crossing96/oncoscreening huggingface dataset:
Video-assisted laparoscopic resection of the esophagus for carcinoma after neoadjuvant therapy.	"BACKGROUND/AIMS: Classical operation approaches, used for decades during subtotal esophageal resection for esophageal carcinoma, have certain disadvantages. The transhiatal ""blind"" approach according to Orringer lacks sufficient radicality, the thoracotomic approach is burdened by serious postoperative complications, primarily respiratory. These disadvantages are eliminated to a great extent by use of the video-assisted laparoscopic transhiatal approach, which is presented in our study. METHODOLOGY: Between 2000-2006 forty-three patients with esophageal cancer underwent video-laparoscopic transhiatal esophagectomy. In all patients passage was renewed by esophagogastroplasty, constructed by placing the neoesophagus in the posterior mediastinum, anastomosis with the cervical esophagus from a laparotomy. Prior to the operation, 27 patients underwent neoadjuvant radio-chemotherapy. Chemotherapy consisted of 5 fluorouracil and cisplatinum, and radiotherapy with a total dose of 50 Gy. RESULTS: The extirpation phase was completed laparoscopically in all patients. Right-sided pneumothorax was seen in 27 patients, in six cases postoperative manifestation of left vocal chord paresis due to damage to the recurrent laryngeal nerve was observed, in 2 patients a fistula developed in the cervical anastomosis, which in all cases healed spontaneously. The operation time ranged between 225-370 minutes, the average time being 256 minutes. The mini-invasive phase took an average of 40 minutes. One patient died 57 days after the operation due to respiratory insufficiency. The average hospital stay was 12.2 days. CONCLUSIONS: The video-assisted laparoscopic transhiatal approach proved to be very useful during subtotal esophageal resection. In tumors localized in the lower portion of the esophagus, it completely replaces the transhiatal ""blind"" approach according to Orringer and, in comparison, eliminates operative hemorrhagic complications, which are more frequent in ""blind"" extirpations, especially in patients after neoadjuvant therapy. It also enables performing a lymphadenectomy, which is not possible using the ""blind"" approach. In tumors of the middle thoracic esophagus, which are inaccessible by the original Orringer's approach, it eliminates the need for a thoracotomy, which significantly contributes to the decrease of respiratory complications."	esophagus
Surgical treatment and prognosis of esophageal cancer after distal gastrectomy.	BACKGROUND: The purpose of the present study was to explore the clinicopathological characteristics and operative therapeutic efficacy of thoracic esophageal cancer after gastrectomy and compare with those without gastrectomy. METHODS: From January 2000 to June 2007, 28 esophageal cancer patients with a history of distal gastrectomy underwent subtotal esophagectomy. Vascularized pedicle colonic conduit was most commonly used for esophageal substitution. Six hundred seventeen patients without a history of gastrectomy treated in the same period form the control group. After the operation, pathological characteristic, tumor staging, and survival statistics were analyzed. RESULTS: Of those patients with esophageal cancer associated with gastric remnant, the majority were male. There was an average of 16.5 years for diagnosing esophageal cancer from the initial partial gastrectomy, 75% (21/28) of them were patients with Billroth I anastomosis. The proportion of lower-third tumors in patients after gastrectomy (12 of 28 patients, 43%) was significantly higher compared with that of the patients with intact stomachs (124 of 617 patients, 20%; P = 0.004). After surgical treatment, the overall 1-, 3-, and 5-year survival rates of gastrectomized and nongastrectomized patients were 100%, 35.00%, and 23.33% versus 98.93%, 59.42%, and 30.85% in stages I-II and 80.00%, 30.00%, and 0% versus 98.59%, 62.03%, and 21.03% in stages III-IV. The log rank test of equality of survival distribution for the gastrectomized vs nongastrectomized patients was not significant in stages I-II (P = 0.5692) but was significant in stages III-IV (P = 0.0166). CONCLUSIONS: The patients with partial gastrectomy for more than 5 years, having upper gastrointestinal symptoms, should be considered having the risk of esophageal cancer associated with gastric remnant. For patients with a history of distal gastrectomy, a vascularized pedicle colonic conduit was most commonly used for esophageal substitution. Surgical efficacy was similar with the no-gastrectomy group in early stages I-II of esophageal cancer associated with gastric remnant but was lower compared with the no-gastrectomy group in stages III-IV. So, early diagnosis and an aggressive surgical approach may be crucial to achieve better outcomes for esophageal cancer patients with gastrectomy.	esophagus
