 12 polymorphisms in 7 DNA repair genes and 2 polymorphisms in the MTHFR gene for association with disease response and prognosis. METHODS: A total of 258 patients included in the study had adenocarcinoma of the esophagus (n = 114) or gastric cancer (n = 144), at stage cT3/4 and cM0, and had been treated with platinum-based neoadjuvant polychemotherapy. The patients were genotyped for polymorphisms in the XPC, XPD, XPG, APEX, XRCC1, NBS1, XRCC3, and MTHFR genes by the allelic discrimination method and the data correlated with various clinical parameters. RESULTS: None of the investigated polymorphisms was associated with histopathological response. XRCC3 polymorphisms rs861539 (P = 0.02) and rs861530 (P = 0.05) showed association with clinical response in gastric cancer. The variants in XRCC3 (rs861539, P = 0.05; rs1799794, P = 0.03) and MTHFR (rs1801131, P = 0.02) were associated with survival in esophageal and gastric cancer, respectively. In R0 resected patients, XRCC3 variants (rs861539, P = 0.04; rs861530, P = 0.02) in esophageal cancer, and XRCC3 (rs1799794, P = 0.02) and MTHFR (rs1801131, P = 0.005) in gastric cancer predicted survival. Cox regression revealed ypT category (P = 0.001) and lymphatic vessel invasion (P = 0.03) to be independent prognostic factors for esophageal cancer, and histopathological response (P = 0.01), MTHFR variant (rs1801131, P = 0.002), and ypN category (P = 0.02) to be prognostic factors for gastric cancer. CONCLUSION: In gastric cancer patients, MTHFR variant (rs1801131) could serve as a potential prognostic marker. In esophageal cancer patients, none of the polymorphisms studied had conclusive results in multivariate analysis, although XRCC3 variant (rs861539) showed an effect on survival in Kaplan-Meier univariate analysis.	esophagus
Comparison between definitive chemoradiotherapy and esophagectomy in patients with clinical stage I esophageal squamous cell carcinoma.	OBJECTIVES: Chemoradiotherapy (CRT) has been proposed as an alternative therapy to esophagectomy for esophageal cancer, because of its favorable survival rate and mild toxicity. However, no comparative studies of esophagectomy and CRT have been reported in patients with clinical stage I esophageal squamous cell carcinoma. METHODS: A total of 54 patients with clinical stage I esophageal squamous cell carcinoma were treated with definitive CRT and 116 patients with esophagectomy at Osaka Medical Center for Cancer and Cardiovascular Diseases between 1995 and 2008, and were included in the analysis. Overall survival and recurrence rates were evaluated. RESULTS: Complete follow-up data were available for 169 of the 170 patients (99%). The median (range) observation period was 67 (10-171) months in the esophagectomy group and 30 (4-77) months in the CRT group (P<0.0001). The 1- and 3-year overall survival rates were 97.4% and 85.5%, respectively, in the esophagectomy group and 98.1% and 88.7%, respectively, in the CRT group (P=0.78). Cox proportional hazards modeling showed that the overall survival was comparable between the two groups after adjusting for age, sex, and tumor size. The hazard ratio of CRT for overall survival was 0.95 (95% confidence interval 0.37-2.47). The incidence of local recurrence, including metachronous esophageal cancer, was significantly higher in the CRT group than in the esophagectomy group (P<0.0001). Most local recurrences in the CRT group were intramucosal carcinomas, and were cured after salvage treatment, mainly using endoscopy. CONCLUSIONS: The overall survival rate of patients with clinical stage I esophageal cancer treated with CRT was comparable to that in those treated with esophagectomy, despite a high local recurrence rate. Locally recurrent carcinoma was endoscopically treatable in most patients, with no effect on overall survival. CRT seems to be a viable alternative to esophagectomy in patients with clinical stage I esophageal cancer.	esophagus
Comparison of chemoradiotherapy with radiotherapy alone in patients with esophageal adenocarcinoma.	Despite the wide use of definitive chemoradiotherapy (CRT) for locally advanced esophageal adenocarcinoma, there is little evidence that CRT improves the survival of patients with esophageal adenocarcinoma compared with radiotherapy (RT) alone. Therefore, we retrospectively evaluated the outcome of patients with esophageal adenocarcinoma treated by CRT and RT alone. Patients were treated at the Gunma Prefectural Cancer Center (Ota, Japan) and the Gunma University Hospital (Maebashi, Japan). Patients provided written informed consent before treatment. Patients with distant metastases were excluded. CRT consisting of RT, nedaplatin, and 5-fluorouracil has been performed since 2002 when patients have adequate bone marrow, liver, and renal function. Between November 1993 and April 2006, 8 patients were treated by CRT and 12 were RT alone. The median follow-up period of surviving patients was 19 months. CRT group had a significantly higher complete response rate than those RT alone group (87% vs. 33%, P = 0.05). Of all patients, 2-year overall survival rate was 41% and the median survival time was 18 months. The 2-year overall survival of patients treated by CRT was 58%, significantly better than 24% of those with RT alone (P = 0.02). CRT can improve outcomes of patients with esophageal adenocarcinoma compared with RT alone.	esophagus
