crossing96/oncoscreening huggingface dataset:
Epidemiology and risk factors for gastroesophageal junction tumors: understanding the rising incidence of this disease.	Gastroesophageal (GE) junction carcinoma is a rare but often lethal condition with increasing importance as a public health problem in recent decades. Whereas diagnosis of this disease has been complicated historically by the lack of uniform classification standards, available data from the Surveillance, Epidemiology, and End Results cancer registry program in the United States show an approximate 2.5-fold increase in the incidence of GE junction adenocarcinoma from 1973 to 1992, with rates stabilizing in the past 2 decades. Similar proportional trends are observed among subgroups defined by race and gender, but rates are significantly higher in males relative to females, and in white males relative to black males. Smoking, obesity, and GE reflux disease are significant risk factors for GE junction adenocarcinoma, and may account for a substantial fraction of total disease burden. Infection with Helicobacter pylori has been associated with reduced incidence, and high dietary fiber intake has also been linked to lower disease risk. Ongoing studies continue to explore a potential role for nonsteroidal anti-inflammatory drugs in chemoprevention.	esophagus
Mechanistic target of rapamycin small interfering RNA and rapamycin synergistically inhibit tumour growth in a mouse xenograft model of human oesophageal carcinoma.	OBJECTIVES: To investigate the effect of mechanistic target of rapamycin (mTOR)-specific small interfering RNA (siRNA) and rapamycin on tumour size and levels of hypoxia inducible factor 1α(HIF-1α), vascular endothelial growth factor (VEGF) and mTOR proteins, and mTOR mRNA, in a mouse xenograft model of human oesophageal carcinoma. METHODS: Tumours were induced in BALB/c nude mice using the human oesophageal squamous cell carcinoma cell line, EC1, injected subcutaneously. Animals were divided into four treatment groups (n = 5 per group) after 7 days: control (phosphate buffered saline, daily intraperitoneal [i.p.] injection); 50 μg/kg rapamycin, daily i.p. injection; 3 μg/kg mTOR siRNA, daily i.p. injection; combined mTOR siRNA and rapamycin, daily i.p. injections. Tumour volume was measured 21 days after xenograft. Levels of mTOR, VEGF and HIF-1α were assessed via immunohistochemistry and in situ hybridization. RESULTS: mTOR siRNA and/or rapamycin significantly decreased tumour volume and levels of HIF-1α, VEGF and mTOR protein, and mTOR mRNA. Combination treatment was significantly more effective than either treatment alone. CONCLUSIONS: mTOR siRNA and/or rapamycin inhibited the growth of oesophageal carcinoma in vivo. This may represent a novel and effective treatment strategy for oesophageal carcinoma.	esophagus
MicroRNA as a new factor in lung and esophageal cancer.	Lung cancer is the most lethal cancer due to late detection in advanced stages; early diagnosis of lung cancer allows surgical treatment and improves the outcome. The prevalence of gastroesophageal reflux-related adenocarcinomas of the esophagus is increasing; repetitive surveillance endoscopies are necessary to detect development of cancer. A blood-based biomarker would simplify the diagnosis and treatment of both diseases. MicroRNAs (miRNAs) are short RNA strands that interfere with protein production. miRNAs play pivotal roles in cell homeostasis, and dysregulation of miRNAs can lead to the development of cancer. miRNAs can be found in all body fluids and have been proposed to serve as messengers between closely localized cells but also distant organs. Cancer cells actively secrete miRNAs, and these miRNA profiles can be found in blood. We outline, here, how these miRNAs may aid in diagnosis and treatment of lung and esophageal cancers, as well as their apparent limitations.	esophagus
Randomized trial comparing minimally invasive esophagectomy and open esophagectomy: early perioperative outcomes appear improved with a minimally invasive approach.	Esophagectomy is an important curative treatment modality for esophageal cancer, but is a complex operation with associated risks. A minimally invasive approach to esophagectomy may decrease the risks associated with resection. Recently, an important study was published in the Lancet by Biere and colleagues that reported the results of a randomized study, with the primary endpoint of postoperative pulmonary infection, comparing minimally invasive esophagectomy versus open esophagectomy for esophageal cancer. The findings from this trial confirm the data from previous, non-randomized studies and highlight the substantial early postoperative benefits of minimally invasive esophagectomy.	esophagus
