crossing96/oncoscreening huggingface dataset:
Serum pepsinogens and Helicobacter pylori in relation to the risk of esophageal squamous cell carcinoma in the alpha-tocopherol, beta-carotene cancer prevention study.	BACKGROUND: Helicobacter pylori can induce gastric atrophy in humans, which in turn increases gastric cancer risk. Whether H. pylori and gastric atrophy also affect the risk of esophageal squamous cell carcinoma (ESCC), however, remains unresolved. METHODS: We performed a nested case-control study within the prospective Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study to assess these relationships. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study is composed of 29,133 Finnish male smokers, ages 50 to 69 years, who were recruited during 1985-1988. Using baseline sera, we assessed H. pylori status (via immunoglobulin G antibodies against whole-cell and CagA antigens) and gastric atrophy status [via the biomarkers pepsinogen I (PGI) and pepsinogen II (PGII)] in 79 ESCC cases and 94 controls. Logistic regression with adjustment for age, date of blood draw, education, cigarette smoking, alcohol, body mass index, and fruit and vegetable intake was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI). RESULTS: Gastric atrophy (PGI/PGII <4) was associated with ESCC (OR, 4.58; 95% CI, 2.00-10.48). There was no evidence for an association between H. pylori and ESCC (OR, 0.94; 95% CI, 0.40-2.24). CONCLUSIONS: These results could be explained by misclassification of H. pylori status due to serologic amnesia, ESCC risk being dependent on the functional consequences or interactions of H. pylori rather than the infection per se, gastric atrophy having a different histogenesis in ESCC without being primarily dependent on H. pylori acquisition, or a lack of statistical power to detect an effect. IMPACT: Validation of these results may warrant mechanistic studies to determine the route of association between gastric atrophy and ESCC.	esophagus
Malignant esophageal dysphagia palliation using insertion of a covered Ultraflex stent without fluoroscopy: a prospective observational study.	BACKGROUND: This study aimed to investigate the efficacy and safety of placing self-expandable metal stents (SEMSs) without fluoroscopy for palliation of malignant esophageal or esophagogastric strictures. METHODS: From January 2003 to June 2008, a prospective observational study investigated the placement of covered proximal-release Ultraflex stents without fluoroscopy in nonoperable malignant esophageal and esophagogastric strictures. The technical success as well as the early and late complications (perforation, migration, severe gastroesophageal reflux, hematemesis, and reobstruction due to tissue ingrowth or overgrowth) were recorded. Dysphagia before and after stent placement was scored on a 5-point scale. All the patients were observed monthly in the outpatient clinic or by telephone contact until death. RESULTS: The study enrolled 89 patients (16 women; mean age, 69.54±7.1 years) with dysphagia due to inoperable esophageal or esophagogastric malignant strictures (29 squamous cell cancers, 52 adenocarcinomas, and 8 obstructive malignant extrinsic compressions). The mean stricture length was 6.2±2.8 cm. Endoscopic deployment was achieved for 83 patients (93.2%), with accurate stent positioning in all the patients except one. An adequate relief of symptoms was noted for 82 of the patients (92.1%). During the follow-up period, 36 patients (43.4%) had recurrent dysphagia, caused by tumor overgrowth in 32 cases and stent migration in 4 cases, after an average time of 82 days (range 67-216 days). A stent-in-stent procedure was performed in 27 cases. For two patients, a third stent-in-stent needed to be placed after 85 and 216 days, respectively. CONCLUSION: In most cases, SEMSs can be accurately and safely positioned without fluoroscopy for palliative treatment of malignant esophageal dysphagia.	esophagus
The resistance of esophageal adenocarcinoma to bile salt insult is associated with manganese superoxide dismutase expression.	