MUC1 induces metastasis in esophageal squamous cell carcinoma by upregulating matrix metalloproteinase 13.	Esophagus squamous cell carcinoma (ESCC) is one of the most deadly malignances because of its high frequency of metastasis. Given the associations of MUC1 with ESCC and tumor metastasis, we explored a potential role of MUC1 in ESCC metastasis. Among 40 ESCC and 20 paired normal tissue specimens examined, we found a significant increase of MUC1 expression in ESCC and more importantly, that expression of MUC1 and MMP13 are strongly correlated in patients who had lymph node metastasis. Studies with cell models indicated that overexpression of MUC1 upregulates the expression of MMP13, leading to increased cell migration. In support of a mode of transcriptional regulation, promoter analysis revealed that MUC1 stimulates MMP13 expression through the Runx-2-binding site. The link of MUC1 to cell motility was further confirmed by the finding that depletion of MUC1 resulted in reduced expression of MMP13 and cell migration, invasion and adhesion. Moreover, the loss of cell metastatic potential was rescued by overexpression of MMP13 completely. Collectively, our findings indicate that MUC1 contributes to ESCC metastasis by stimulating MMP13 expression, suggesting MUC1 as a novel diagnostic biomarker and therapeutic target in ESCC.	esophagus
Comparison of lifestyle and living environment among high risk immigrant and low risk host residents: implications for esophageal cancer etiology.	BACKGROUND: It has been hypothesized that the high prevalence of esophageal squamous cell carcinoma (ESCC) in China is associated with specific environments and lifestyles. A previous study found that immigrant residents (IR) from Henan, residing long term in the town of Caihu, had significantly greater risk of dying from ESCC than host residents (HR). OBJECTIVES: This study was conducted to compare lifestyle and living environments between high risk IR and low risk HR to determine risk factors for ESCC. METHODS: The subjects included randomly selected IR and HR living in Caihu. Information on lifestyle and the living environment of participants was collected by interview using a structured questionnaire. RESULTS: The IR were found to have a higher consumption of hot food (P<0.05), pickled vegetables (P<0.05) and a lower consumption of fresh fruits and vegetables, and alcohol (P<0.05), compared with the HR. There were no significant differences in income and cigarette smoking between the two populations. Fewer IR families had a separate kitchen (P<0.05) than host families. CONCLUSIONS: Our study provided some epidemiological evidence indicating that dietary factors, such as hot food, pickled vegetables, salt, and low fruit and vegetable intake, as well as a poor living environment, are possibly related to the higher prevalence of ESCC in IR. However, cigarette smoking, alcohol drinking and income were not shown to be risk factors for immigrant susceptibility to ESCC in our study.	esophagus
Population-based case-control study on risk factors for esophageal cancer in five high-risk areas in China.	OBJECTIVE: To study major etiological factors for esophageal cancer in upper gastrointestinal cancer high risk areas in China. METHODS: Five areas with high incidences of esophageal and gastric cancer with good quality cancer registration data were selected for the study: Cixian, Shexian from Hebei Province, Linxian from Henan Province, Feicheng from Shandong Province and Zhuanghe from Liaoning Province. A total of 250 cases were randomly recruited from the cancer registration database diagnosed as arising in the lower esophageal segment since January 1, 2009. Three controls were identified and matched with each case as having similar characteristics, such as gender, sex and residency. Questionnaires were applied by face to face interview with trained staff, and data entry was conducted using EPIDATA software. Conditional logistic models were employed for univariate and multivariate analyses to evaluate odd ratios and 95% confident intervals, with SPSS 13.0 statistic software. RESULTS: In single variable analysis, gastrointestinal history, GERD, smoking, passive smoking, alcohol drinking, hot food, pickled food, overnight vegetable, dried food, no breakfast, false dining posture were found to be risk factors of esophageal cancer. Eating more fresh vegetables and high BMI were protective factors. Gastrointestinal history (OR=12.658), not taking regular meals (3.465), overnight vegetables (OR=3.296), GERD (OR=3.044), hot food (OR=2.510), passive smoking (OR=2.423), pickled food (OR=2.273), alcohol drinking (OR=2.074), seldom eating breakfast(OR=1.987), and false dining posture (OR=1.977) increased the risk of esophageal cancer on multivariate logistic analysis, and fresh vegetables (OR=0.279) and BMI≥25 (OR=0.528) continued to be protective. CONCLUSIONS: Esophageal cancer could be caused by genetics acting in synergy with environmental factors. Health education for the general population in high risk areas should be strengthened, with intervention programs of nutrition and lifestyle focusing on effective prevention and control for upper gastrointestinal cancer.	esophagus
PET and PET-CT in esophageal and gastric cancer.	Esophageal cancer ranks among the ten most common malignancies in the world and is a frequent cause of cancer-related death. Almost all therapeutic modalities for esophageal cancer are associated with considerable mortality and morbidity. Consequently, there has been growing concern regarding effective management of esophageal cancer. Imaging plays an important role in the initial selection of patients. 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET) is playing an increasing role in the management of esophageal cancer. The role of FDG-PET in diagnosis, preoperative staging, monitoring of response to neoadjuvant therapy, and detection of disease recurrence is evaluated in this chapter.	esophagus