crossing96/oncoscreening huggingface dataset:
Vitamin deficiency in Golestan Province, northern Iran: a high-risk area for esophageal cancer.	OBJECTIVE: Dietary factors seem to play a major role in esophageal carcinogenesis in Golestan Province, a high-incidence area for esophageal cancer in northern Iran. The current study was conducted to evaluate previous reports on severe deficiency of vitamin intake in Golestan. METHODS: Using a food frequency questionnaire, food intake data were collected from 30,463 healthy participants in the Golestan Cohort Study. Intake of selected nutrients was compared with recommended daily allowance and lowest threshold intake values. RESULTS: Vitamin A intake in the majority of participants was lower than recommended values. The proportion of participants with intakes lower than lowest threshold intake was as follows: urban men, 20%; urban women, 31%; rural men, 48%; and rural women, 64%. The pattern of vitamin C deficiency was similar to that of vitamin A, however, vitamin C deficiency was less common. Daily intake of vitamin C lower than the LTI was as follows: urban men, 6%; urban women, 9%; rural men, 13%; and rural women, 19%. On the other hand, protein intake in the majority of the general population in Golestan was higher than recommended values. CONCLUSION: Severe deficiency in vitamin intake among women and rural dwellers may partly explain the high incidence of EC among inhabitants in rural areas and the male:female ratio that is approximately 1 in Golestan; while EC is much more common in men in many low-incidence areas.	esophagus
STC2: a predictive marker for lymph node metastasis in esophageal squamous-cell carcinoma.	BACKGROUND: We sought to identify genes associated with the progression and metastasis of esophageal squamous-cell cancer by comparing the expression profiles of normal, primary cancer, and metastatic cancer cells isolated with laser microdissection. METHODS: Oligo microarray analysis identified several lymph node-specific, metastasis-related genes. STC2 (stanniocalcin 2), which was overexpressed in esophageal cancer cases, was chosen for further characterization. Quantitative reverse transcriptase-polymerase chain reaction and immunohistochemistry were used to explore the clinicopathologic significance of STC2 expression status in 70 cases. Additionally, the functional role of STC2 in esophageal cancer was studied by the attenuation of STC2 in an esophageal cancer cell line. RESULTS: Laser microdissection and oligo microarray analysis identified 63 candidate genes. Among them, STC2 showed higher expression in cancer tissue than in corresponding normal tissue (P < 0.001). STC2 expression was significantly correlated with lymph node metastasis, lymphatic invasion, and distant metastasis (P = 0.005, 0.007, and 0.038, respectively). Patients whose tumors had high STC2 expression had a worse 5-year survival rate than patients whose tumors had a low STC2 expression level (P = 0.016). STC2 transfected cells had a significantly higher proliferation rate than control cells (P < 0.001). Additionally, STC2 transfected cells were more invasive in vitro (P < 0.001) than control cells. These findings were validated by means of RNA interference assays. CONCLUSIONS: We identified lymph node-specific, metastasis-related genes in esophageal cancer cells. One of these, STC2, may be associated with lymph node metastasis, making it a potential prognostic marker for esophageal cancer patients.	esophagus
"Prevention of early delayed gastric emptying after high-level esophagogastrostomy by ""pyloric digital fracture""."	OBJECTIVE: This study was designed to evaluate the clinical efficacy of pyloric digital fracture for the prevention of early delayed gastric emptying (DGE) after high-level esophagogastrostomy. METHODS: From January 2004 to March 2009, we sequentially enrolled 78 patients after esophagogastrostomy: 48 patients with pyloric digital fracture (DF group) and 30 patients without any drainage procedure (non-DF group). Intraoperative manometric study was performed in 48 patients of the DF group. Postoperative evaluation was performed, including symptomatic questionnaire, radiographic study, and gastric scintigraphy. RESULTS: Intraoperative manometric study revealed that basal pyloric pressure and peak pressure of pylorus in phase III of the migrating motor complex increased significantly after gastric conduit was made and anastomosed, but decreased appreciably following digital fracture. Compared with the peak pressure of IPPW before digital fracture (88.52 ± 19.88 mmHg), it appreciably decreased following digital fracture (40.45 ± 13.52 mmHg). Occurrences of IPPW (in 10 min) and duration time of each occurrence (s) had similar trends for before and after digital fracture (11.5 ± 4.5 vs. 5.0 ± 3.5 and 7.0 ± 2.0 vs. 3.0 ± 1.0, respectively). Postoperative evaluation demonstrated that early DGE occurred in four patients in the non-DF group (13.3%), and there was no DGE patient in the DF group. There was significant difference regarding gastric scores between the DF group and the non-DF group (10.5 ± 3.4 vs. 16.7 ± 3.8, t = 2.8271, P < 0.05). Gastric scintigraphy revealed that either semi-emptying-time or percent of retention at 4 h of the DF group was significantly lower than that of the non-DF group. CONCLUSION: Pyloric digital fracture can prevent early DGE after high-level esophagogastrostomy efficaciously and conveniently.	esophagus