BACKGROUND: Bile acids are implicated as etiologic agents in esophageal cancer. We sought to analyze the impact of bile acid exposure on esophageal epithelial cells, Barrett's metaplastic cells (BE), esophageal adenocarcinoma cells (EAC), and esophageal squamous carcinoma cell (ESC). We sought to determine if cellular resistance is related to manganese superoxide dismutase expression. METHODS: Cells were exposed to sodium choleate (CA), sodium deoxycholate (DCA), sodium glycocholate (GCA), sodium taurocholate (TCA), or a 1:1 mixture (MIX) of reagents at concentrations in the range 0.2-0.8 mM. Cell viability was evaluated by MTT assay. Manganese superoxide dismutase (MnSOD) expression was analyzed by Western blot. Statistical analysis was performed using SPSS ver. 17.0, SPSS Inc., Chicago, IL. RESULTS: Bile salt exposure inhibited cell viability in esophageal squamous cells in time- and growth-dependent manner. There was a 50% decrease in cell viability from 4 to 24 h. BE, EAC, and ESC cell lines were more resistant to bile insult. In untreated cell lines, MnSOD expression was significantly decreased in EAC and ESC cell lines compared with esophageal squamous epithelial cells and BE cells (P=0.002). Exposure of ESC cells to bile salt increased MnSOD expression. CONCLUSION: The confirmation of the role of reactive oxygen species (ROS) and bile acids in esophageal carcinogenesis has interesting implications for chemoprevention in patients with reflux esophagitis and Barrett's esophagus. Further studies are necessary to assess the preventative role of antioxidant supplementation.	esophagus
Tumour budding and a low host inflammatory response are associated with a poor prognosis in oesophageal and gastro-oesophageal junction cancers.	AIMS: Tumour budding and host inflammatory response are parameters easily assessed histologically that have prognostic significance in many cancers. There have been few studies examining these parameters in oesophageal or gastro-oesophageal cancers. This study aims to address that deficiency. METHODS AND RESULTS: A two-centre, retrospective study was carried out on 356 patients. Tumour budding and host inflammatory response at the invasive front were assessed histologically. Statistical analysis was performed to determine the prognostic significance of these factors. The median number of tumour buds was four (range 0-50) with 172 of 356 cases having five or more buds at the invasive front. The presence of five or more buds was associated with a poor prognosis on univariate analysis (P = 0.0001), as was a sparse or moderate host inflammatory response (P = 0.001). Tumour budding retained prognostic significance when tumours were separated into adenocarcinomas (n = 287) and squamous cell carcinomas (n = 69), but host inflammatory response was a significant prognostic factor only for adenocarcinomas. On multivariate analysis the presence of five or more buds retained significance (P = 0.002). CONCLUSIONS: Tumour budding and host inflammatory response are important prognostic factors in patients with oesophageal/gastro-oesophageal cancer and can be used to identify high-risk patients who would benefit from closer follow-up and adjuvant therapies.	esophagus
Assessment of genetic damage in inflammatory, precancerous, and cancerous pathologies of the esophagus using the comet assay.	The last few decades of cancer research indicate that DNA damage is a prerequisite for development of malignancies. An increase in damage points to reduced repair capacity and risk for progression. We have used the comet assay to assess DNA damage in individuals with various disorders of the upper gastrointestinal (GI) tract in a cohort of patients from South India. After thorough clinical, endoscopic, and histopathological evaluation, patients were categorized into cancers, precancers, inflammatory pathologies, and controls. Results from the comet assay performed on esophageal tissue cells and blood from the same patients showed good correlation of damage in the paired samples; subsequent assays were performed in blood. There was more DNA damage in cancers when compared with controls. A significant increase in damage in cancers (37%) and precancers (30.7%) when compared with the inflammatory pathologies (15.6%) and controls (10.03%) was noted. The interindividual variation observed was independent of confounding factors such as tobacco and alcohol. We suggest that the damage seen in the esophageal tissue is likely to be disease-related, whereas that seen in blood may be a reflection of disease. Individuals with greater damage may be prone to disease progression and the comet assay can be used as a cost-effective biomonitoring tool to assess damage and identify these individuals at risk for a progressive pathology, even to malignancy.	esophagus