Oesophageal tumour progression between the diagnostic ¹⁸F-FDG-PET and the ¹⁸F-FDG-PET for radiotherapy treatment planning.	BACKGROUND AND PURPOSE: To test whether the interval between diagnostic and therapeutic FDG-PET-scanning is associated with early tumour progression. MATERIAL AND METHODS: All patients (n=45) underwent two PET scans, one for staging ('baseline PET') using an HR+ positron camera or PET/CT-scanner and one for radiotherapy planning ('therapeutic PET') using a PET/CT-scanner. All images were reviewed in random order by an experienced nuclear physician. If there were any discrepancies, the images were also compared directly. SUVmax, tumour length, lymph node metastases and distant metastases were assessed. RESULTS: The median time between the PET scans was 22 days (range: 8-49). The SUVmax increased (>10%) (19 patients, 42%) or decreased (11 patients, 24%). Fourteen patients (31%) showed tumour length progression (>1cm). TNM progression was found in 12 patients (27%), with newly detected mediastinal nodes (N) in eight patients (18%) and newly detected distant metastases (M) in six patients (13%). No significant prognostic factors were found. However, a trend was noted towards TNM progression for the type of PET-camera (p=0.05, 95% CI 0.01-0.66) and for the interval between the PET scans (p=0.09, 95% CI -0.9 to 12.5). CONCLUSION: This study suggests rapid oesophageal tumour progression. Therefore, the interval between relevant imaging and start of the radiotherapy should be minimized. Furthermore, 'state of the art' PET scanners should be used.	esophagus
Dietary intake of lignans and risk of esophageal and gastric adenocarcinoma: a cohort study in Sweden.	High intake of phytoestrogen lignans has been found to be associated with decreased risk of esophageal adenocarcinoma in our previous population-based case-control study in Sweden. To further evaluate this possible association, we tested the hypothesis of an inverse association between dietary lignan intake and risk of esophageal and gastric adenocarcinoma using a prospective design. In a population-based cohort study in Sweden, 81,670 participants who were cancer-free at baseline were followed up during 1998 to 2009. All participants completed a 96-item food frequency questionnaire (FFQ), which was used to assess dietary exposure to lignans (secoisolariciresinol, matairesinol, lariciresinol, pinoresinol, medioresinol, and syringaresinol). All cases of esophageal, gastroesophageal junctional, and gastric adenocarcinoma were identified through linkage to the Swedish Cancer Register. Cox proportional hazard models were used to estimate HRs and 95% confidence intervals (CI), with adjustment for potential confounding factors. During an average follow-up of 9.9 years, a total of 211 cases were identified, including 83 cases of esophageal or junctional adenocarcinoma, and 128 cases of gastric adenocarcinoma. There was no statistically significant association between dietary intake of lignans and any of the studied adenocarcinomas. Compared with participants in the lowest quartile of lignan intake, the adjusted HR of the highest quartile was 0.96 (95% CI, 0.46-2.00; P(trend) = 0.70) for adenocarcinoma of the esophagus or gastroesophageal junction, and 0.89 (95% CI, 0.52-1.55: P(trend) = 0.78) for gastric adenocarcinoma. No clear support for a protective role of dietary intake of lignans in the development of esophageal or gastric adenocarcinoma was found.	esophagus
Epigenetic inactivation of Wnt inhibitory factor-1 in human esophageal squamous cell carcinoma.	Wnt inhibitory factor-1 (WIF1), as one of most important Wnt antagonists, has been detected frequently silenced by promoter hypermethylation in various types of cancer. In this study, we aimed to investigate the promoter methylation profiles of WIF1 in human esophageal squamous cell carcinoma (ESCC) tissues and cell lines, as well as the functional roles of WIF1 in the human ESCC metastatic behavior. WIF1 mRNA levels and promoter methylation status in ESCC tissues and cell lines were detected using RT-PCR and methylation-specific PCR (MS-PCR), respectively. WIF1 protein levels were assessed by Western blot. Stable ESCC cell line with restoration of WIF1 was generated in EC109 cells, which naturally do not express detectable WIF1 mRNA. The effects of reexpressed WIF1 on EC109 cell proliferation and migration were investigated using crystal violet and wound healing assay, respectively. Also the effects of WIF1 