Resection of a giant esophageal fibrovascular polyp.	Fibrovascular polyps of the esophagus are rare benign neoplasms of the esophagus. They frequently reach giant proportions before patients develop symptoms and a diagnosis is made. Endoscopic or surgical excision is the treatment of choice. We report a case of a giant fibrovascular polyp in a 79-year-old man that was detected incidentally. The mass was resected through a left neck approach. The patient remains symptom- and recurrence-free after a 2-year follow-up.	esophagus
Validation of a nomogram predicting complications after esophagectomy for cancer.	BACKGROUND: A nomogram has been developed recently in order to predict the occurrence and severity of postoperative complications after esophagectomy for cancer. In the present study, we externally validated this nomogram in a new cohort of patients who underwent esophagectomy for cancer in a different high-volume center. METHODS: An independent dataset of 777 patients who underwent esophagectomy for cancer was used for validation. The discriminatory capability of the nomogram was determined by using the concordance index (C statistic). Calibration was evaluated by comparing the observed with the expected number of patients with complications, as predicted by the original nomogram across patients with different risk profiles. We also examined whether adjusting the value of the original coefficients of the predictors or adding new predictors would improve the fit of the nomogram. RESULTS: Discrimination of the original nomogram was similar in the validation cohort: the C statistic hardly decreased from 0.65 in the original cohort to 0.64 in the validation cohort. Observed and expected number of patients with complications were in close agreement, reflecting a good calibration (p = 0.84). Reestimation of the coefficients in the validation cohort did not lead to any significant changes of the original nomogram values. CONCLUSIONS: External validation of a nomogram predicting the occurrence and severity of complications after esophagectomy showed that the model is applicable in other high-volume hospitals. Nevertheless, preoperative prediction of complications in individual patients remains difficult, most likely due to the complexity of mechanisms causing these complications.	esophagus
Pathologic T0N1 esophageal cancer after neoadjuvant therapy and surgery: an orphan status.	BACKGROUND: Patients with esophageal carcinoma who appear to have a complete response at the primary tumor site after undergoing neoadjuvant chemoradiotherapy may still have residual disease in regional lymph nodes despite clinically negative restaging (ypT0N1). We hypothesized that these patients would have similar survival to patients with incomplete response to therapy. METHODS: We reviewed 336 esophageal cancer patients who received neoadjuvant chemoradiotherapy followed by complete resection. We identified 20 patients who obtained complete pathologic response at the primary tumor with persistent metastatic disease to regional lymph nodes (ypT0N1). These patients were compared to 123 patients with pathologic complete response and 193 with partial response for overall survival. RESULTS: Demographics among the three groups of patients were similar except that this cohort of patients with ypT0N1 had higher initial clinical stage (p = 0.013) and had more squamous cell carcinoma pathology (p = 0.005). Eighty-six percent of the ypT0N1 patients who had modern preoperative staging were felt to have clinical complete response. Five-year survival of ypT0N1 patients was intermediate, similar to pathologic partial response stage II patients in both the sixth and seventh editions of the American Joint Committee on Cancer staging criteria. CONCLUSIONS: Clinical staging of complete response to chemoradiotherapy may not translate to pathologic complete response. Patients with ypT0N1 disease at resection have intermediate but reasonable survival, justifying an aggressive approach to curative therapy. Future revisions of the staging system should place this group of patients with patients who have metastatic regional lymph nodes, stratified by number of nodes involved.	esophagus