Associations between leptin and adiponectin receptor upregulation, visceral obesity and tumour stage in oesophageal and junctional adenocarcinoma.	BACKGROUND: Obesity is associated with oesophageal adenocarcinoma, but mechanisms linking fat and carcinogenesis remain poorly understood. Altered circulating adipocytokines may be important. This study aimed to identify pathways through which visceral fat impacts on tumour biology. METHODS: Seventy-five patients with oesophageal adenocarcinoma underwent anthropometric and radiological assessment of obesity. Expression of leptin receptor (ObR) and adiponectin receptors 1 and 2 (AdipR1, AdipR2) was quantified by real-time reverse transcriptase-polymerase chain reaction. The human oesophageal adenocarcinoma cell line OE33 was used as the calibrator sample. RESULTS: Ninety-one per cent of tumours expressed ObR, 95 per cent expressed AdipR1 and 100 per cent expressed AdipR2. Relative expression of ObR was upregulated in 67 per cent, and AdipR1 and AdipR2 were downregulated in 55 and 68 per cent respectively, relative to the calibrator sample. Upregulated ObR and AdipR2 expression was significantly associated with anthropometric and radiological measures of obesity. Upregulated ObR was associated with advanced tumour and node category (P = 0.036 and P = 0.025 respectively), and upregulated AdipR2 with nodal involvement (P = 0.037). CONCLUSION: Obesity is associated with upregulated ObR and AdipR2 expression in oesophageal adenocarcinoma. The association of ObR and AdipR2 with tumour stage suggest that pathways involving adipocytokines affect tumour biology.	esophagus
The pharmacokinetics and safety of porfimer after repeated administration 30-45 days apart to patients undergoing photodynamic therapy.	BACKGROUND: Porfimer is an intravenous (i.v.) injectable photosensitizing agent used in the photodynamic treatment of tumours and of high-grade dysplasia in Barrett's oesophagus. AIM: To assess the pharmacokinetics as well as the safety profiles of porfimer after a first and a second dose administered 30-45 days apart in patients undergoing photodynamic therapy. METHODS: Nineteen patients (16 with cholangiocarcinoma) were enrolled. Porfimer sodium was administered by i.v. injection over 3-5 min. Blood samples were collected prior to starting i.v. drug injection and postdose at different time points after the first and second administrations. RESULTS: Porfimer exposure values after the second administration were statistically higher than those observed after the first administration, suggesting a slight accumulation of porfimer following repeated administration. The apparent mean elimination half-life of porfimer increased from 410 h after the first administration to 725 h after the second administration. The safety profiles of porfimer after a first and a second administration were similar and did not raise additional concern. Eight patients experienced nine serious adverse events. Only photosensitivity was deemed study-drug related. CONCLUSION: Porfimer appears to display a safe and tolerable profile when used in patients requiring a second photodynamic therapy within 45 days.	esophagus
[Effects of RNAi-silenced id1 gene on the biology behavior of esophageal cancer cell lines Eca-109].	OBJECTIVE: To study the effect of shRNA expressing vector targeting to id1 gene on the biological behavior of the esophageal cancer cell. METHODS: The specific shRNA sequence was designed, synthesized and cloned into pGFU6/neo vector. Then, the resulting recombinants were transfected into Eca-109 cells using Lipofetamine 2000 following the instruction of the manufactures. The expression levels of id1 mRNA were analyzed by RT-PCR and the levels of Id1, p16 and PCNA protein were detected by Western blot assay. The growth of Eca-109 cells was analyzed using clone formation assay and trypan blue exclusion assay. Distribution of cell cycle and proliferation of Eca-109 cells were assessed by flow cytometry. RESULTS: The sequence of recombinant plasmid was confirmed by sequence analysis. The expression levels of id1 mRNA and Id1 protein significantly decreased in Eca-109 cells transfected with pGFU6/neo-Id1-1 vector compared to the negative control group (P < 0.05). The recombinant plasmid expressing id1 shRNA could effectively inhibit cell proliferation and induce cell cycle arrest in G0/G1 phase with a remarkably decrease of cells in S phase (P < 0.05). CONCLUSION: All the above data suggested that the expression of id1 gene was significantly inhibited in Eca-109 cells transfected with pGFU6/neo-id1-1 recombinant. Furthermore, the proliferation of id1 knockdown cells was depressed.	esophagus