reexpression on the beta-catenin/T-cell factor-dependent transcription activity was measured by luciferase assay. WIF1 promoter methylation was frequently observed in ESCC tissues (46%, 23/50) and cell lines (50%, 2/4). Treatment with demethylating agent, 5-aza-2'-deoxycytidine (5-aza-dC), increased or restored WIF1 expression in these ESCC cell lines. Restoration of the WIF1 in EC109 cells resulted in a significant inhibition on both cell proliferation and migration. Moreover, reexpression of WIF1 caused significant decrease of beta-catenin/T-cell factor-dependent transcription activity. These findings demonstrated that WIF1 silencing due to promoter hypermethylation is a major mechanism during carcinogenesis of ESCC. This would be an opportunity to prevent the development and progression of HCC through modulation of WIF1.	esophagus
Dietary N-nitroso compounds, endogenous nitrosation, and the risk of esophageal and gastric cancer subtypes in the Netherlands Cohort Study.	BACKGROUND: Dietary N-nitroso compounds and endogenous nitrosation are important carcinogenic factors, but human evidence of their role is scarce for esophageal cancer and inconsistent for gastric cancer. OBJECTIVE: We studied the relation between risks of esophageal and gastric cancer subtypes and dietary intake of N-nitrosodimethylamine, heme iron, nitrite, and nitrate in the Netherlands Cohort Study. DESIGN: A total of 120,852 men and women aged 55-69 y were recruited in 1986, and diet, based on a 150-item food-frequency questionnaire, and other risk factors were assessed. The cohort was followed for 16.3 y, and 110 esophageal squamous cell carcinoma (ESCC), 151 esophageal adenocarcinoma, 166 gastric cardia adenocarcinoma, and 497 gastric noncardia adenocarcinoma (GNCA) cases were analyzed along with 4032 subcohort members in a case-cohort analysis. RESULTS: Positive associations were observed between N-nitrosodimethylamine intake and ESCC risk (HR for 0.1-μg/d increase in intake: 1.15; 95% CI: 1.05, 1.25; P-trend = 0.01 based on tertiles of intake) and GNCA risk (1.06; 95% CI: 1.01, 1.10; P-trend = 0.09) in men. ESCC risk was associated with nitrite intake (HR for 0.1-mg/d increase: 1.19; 95% CI: 1.05, 1.36; P-trend = 0.06) and heme-iron intake (HR for 1-mg/d increase: 1.83; 95% CI: 0.98, 3.39; P-trend = 0.03). Among women, exposure levels were lower, and we found no convincing positive associations. CONCLUSION: These results suggest that N-nitroso compounds may influence the risk of ESCC in men, but there are no clear associations for other esophageal and gastric subtypes.	esophagus
Vibrational spectroscopic changes of B-lymphocytes upon activation.	The first study interpreting B-lymphocyte activation in normal lymph nodes using vibrational micro-spectral imaging is reported. Lymphocyte activation indicates the presence and response against a pathogen, regardless of the inciting pathogen's etiology, whether a benign, reactive or malignant process. Understanding the biochemical makeup of lymphocyte activation during early stages of disease and immune response may offer significant aid in determining a tumor's origin without the presence of malignant metastatic cells but within lymph nodes that are reactive and displaying regions of hyperplasia. Infrared and Raman data scrutinized via unsupervised multivariate methods may provide a physical and reproducible method to determine the biochemical components and variances therein of activated lymph nodes with distinguishing characteristics depending on the malignancy present in the region or elsewhere in the body. The results reported here provide a proof-of-concept study that reveal a potential to screen lymph nodes for disease without the presence of metastatic cells.	esophagus
Patient-reported outcomes evaluating palliative radiotherapy and chemotherapy in patients with oesophageal cancer: a systematic review.	BACKGROUND: Patient-reported outcomes (PROs) and assessments of treatment-related toxicity provide important information on the effect of palliative chemotherapy and/or radiotherapy. The aim of this study was to review the effect of palliative radiotherapy and/or chemotherapy on symptoms and quality of life assessed by PROs and measurement of toxicity for patients with oesophageal cancer. METHODS: The Central, Medline and Embase databases (1990 to November 2011) were systematically searched for prospective studies of palliative chemotherapy and/or radiotherapy in patients with advanced oesophageal cancer with PRO- and/or toxicity outcomes. The risks of bias were assessed. RESULTS: Of 2677 records identified, only 32 included