Genetics in the pathogenesis of esophageal cancer: possible predictive and prognostic factors.	INTRODUCTION: Esophageal adenocarcinoma is the most rapidly increasing cancer in Western countries. Like esophageal squamous-cell carcinoma, these tumors are often detected at an advanced stage, requiring a multimodal concept. Despite improvements in detection, surgical resection, and (neo-) adjuvant therapy, the overall survival of esophageal cancer remains lower than other solid tumors. In fact, just 30-40% of the patients with advanced esophageal cancer benefit from a neoadjuvant therapy. Therefore, predictive/prognostic markers are needed to allow tailored multimodality therapy with increased efficacy. DISCUSSION: In recent years, there has been an exponential growth in our understanding of the cellular and molecular events associated with cell cycle regulation, programmed cell death, angiogenesis, and tumor growth. In this review, the classification of Hanahan and Weinberg is used concerning the six essential changes in carcinogenesis, i.e., the six hallmarks of cancer: (1) self-sufficiency in growth signals; (2) insensitivity to antigrowth signals; (3) avoidance of apoptosis; (4) limitless replicative potential; (5) sustained angiogenesis; and (6) tissue invasion and metastasis. CONCLUSIONS: According to these six steps, this review provides an update of the most recent data about predictive/prognostic molecular markers in patients with esophageal cancer.	esophagus
Heparanase expression by Barrett's epithelium and during esophageal carcinoma progression.	Enzymatic activity responsible for the cleavage of heparan sulfate, commonly known as heparanase, is abundant in tumor-derived cells. Heparanase cleaves heparan sulfate side chains, presumably at sites of low sulfation, thus facilitating structural alterations of the extracellular matrix and basement membrane underlying epithelial and endothelial cells. Traditionally, heparanase activity was correlated with the metastatic potential of tumor-derived cells, attributed to enhanced cell dissemination as a consequence of heparan sulfate cleavage and remodeling of the extracellular matrix barrier. More recently, heparanase upregulation was documented in an increasing number of human carcinomas and hematological malignancies, correlating with increased tumor metastasis, vascular density, and shorter post-operative survival of cancer patients. Although heparanase upregulation and its pro-malignant features are well documented, the instance of its induction in the course of tumor development was less investigated. Here, we used immunohistochemical analysis to investigate heparanase expression in normal esophagus, Barrett's esophagus without dysplasia, Barrett's esophagus with low-grade dysplasia, Barrett's esophagus with high-grade dysplasia, and adenocarcinoma of the esophagus. We report that heparanase expression is already induced in Barrett's epithelium without dysplasia, and is further increased during progression through distinct pathological stages, namely, low-grade dysplasia, high-grade dysplasia, and adenocarcinoma. Notably, heparanase induction correlated with increased cell proliferation index revealed by Ki-67 staining. These findings suggest that heparanase function is not limited to the process of tumor metastasis, but rather is engaged at the early stages of esophagus carcinoma initiation and progression.	esophagus
Microsomal prostaglandin E synthase-1 inhibition blocks proliferation and enhances apoptosis in oesophageal adenocarcinoma cells without affecting endothelial prostacyclin production.	Prostaglandins are important in the progression of various gastrointestinal cancers including oesophageal adenocarcinoma (OAC). Cyclo-oxygenase (COX)-2 inhibitors reduce OAC prostaglandin production but also have potentially detrimental effects on vascular endothelial function by reducing prostacyclin production and increasing the risk of cardiovascular events. We have examined the effects of inhibiting microsomal prostaglandin synthase-1 (mPGES-1), the enzyme downstream of COX-2 in the prostaglandin synthetic cascade. In OAC cells, reduction of mPGES-1 with RNA interference blocked PGE2 production, inhibited serum-induced proliferation and enhanced apoptosis in the COX-2 expressing cell lines (OE33 and FLO) but had no effect in COX-2 deficient BIC-1 cells. Three different methods of inhibiting mPGES-1 (RNA interference, a novel small molecule inhibitor and the endogenous inhibitor 15-deoxy-Delta(12,14)-PGJ(2)) also blocked leptin induced mPGES-1 expression and PGE2 production and abolished