[Small bowel ileus caused by migration of oesophageal stent].	Stents are used for the treatment of malignant strictures and stenoses in the oesophagus. Both the ease of placement and the safety of these oesophageal stents have increased considerably over the years; however, complications still occur. We describe a patient who developed small bowel obstruction and perforation due to migration of the stent. Laparotomy with resection of the diseased bowel section including the stent was performed, and the patient recovered uneventfully. Our report shows that bowel obstruction and perforation is a seldom but severe complication of migrated oesophageal stents.	esophagus
Identification of GPX3 epigenetically silenced by CpG methylation in human esophageal squamous cell carcinoma.	BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is one of the most common causes of cancer mortality in the gastrointestinal tract. Promoter hypermethylation of tumor suppressor genes contributes to gene inactivation during development of ESCC. AIM: To identify novel methylation-silenced genes in ESCC. METHODS: Genome-wide microarrays were applied to search for genes that were markedly upregulated after treatment with 5-aza-2'-deoxycytidine (5-Aza-dC) and that were markedly decreased in tumor tissue compared with paired adjacent nontumor tissue. Reverse-transcription polymerase chain reaction (PCR), immunohistochemistry, methylation-specific PCR, and bisulfite genomic sequencing were employed to investigate expression and methylation of candidate genes in five human ESCC cell lines, two human immortalized normal esophageal epithelial cell lines, primary ESCC tumor tissues, and paired adjacent nontumor tissues. RESULTS: GPX3 was selected as a novel candidate hypermethylated gene in ESCC through microarray analysis. In most ESCC cell lines, GPX3 messenger RNA (mRNA) expression was downregulated and the CpG island of GPX3 promoter was methylated. Demethylation treatment with 5-Aza-dC restored GPX3 mRNA expression. Methylation of GPX3 promoter was more frequent in ESCC tumor tissues (71.4%) than in adjacent nontumor tissues (10.7%) (P < 0.001), and methylation of GPX3 promoter correlated significantly with GPX3 mRNA downregulation. Finally, GPX3 protein expression was also significantly lower in ESCC tumor tissues than in adjacent nontumor tissues. CONCLUSION: GPX3 is downregulated through promoter hypermethylation in ESCC, which may be a potential biomarker of ESCC.	esophagus
[Characteristics of the lymph node metastases and influencing factors and their value in target region delineation in postoperative radiotherapy for thoracic esophageal carcinoma].	OBJECTIVE: To explore the distribution of lymph node metastases, to analyze the cliniopathologic factors of thoracic esophageal carcinoma after curative resection, and to provide the criteria of irradiated region delineation in radiotherapy for esophageal carcinoma. METHODS: The clinicopathological data of 763 patients who underwent esophagecotomy from Jun 2002 to Jun 2006 were retrospectively analyzed. The regularity of lymph node metastases of thoracic esophageal cancer and clinicopathological factors were stratified and analyzed with SPSS13.0 software. RESULTS: Of the 763 patients, a total of 5846 lymph nodes were dissected with an average of 7.7 lymph nodes in each case. Metastatic lymph nodes were 711, the ratio of metastatic lymph node was 12.2%, and 297 patients had lymph node involved, the lymph node metastasis rate was 38.9%. The metastatic lymph nodes of upper-thoracic esophagus were mainly observed in the supraclavicular and paratracheal regions (P < 0.05), the metastatic lymph nodes of middle-third thoracic esophagus were bidirectional, and those of the lower-third thoracic esophagus mainly metastasized to the regions adjacent to the esophagus, gastric cardia and gastric artery (P < 0.05). Both the metastasis ratio and rate of lymph nodes adjacent to the gastric artery in the lower-thoracic esophageal cancer were significantly higher than those in the middle-third and upper-third thoracic esophageal cancers (P = 0.007, P = 0.001). The multiple factors logistic regression analysis showed that tumor length, depth of tumor invasion, vascular tumor emboli and distant metastasis were major factors for lymphatic metastasis (P < 0.01). For the whole group of patients the lymph node metastatic rate was 28.5% in upper-thoracic esophageal cancer, significantly lower than 38.8% of the lower-thoracic esophageal cancer (P = 0.039) and 43.4% in the middle-thoracic esophageal cancer (P = 0.010). However, the lymph node metastatic rates were 37.0%, 37.9% and 41.4% in the upper-, middle- and lower-thoracic esophageal cancers of the 592 cases receiving left chest notches, with a non-significant difference among them (P = 0.715). CONCLUSION: The lesion length, depth of tumor invasion, vascular tumor embolus and distant metastasis are the most important parameters for lymph node metastases. Operative modes have obvious influence on the distribution of regional lymph node metastases. Therefore, in the clinical management, a postoperative prophylactic radiotherapy may be selected according to the tumor length, depth of tumor invasion, vascular tumor embolus and distant lymph node metastasis.	esophagus