PROs, of which eight were randomised controlled trials. In studies with sufficient standard of PRO (n = 18), either Health Related Quality of Life (HRQL) (n = 14) or patient-reported dysphagia (n = 4), were assessed. Docetaxel added to cisplatin + fluorouracil (CF) improved HRQL compared to CF only, even though toxicity increased. Epirubicin added to CF resulted in longer preserved HRQL than its comparator in two trials, and non-inferiority in one. All phase II chemotherapy studies reported maintained HRQL or improved dysphagia combined with low level of toxicity. Brachytherapy resulted in better HRQL compared to stent placement in two trials, and external radiotherapy relieved dysphagia. The quality of the HRQL methodology and the interpretation and presentation of the PRO results varied, and clinical significance was seldom discussed. CONCLUSION: PRO endpoints are seldom used and further studies of homogenous patient groups with valid measures and methodology of PROs should be encouraged in the evaluation of palliative treatment. Brachytherapy, external radiotherapy and combination chemotherapy improved HRQL and dysphagia in the few identified studies with sufficient PRO methodology.	esophagus
[The molecular mechanisms of curcuma wenyujin extract-mediated inhibitory effects on human esophageal carcinoma cells in vitro].	OBJECTIVE: To study the molecular mechanisms of Curcuma Wenyujin extract-mediated inhibitory effects on human esophageal carcinoma cells. METHODS: The Curcuma Wenyujin extract was obtained by supercritical carbon dioxide extraction. TE-1 cells were divided into 4 groups after adherence. 100 microL RMPI-1640 culture medium containing 0.1% DMSO was added in Group 1 as the control group. 100 microL 25, 50, and 100 mg/L Curcuma Wenyujin extract complete culture medium was respectively added in the rest 3 groups as the low, middle, and high dose Curcuma Wenyujin extract groups. The effects of different doses of Curcuma Wenyujin extract (25, 50, and 100 mg/L) on the proliferation of human esophageal carcinoma cell line TE-1 in vitro were analyzed by MTT assay. The gene expression profile was identified by cDNA microarrays in esophageal carcinoma TE-1 cells exposed to Curcuma Wenyujin extract for 48 h. The differential expression genes were further analyzed by Gene Ontology function analysis. RESULTS: Compared with the control group, MTT results showed that Curcuma Wenyujin extract significantly inhibited the proliferation of TE-1 cells in a dose-dependent manner (P<0.05). The expression level of 88 genes changed with significance, including 66 up-regulation genes and 22 down-regulation genes. Gene Ontology analysis indicated the genes coding for proteins was involved in signal transduction (6), cell cycle (8), apoptosis (14), and cell differentiation (10). CONCLUSIONS: The Curcuma Wenyujin extract could inhibit the growth of human esophageal carcinoma cell line TE-1 in vitro. The molecular mechanisms might be associated with regulating genes expressions at multi-levels.	esophagus
Clinicopathological characteristics of human epidermal growth factor receptor 2-positive Barrett's adenocarcinoma.	AIM: To compare the clinicopathological characteristics of human epidermal growth factor receptor 2 (HER2)-positive and HER2-negative Barrett's adenocarcinoma in Japan. METHODS: We performed immunohistochemical analysis of HER2 in 30 samples taken from patients with Barrett's adenocarcinoma and dual color in situ hybridization in cases showing 2+ reactions. We compared the clinicopathological characteristics of HER2-positive and HER2-negative patients. RESULTS: HER2 positivity was identified in 8 (27%) carcinoma samples. We found that HER2 expression was associated with p53 overexpression (100% vs 52.6% in pT1 tumor; 100% vs 54.5% in all stage tumor, P < 0.05) and protruding lesions at the early disease stage. There was no association between the mucin phenotype of the carcinomas and prognosis. HER2 expression and low clinical stage were unexpectedly different between Barrett's adenocarcinoma patients and gastric cancer patients, but the macroscopic features may be associated with earlier diagnosis in these patients. CONCLUSION: Our results suggest that HER2-positive Barrett's adenocarcinomas are associated with p53 overexpression and lesion protrusion at the early disease stage.	esophagus