the leptin-induced proliferative and anti-apoptotic effects in OE33 cells, without affecting COX-2 expression. The anti-proliferative effects were equivalent to those produced by COX-2 inhibitory concentrations of celecoxib and NS-398. However, unlike the two COX-2 inhibitors, mPGES-1 inhibition did not reduce endothelial prostacyclin production. In contrast to the effects of the COX-2 inhibitor celecoxib, mPGES-1 inhibition had no effects on Akt kinase activity in OAC cells. We conclude that inhibition of mPGES-1 has potentially beneficial effects in OAC without the potentially detrimental effects on vascular endothelial prostacyclin synthesis. We have also confirmed that celecoxib has anticancer actions separate from the inhibition of COX-2. Inhibition of mPGES-1 may be therapeutically useful in the treatment and prevention of OAC.	esophagus
MicroRNA expression signatures in Barrett's esophagus and esophageal adenocarcinoma.	PURPOSE: Esophageal adenocarcinoma is a highly aggressive malignancy that frequently develops from Barrett's esophagus, a premalignant pathologic change occurring in the lower end of the esophagus. Identifying Barrett's esophagus patients at high risk of malignant transformation is essential to the prevention of esophageal adenocarcinoma. Although microRNA (miRNA) expression signatures have been associated with the etiology and prognosis of several types of cancers, their roles in the development of esophageal adenocarcinoma have not been extensively evaluated. EXPERIMENTAL DESIGN: In this study, we analyzed the expression patterns of 470 human miRNAs using Agilent miRNA microarray in 32 disease/normal-paired tissues from 16 patients diagnosed with Barrett's esophagus of either low- or high-grade dysplasia, or esophageal adenocarcinoma. RESULTS: Using unsupervised hierarchical clustering and class comparison analyses, we found that miRNA expression profiles in tissues of Barrett's esophagus with high-grade dysplasia were significantly different from their corresponding normal tissues. Similar findings were observed for esophageal adenocarcinoma, but not for Barrett's esophagus with low-grade dysplasia. The expression patterns of selected miRNAs were further validated using quantitative reverse transcription real-time PCR in an independent set of 75 pairs of disease/normal tissues. Finally, we identified several miRNAs that were involved in the progressions from low grade-dysplasia Barrett's esophagus to esophageal adenocarcinoma. CONCLUSIONS: We showed that miRNAs were involved in the development and progression of esophageal adenocarcinoma. The identified significant miRNAs that may become potential targets for early detection, chemoprevention, and treatment of esophageal cancer.	esophagus
Oesophageal stenting in a district general hospital.	BACKGROUND: Oesophageal carcinoma is the ninth most common malignancy in the UK with five year survival rate of only 8%. Most patients with dysphagia present at an advanced stage. Endoscopic stent insertion is a valid method of palliation. We present the outcomes of patients stented at a district general hospital. METHOD: This is a retrospective study of patients presenting to a district general hospital with inoperable oesophageal obstruction resulting in stent insertion from December 2000 to September 2006. Case notes were reviewed for demographics, diagnosis, treatment, complication and outcome. RESULTS: Fifty-seven patients were stented endoscopically by a single surgeon during the study period for incurable oesophageal obstruction. Forty were male and 17 female (mean age 71.9 range 39-92). Most common causes were advanced adenocarcinoma (34; 60%) and squamous cell carcinoma (16; 28%). Other rarer causes were benign stricture of the oesophagus, lung carcinoma, non-Hodgkin's lymphoma and salivary gland tumour. Of the 50 patients with oesophageal carcinoma, strictures were in the lower third (in 68%), middle third (in 30%) and proximal third (in 2%). Twenty-four (42%) patients developed a complication, including overgrowth (14; 25%), migration (8; 14%), tracheo-oesophageal fistula (2; 4%) and perforation (1; 2%). There was an overall improvement in dysphagia in 41 (72%). CONCLUSION: Endoscopic stenting for advanced oesophageal obstruction is a well-tolerated procedure, which is acceptable to patients. Despite a significant complication rate, it allows the relief of dysphagia in most patients and therefore should be considered for all patients in this category.	esophagus