[Simulation of thoracoscopic esophagectomy for esophageal cancer by three-dimensional computed tomography and usefulness for preservation of bronchial arteries].	Thoracoscopic esophagectomy for esophageal cancer was simulated preoperatively by 3-dimensional computed tomography (3D-CT). The anatomical structures such as major vessels, bone, trachea and bronchi, esophagus, lymph nodes, and broncial arteries were extracted from multi-detector row CT scanning and integrated to build the virtual operative field by multi-volume fusion. The virtual thoracoscopy was helpful to understand the location of lymph nodes and bronchial arteries in relation to the adjacent anatomical structures. Preservation of bronchial arteries is important to avoid tracheobronchial ischemia which is a fatal complication in salvage esophagectomy after definitive chemoradiotherapy. 3D-CT revealed anatomical variations of bronchial arteries and was useful for identification and preservation of bronchial arteries in thoracoscopic esophagectomy.	esophagus
[Basic technique for reconstruction after esophagectomy].	The stomach as a conduit after esophagectomy is preferred to the colon because it is much simpler to prepare and involves only 1 anastomosis. The following principles should be followed in preparing the stomach as an esophageal substitute: the complete removal of lymphatics within the left gastric area, and careful preservation of the gastric intramural vascular network. The line of resection, where the vessels of the left gastric area enter the gastric wall, should be cautiously decided. Border between the left and right gastric area of the lesser curvature is identified by the courses of these arteries. The 1st GIA should be inserted slightly toward the caudal side, and the 2nd GIA should be fired along the resection-line. The final GIA should be advanced to the highest point. The space beneath the sternum in the anterior mediastinum is easily created with minimal blood loss. The space is initially created by blunt finger dissection through the abdominal and cervical incisions, and further developed by insertion of a flat malleable intestinal retractor with a hole on 1 side, which is useful for elevating the esophageal substitute without a twist.	esophagus
Ethanol-mediated carcinogenesis in the human esophagus implicates CYP2E1 induction and the generation of carcinogenic DNA-lesions.	Chronic alcohol consumption is a major risk factor for esophageal cancer. Various mechanisms may mediate carcinogenesis including the genotoxic effect of acetaldehyde and oxidative stress. Ethanol exerts its carcinogenic effect in the liver among others via the induction of cytochrome P450 2E1 (CYP2E1) and the generation of carcinogenic etheno-DNA adducts. Here we investigated if such effects can also be observed in the human esophagus. We studied nontumorous esophageal biopsies of 37 patients with upper aerodigestive tract cancer and alcohol consumption of 102.3 ± 131.4 g/day (range: 15-600 g) as well as 16 controls without tumors (12 teetotalers and 4 subjects with a maximum of 25 g ethanol/day). CYP2E1, etheno-DNA adducts and Ki67 as a marker for cell proliferation were determined immunohistologically. Chronic alcohol ingestion resulted in a significant induction of CYP2E1 (p = 0.015) which correlated with the amount of alcohol consumed (r = 0.6, p < 0.001). Furthermore, a significant correlation between CYP2E1 and the generation of the carcinogenic exocyclic etheno-DNA adducts 1,N(6)-ethenodeoxyadenosine (r = 0.93, p < 0.001) and 3,N(4)-ethenodeoxycytidine (r = 0.92, p < 0.001) was observed. Etheno-DNA adducts also correlated significantly with cell proliferation (p < 0.01), which was especially enhanced in patients who both drank and smoked (p < 0.001). Nonsmokers and nondrinkers had the lowest rate of cell proliferation, CYP2E1 expression and DNA lesions. Our data demonstrate for the first time an induction of CYP2E1 in the esophageal mucosa by ethanol in a dose dependent manner in man and may explain, at least in part, the generation of carcinogenic DNA lesions in this target organ.	esophagus