Critical role of surgery in patients with gastroesophageal carcinoma with a poor prognosis after chemoradiation as defined by positron emission tomography.	BACKGROUND: The prognosis of patients with localized gastroesophageal carcinoma (LGC) can be defined after chemoradiation by the standardized uptake value (SUV) of positron emission tomography (PET). High SUV (HSUV) after chemoradiation portends a poor prognosis. The authors retrospectively examined the role of surgery in patients with HSUV after chemoradiation. METHODS: The authors analyzed the postchemoradiation PET scans of 204 LGC patients. One hundred twenty-nine patients had HSUV. Two postchemoradiation variables were evaluated: SUV and surgery and their association with overall survival (OS) and event-free survival (EFS). The log-rank test, multivariate Cox proportional hazards model, and Kaplan-Meier survival plots were used to assess the association between OS or EFS and the dichotomized SUV (using the median SUV as the cutoff) and surgery. RESULTS: The median SUV was 4.6. The OS of the 52 patients who had an SUV above the median and did not undergo surgery (HSUV-NS) (median OS, 1.22 years; 95% confidence interval [95% CI], 1.02-2.16 years) was much shorter than that of the 77 patients with an SUV above the median who underwent surgery (HSUV-S) (median OS, 2.7 years; 95% CI, 2.43 years to not reached [P<.0001]). Similarly, the EFS for patients with HSUV-NS was significantly shorter than that for patients with HSUV-S (P=.001). In the multivariate analyses, patients who underwent surgery (irrespective of SUV) had a lower risk of death (P=.0001) and disease progression (P=.002). CONCLUSIONS: The data from the current study suggest that surgery may prolong OS and EFS in patients with a poor prognosis after chemoradiation as defined by PET. However, these data need confirmation.	esophagus
MiRNAs and their association with locoregional staging and survival following surgery for esophageal carcinoma.	BACKGROUND: Prognostic and staging information for esophageal cancer impacts clinical decision making. miRNAs, a newly discovered class of biomarkers and their expression might add additional information relevant to this. In this study we evaluated the expression of selected miRNAs and their relationship to tumor stage and survival in patients with locally advanced tumors following esophagectomy. MATERIALS AND METHODS: A total of 43 individuals undergoing esophagectomy (without neoadjuvant therapy) for locally advanced but not metastatic (pT2/3; pN0/1) disease (22 adenocarcinoma [EAC], 21 squamous cell carcinoma [SCC]) were included in this study. Perioperative clinical and survival data were collected and managed on a database. The expression of miR-21, miR-106a, miR-148a, miR-205 in formalin-fixed paraffin-embedded specimens was evaluated by TaqMan qPCR assays. Expression was compared with clinicopathological features of the cancers and outcome. RESULTS: In EAC, miR-148a expression levels were inversely associated with cancer differentiation. miR-21 expression levels were higher in SCC if distant lymph node metastases were present. miR-148a levels were lower when EAC was more proximally located, and miR-21 levels were lower when SCC was more proximal. miR-106a and miR-148a were lower in patients with SCC who developed recurrent disease or had a tumor-related death. CONCLUSIONS: In patients with locally advanced esophageal squamous cell carcinoma, but not adenocarcinoma, alterations in the expression of miR-21 correlate with tumor location and lymph node status. Furthermore, miR-106a and miR-148a expression correlates with disease recurrence and tumor-related mortality. miRNA markers might inform the initial assessment of these patients, and predict those at higher risk of postsurgical recurrence.	esophagus
Vessel probe CT protocol in the study of esophageal carcinoma: can it improve preoperative T staging?	AIMS: This study aims to compare transverse images and vessel probe (VP) in MPR mode reconstructions obtained by 16-row MDCT with the histological findings in the preoperative T staging of esophageal cancer. MATERIALS AND METHODS: Thirty-one patients (23 M, 8 F, mean age 63.2) with endoscopic and histological diagnosis of esophageal carcinoma underwent CT examination. Esophageal lumen was distended by CO2 and a biphasic technique with 35 s and 70 s delay was used after intravenous injection of contrast material. Transverse and VP in MPR mode images were evaluated and the following parameters were considered: presence and location of the tumor; esophageal wall thickness and enhancement; depth of visceral wall invasion; periesophageal fat morphology and infiltration of adjacent organs. Preoperative staging was performed and then it was compared with the histological findings considered as reference standard. RESULTS: Sensibility, negative predictive and accuracy values were 67%, 64% and 79% by using axial images for preoperative T staging, while the use of VP increased the previous values up to 83%, 78% and 89%, respectively. CONCLUSIONS: In the preoperative staging of esophageal cancer, VP in MPR mode reconstructions obtained by 16-row MDCT increase the sensibility and diagnostic accuracy values in the T parameter evaluation compared with axial images.	esophagus