Prospective comparison of surgery alone and chemoradiotherapy with selective surgery in resectable squamous cell carcinoma of the esophagus.	PURPOSE: Esophagectomy remains the mainstay treatment for esophageal cancer, although retrospective studies have suggested that chemoradiotherapy (CRT) is as effective as surgery. To determine whether CRT can substitute for surgery as the primary treatment modality, we performed a prospective direct comparison of outcomes after treatment in patients with resectable esophageal cancer who had received CRT and those who had undergone surgery. METHODS AND MATERIALS: Eligible patients had resectable T1-3N0-1M0 thoracic esophageal cancer. After the surgeon explained the treatments in detail, the patients selected either CRT (CRT group) or surgery (OP group). The CRT course consisted of two cycles of cisplatin and fluorouracil with split-course concurrent radiotherapy of 60Gy in 30 fractions. Patients with progressive disease during CRT and/or with persistent or recurrent disease after CRT underwent salvage resection. RESULTS: Of 99 eligible patients with squamous cell carcinoma registered between January 2001 and December 2005, 51 selected CRT and 48 selected surgery. Of the patients in the CRT group, 13 (25.5%) underwent esophagectomy as salvage therapy. The 3- and 5-year survival rates were 78.3% and 75.7%, respectively, in the CRT group compared with 56.9% and 50.9%, respectively, in the OP group (p = 0.0169). Patients in the OP group had significantly more metastatic recurrence than those in the CRT group. CONCLUSIONS: Treatment outcomes among patients with resectable thoracic esophageal squamous cell carcinoma were comparable or superior after CRT (with salvage therapy if needed) to outcomes after surgery alone.	esophagus
[A case of early esophageal adenocarcinoma arising from esophageal cardiac glands].	A 54-year-old man was referred to our hospital with an esophageal lesion. On esophagogastroduodenoscopy a pedunculated elevated lesion about 15mm in diameter was identified in the abdominal esophagus. The surface of the lesion had irregular nodules with white coating. We found no Barrett's mucosa around the lesion. A biopsy specimen of this tumor showed well-differentiated adenocarcinoma. A lower esophagus-proximal gastrectomy was performed because this tumor was suspected to invade the submucosal layer. Eventually, the histological diagnosis after resection was esophageal adenocarcinoma arising from cardiac glands, limited to the mucosal layer (M2). This origin of the esophageal adenocarcinoma is rare. Furthermore, this form of the tumor is especially unusual, and there have been few reports of similar cases.	esophagus
Phase I study of concurrent selective lymph node late course accelerated hyper-fractionated radiotherapy and Capecitabine, Cisplatin for locally advanced esophageal squamous cell carcinoma.	Twelve patients with locally advanced esophageal squamous cell carcinoma were enrolled to evaluate the safety and efficacy of concurrent chemo-radiotherapy. Dose-limiting toxicity was mainly observed at Capecitabine 1500 mg. The maximum-tolerated dose/recommended dose of Capecitabine was 1000 mg. The Kaplan-Meier estimated overall l-year survival rate was 100%.	esophagus
The value of protecting the longitudinal staple line with invaginating sutures during esophageal reconstruction by gastric tube pull-up.	BACKGROUND: Radical surgery with lymphadenectomy offers the best chance of curing esophageal cancer, but it carries considerable risks. Generally, the resected esophagus is replaced with a gastric tube. Rupture of the gastric tube staple line is a rare but serious surgical complication. One unresolved issue is whether oversewing of the longitudinal gastric staple line is necessary to avoid staple line rupture or insufficiency. PATIENTS AND METHODS: Between 2000 and February 2008, 199 patients underwent esophageal resection for cancer or perforation at the Vienna General Hospital, Medical University of Vienna. Data were collected prospectively. Of these patients, 151 (75.9%) underwent reconstruction by pulling up a gastric tube. These comprised the study population. In 83 patients (55.0%) the longitudinal gastric staple line was not oversewn (group A). In 68 patients (45.0%) the staple line was reinforced by invaginating sutures (group B). RESULTS: The mean age of the patients was 62.0 +/- 10.6 years (median: 63.1 years). Males comprised 75.5% of the population. Adenocarcinoma was diagnosed in 77 patients (51.0%), 63 patients (41.7%) suffered from a squamous cell carcinoma, 10 patients (6.6%) had esophageal perforation, and in 1 patient (0.7%) a gastrointestinal stromal tumor was diagnosed. In group A, a leak within the staple line was observed in 4 of 83 patients (4.9%). No leak was found in group B (p = 0.09). Major surgical complications included anastomotic leakage (21 patients; 13.9%), gastric tip necrosis (3 patients; 2%), postoperative ileus (3 patients; 2.0%) and chylothorax (7 patients; 4.6%). Two major intraoperative complications (1.3%) were splenic injury and aortic bleeding. CONCLUSION: A remarkable but not statistically significant difference was found regarding staple line rupture between study groups. However, all leaks were seen in patients without a staple line suture.	esophagus