Programmed cell death 4 (PDCD4) expression during multistep Barrett's carcinogenesis.	AIM: To test the contribution of programmed cell death 4 (PDCD4) tumour suppressor gene in Barrett's carcinogenesis. METHODS: PDCD4 immunohistochemical expression was assessed in 88 biopsy samples obtained from histologically proven long-segment Barrett's mucosa (BM; 25 non-intestinal columnar metaplasia, 25 intestinal metaplasia (IM), 16 low-grade intraepithelial neoplasia (LG-IEN), 12 high-grade IEN (HG-IEN) and 10 Barrett's adenocarcinoma (BAc)). As controls, 25 additional samples of native oesophageal mucosa (N) were obtained from patients with dyspepsia. To further support the data, the expression levels of miR-21, an important PDCD4 expression regulator, in 14 N, 5 HG-IEN and 11 BAc samples were determined by quantitative real-time PCR analysis. Results PDCD4 immunostaining decreased progressively and significantly with the progression of the phenotypic changes occurring during Barrett's carcinogenesis (p<0.001). Normal basal squamous epithelial layers featured strong PDCD4 nuclear immunoreaction (mostly coexisting with weak-moderate cytoplasmic staining). Non-intestinal columnar metaplasia and intestinal metaplasia preserved a strong nuclear immunostaining; conversely, a significant decrease in PDCD4 nuclear expression was seen in dysplastic (LG-IEN and HG-IEN) and neoplastic lesions. Weak-moderate cytoplasmic immunostaining was evident in cases of LG-IEN, while HG-IEN and BAc samples showed weak cytoplasmic or no protein expression. As expected, miR-21 expression was significantly upregulated in HG-IEN and BAc samples, consistently with PDCD4 dysregulation. CONCLUSIONS: These data support a significant role for PDCD4 downregulation in the progression of BM to BAc, and confirm miR-21 as a negative regulator of PDCD4 in vivo. Further efforts are needed to validate PDCD4 as a potential prognostic marker in patients with Barrett's oesophagus.	esophagus
The standardized uptake value of 18-fluorodeoxyglucose positron emission tomography after chemoradiation and clinical outcome in patients with localized gastroesophageal carcinoma.	BACKGROUND: Empirical trimodality (TM) or bimodality (BM) approaches lead to unpredictable outcomes in patients with localized gastroesophageal carcinoma (LGC). We hypothesized that the standardized uptake value (SUV) of positron emission tomography (PET) after chemoradiation would define the clinical outcome in patients. METHODS: We analyzed 272 (TM = 155 and BM = 117) LGC patients after chemoradiation PET and studied its association with overall survival (OS) and disease-free survival (DFS). The log-rank test, multivariate Cox proportional hazards model, and Kaplan-Meier survival plots were used to analyze the dichotomized data (using the median as a cutoff). RESULTS: The median survival of TM patients was 49 months (95% CI: 36 to not reached) and that of BM patients was 20 months (95% CI: 15-34; p < 0.0001); however, if the postchemoradiation SUV was <4.6 (4.6 = median SUV), the OS of TM and BM patients was not significantly different (p = 0.22). In the multivariate Cox model, postchemoradiation SUV (p = 0.02), baseline stage (p = 0.03), histology grade (p = 0.01), and having surgery (p = 0.004) were independent prognosticators for OS and DFS. CONCLUSIONS: These data document that the low postchemoradiation SUV in both TM and BM patients defines clinical aggression and has a similar clinical outcome. Systematic validation of PET changes, in this setting, can facilitate individualization of therapy of LGC patients.	esophagus
Initial institutional experience with thoracoscopic assisted esophagectomy.	We report our initial experience with thoracoscopic assisted esophagectomy (TAE) in patients with esophageal carcinoma. Clinical outcome measures are reported for 14 consecutive patients who underwent thoracoscopically assisted esophagectomy at our institution between January 2007 and June 2009. These outcomes were compared with 18 patients who underwent open esophagectomy (OE) during this time. All 14 patients were male, with a median age of 63. All had distal esophageal adenocarcinoma: stage I (7), II A (2), II B (3), and III (2). Surgical approaches included laparotomy combined with thoracoscopy and cervical (n=12), or intrathoracic anastomosis (n=2). Compared with an open approach, the thoracoscopic assisted esophagectomies were longer (median time 460 vs. 386 minutes), and they were associated with less blood loss (250 mL vs. 500 mL) and less respiratory complications (14.3% vs. 27.8%). In our TAE group more lymph nodes were removed (median number 12 in TAE vs. 10 in OE). The overall morbidity was similar in both groups (42.8% in TAE vs. 50% in OE group), but the in-hospital mortality was reduced with TAE (7.1% with TAE vs. 16.7% with OE). TAE is feasible with a low conversion rate, acceptable morbidity, and low mortality.	esophagus