Esophageal verrucous carcinoma arising from hyperkeratotic plaques associated with human papilloma virus type 51.	Esophageal verrucous carcinoma is a rare variant of esophageal squamous cell carcinoma. We report a case of esophageal verrucous carcinoma associated with human papilloma virus (HPV) type 51. The patient had long-standing dysphagia and odynophagia, and white esophageal plaques showing hyperkeratosis on biopsy. At repeat endoscopy, the esophagus was covered with verrucous white plaques and areas of nodular mucosa with white fronds, with a distal 10-cm smooth mass protruding into the lumen. Biopsies demonstrated an atypical squamoproliferative lesion but no frank malignancy. HPV type 51 DNA was detected in endoscopic biopsy specimens by polymerase chain reaction. Because the size of the lesion favored an underlying verrucous carcinoma, our patient underwent minimally invasive esophagectomy with gastric pull-up and cervical anastomosis. The pathologic diagnosis was a well-differentiated esophageal verrucous carcinoma. One year after esophagectomy, the patient feels well and is free of disease. Although HPV DNA was not detected in the cancer tissue obtained at surgery, our case suggests an association between HPV type 51 and esophageal verrucous carcinoma. The clinical evolution in this case highlights the importance of endoscopic surveillance in patients with exuberant esophageal hyperkeratosis, and of definitive surgical resection when malignancy is suspected even if frank malignancy is not demonstrated on superficial biopsies.	esophagus
Risk of Barrett's oesophagus, oesophageal adenocarcinoma and reflux oesophagitis and the use of nitrates and asthma medications.	OBJECTIVE: To investigate the relationship between use of asthma medication and nitrates and risk of reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma. MATERIAL AND METHODS: Data were collected on use of asthma medication and nitrates at least 1 year before interview from patients with reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma. Associations between use of asthma medications and nitrates and the risk of reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma were estimated using multiple logistic regression. RESULTS: Nine hundred and forty-one subjects were recruited: 230 reflux oesophagitis, 224 Barrett's oesophagus, 227 oesophageal adenocarcinoma patients and 260 population controls. Barrett's oesophagus patients were more likely than controls to have had a diagnosis of asthma (odds ratio 2.15, 95% confidence interval 1.15-4.03) and to have used asthma medications (odds ratio 2.13, 95% confidence interval 1.09-4.16). No significant associations were observed between use of asthma medication or nitrates and reflux oesophagitis or oesophageal adenocarcinoma. CONCLUSIONS: Gastro-oesophageal reflux symptoms appear to confound the association between asthma medication use and Barrett's oesophagus. However, it is possible that asthma medications may increase the risk of Barrett's oesophagus by other mechanisms.	esophagus
Dietary factors and the risks of oesophageal adenocarcinoma and Barrett's oesophagus.	Incidence rates for oesophageal adenocarcinoma have increased by over 500% during the past few decades without clear reasons. Gastro-oesophageal reflux disease, obesity and smoking have been identified as risk factors, although the demographic distribution of these risk factors is not consistent with the demographic distribution of oesophageal adenocarcinoma, which is substantially more common among whites and males than any other demographic groups. Numerous epidemiological studies have suggested associations between dietary factors and the risks of oesophageal adenocarcinoma and its precursor, Barrett's oesophagus, though a comprehensive review is lacking. The main aim of the present review is to consider the evidence linking dietary factors with the risks of oesophageal adenocarcinoma, Barrett's oesophagus, and the progression from Barrett's oesophagus to oesophageal adenocarcinoma. The existing epidemiological evidence is strongest for an inverse relationship between intake of vitamin C, β-carotene, fruits and vegetables, particularly raw fruits and vegetables and dark green, leafy and cruciferous vegetables, carbohydrates, fibre and Fe and the risk of oesophageal adenocarcinoma and Barrett's oesophagus. Patients at higher risk for Barrett's oesophagus and oesophageal adenocarcinoma may benefit from increasing their consumption of fruits and vegetables and reducing their intake of red meat and other processed food items. Further research is needed to evaluate the relationship between diet and the progression of Barrett's oesophagus to oesophageal adenocarcinoma. Evidence from cohort studies will help determine whether randomised chemoprevention trials are warranted for the primary prevention of Barrett's oesophagus or its progression to cancer.	esophagus