Management strategies of Barrett's esophagus.	Barrett's esophagus is a condition resulting from chronic gastro-esophageal reflux disease with a documented risk of esophageal adenocarcinoma. Current strategies for improved survival in patients with Barrett's adenocarcinoma focus on detection of dysplasia. This can be obtained by screening programs in high-risk cohorts of patients and/or endoscopic biopsy surveillance of patients with known Barrett's esophagus (BE). Several therapies have been developed in attempts to reverse BE and reduce cancer risk. Aggressive medical management of acid reflux, lifestyle modifications, antireflux surgery, and endoscopic treatments have been recommended for many patients with BE. Whether these interventions are cost-effective or reduce mortality from esophageal cancer remains controversial. Current treatment requires combinations of endoscopic mucosal resection techniques to eliminate visible lesions followed by ablation of residual metaplastic tissue. Esophagectomy is currently indicated in multifocal high-grade neoplasia or mucosal Barrett's carcinoma which cannot be managed by endoscopic approach.	esophagus
Leukocyte telomere length-related genetic variants in 1p34.2 and 14q21 loci contribute to the risk of esophageal squamous cell carcinoma.	Short leukocyte telomere length has been associated with significantly increased risk of esophageal cancer. A previous genome-wide association study demonstrated that four SNPs (rs398652 on 14q21, rs621559 on 1p34.2, rs6028466 on 20q11.22 and rs654128 on 6q22.1) were associated with leukocyte telomere length in Caucasians. However, the role of these genetic variants on esophageal squamous cell carcinoma (ESCC) susceptibility is still unknown. Therefore, we investigated whether these polymorphisms have impact on leukocyte telomere length and the risk of ESCC in Chinese. After measuring leukocyte telomere length of 550 healthy individuals, we observed that both rs621559 and rs398652 genetic variants are significantly associated with leukocyte telomere length. On the basis of analyzing 1550 ESCC patients and frequency-matched 1620 controls from 4 medical centers in China, we found that 0.71-fold decreased risk of ESCC is associated with the rs621559 AA genotype compared with the rs621559 GG genotype (p = 5.9 × 10(-6) ). We also detected a moderately increased OR for ESCC that was associated with the 14q21 rs398652 G allele (p = 6.5 × 10(-4) ). It has been shown that both rs621559 and rs398652 polymorphisms were significantly associated with ESCC risk in additive, recessive or dominant genetic models. Stratified analyses demonstrated that these associations were more pronounced in males. Our results highlight the complexity of genetic regulation of telomere length and further support the important role of telomere in carcinogenesis.	esophagus
Differences in outcomes of oesophageal and gastric cancer surgery across Europe.	BACKGROUND: In several European countries, centralization of oesophagogastric cancer surgery has been realized and clinical audits initiated. The present study was designed to evaluate differences in resection rates, outcomes and annual hospital volumes between these countries, and to analyse the relationship between hospital volume and outcomes. METHODS: National data were obtained from cancer registries or clinical audits in the Netherlands, Sweden, Denmark and England. Differences in outcomes were analysed between countries and between hospital volume categories, adjusting for available case-mix factors. RESULTS: Between 2004 and 2009, 10 854 oesophagectomies and 9010 gastrectomies were registered. Resection rates in England were 18·2 and 21·6 per cent for oesophageal and gastric cancer respectively, compared with 28·5-29·9 and 41·4-41·9 per cent in the Netherlands and Denmark (P < 0·001). The adjusted 30-day mortality rate after oesophagectomy was lowest in Sweden (1·9 per cent). After gastrectomy, the adjusted 30-day mortality rate was significantly higher in the Netherlands (6·9 per cent) than in Sweden (3·5 per cent; P = 0·017) and Denmark (4·3 per cent; P = 0·029). Increasing hospital volume was associated with a lower 30-day mortality rate after oesophagectomy (odds ratio 0·55 (95 per cent confidence interval 0·42 to 0·72) for at least 41 versus 1-10 procedures per year) and gastrectomy (odds ratio 0·64 (0·41 to 0·99) for at least 21 versus 1-10 procedures per year). CONCLUSION: Hospitals performing larger numbers of oesophagogastric cancer resections had a lower 30-day mortality rate. Differences in outcomes between several European countries could not be explained by differences in hospital volumes. To understand these differences in outcomes and resection rates, with reliable case-mix adjustments, a uniform European upper gastrointestinal cancer audit with recording of standardized data is warranted.	esophagus