Biomarkers of apoptosis and survival in esophageal squamous cell carcinoma.	BACKGROUND: Cancer of the esophagus is a deadly malignancy, and development of biomarkers that predict survival is an urgent need. The apoptotic pathways have been hypothesized as important in progression of esophageal squamous cell carcinoma (ESCC). We investigated a panel of proteins that regulate apoptosis as candidate of biomarkers of prognosis in ESCC. METHODS: Tissue microarray (TMA) including 313 surgically-resected cases of ESCC specimens was built for immunohistochemical interrogation. We evaluated seven genes in the FasL-Fas apoptotic pathway - FasL, Fas, FAS-associated death domain protein (FADD), phosphorylated-FADD, and caspase 8 and 10, and the antiapoptotic protein bcl-2. We studied pathway integrity and relations to risk and clinical factors, and determined the prognostic significance of each marker. RESULTS: Five markers showed strong inter-marker correlations (r > or = 0.28, p < 0.001), including FasL, Fas, FADD, and caspases 8 and 10. FasL and FADD also showed modest correlations with one or more cancer risk factors, but none of the markers was significantly associated with either tumor stage or lymph node metastasis, the only two clinical factors that predicted survival in these ESCC cases. Multivariate-adjusted proportional hazard regression models showed no association between protein expression and risk of death for any of the seven markers examined. CONCLUSION: Individual biomarkers in the apoptosis pathway do not appear to predict survival of patients with ESCC.	esophagus
[Characterization of the changes in comparative genomic hybridization in esophageal cancer patients with family history].	OBJECTIVE: To characterize the profile of chromosomal imbalances in esophageal cancer (EC) with or without family history in Linzhou, Henan Province of China. METHODS: Comparative genomic hybridization (CGH) was used to examine 13 cases with positive family history of EC and 32 cases with negative family history of EC. RESULTS DNA copy number gains on chromosome 10q was observed only in the cases with postivie family history of EC (30%), and none in cases with a negative family history (P<0.05). DNA copy number losses on chromosome 15q were significantly higher in cases with postivie family history (38% vs 6%, P<0.05). The frequency of DNA copy number gains in 3q, 5p, 7p, 8q and DNA copy number losses in 3p, 19q, 9q were similar in the two groups (both beyond 20%) (P>0.05). CONCLUSIONS: Frequent DNA copy number gains on chromosome 10q and losses on chromosome 15q in EC casers with postivie family history indicate that these chromosome sites may harbor the genes related to high susceptibility to EC. Such chromosomal sites as 3q, 5p, 7p, 8q, 3p, 19q, and 9q may contain important genes related with the environmental risk factors of esophageal carcinogenesis.	esophagus
Expression and clinical significance of S100A2 and p63 in esophageal carcinoma.	AIM: To investigate the expression and clinical significance of S100A2 mRNA and protein, p63 protein in esophageal squamous cell carcinoma (ESCC) and their roles in carcinogenesis and progression of esophageal carcinoma (EC). METHODS: Immunohistochemical staining (S-P method) for S100A2 and p63 protein were performed in 40 samples of ESCC and 40 samples of normal esophageal mucosa. In situ hybridization (ISH) was used to detect the expression of S100A2 mRNA. RESULTS: Expression of S100A2 mRNA in ESCC was positive in 77.5% of samples, which was lower than that in normal mucosa (100%) by ISH (P = 0.002). The expression level of S100A2 mRNA was closely related to differentiation and and node-metastasis (P = 0.012, P = 0.008). Expression of S100A2 protein was positive in 72.5% of ESCC samples and expression of p63 protein was positive in 37.5% of ESCC samples, and was lower than that in normal mucosa (100%) (P = 0.000). The expression of S100A2 protein was correlated with the differentiation and node-metastasis (P = 0.007, P = 0.001), but no relationship was observed between the expression of p63 protein and clinical pathological manifestations. S100A2 protein was positively correlated with the expression of S100A2 mRNA, and negatively associated with the expression of p63 protein (P = 0.000, P = 0.002). CONCLUSION: S100A2 and p63 protein both play important roles in the carcinogenesis of ESCC. An investigation into the combined expression of S100A2 and p63 may be helpful in early diagnosis and in evaluating the prognosis of ESCC.	esophagus