crossing96/oncoscreening huggingface dataset:
Giant fibrovascular polyp of the esophagus: report of a case.	A fibrovascular polyp is a peculiar nonepithelial tumor of the esophagus that invariably arises in the cervical esophagus at the level of the thoracic inlet and grows distally into a massive elongated, pedunculated, intraluminal lesion. Although it is a benign lesion that is eminently resectable, it is a dramatic entity owing to its tendency to cause bizarre complications such as asphyxia and sudden death when it regurgitates into the pharynx and causes laryngeal impaction. This report describes the multimodality imaging appearance of an archetypal case of a giant fibrovascular polyp in a patient with a seemingly innocuous presentation for the size of the lesion. The essential role of cross-sectional imaging in establishing a prompt diagnosis, defining the tissue elements of the mass, and delineation of the exact extent of the lesion in guiding the treatment approach is highlighted. The appearance of fibrovascular polyp in a single patient with a combination of barium swallow, multidetector computed tomography, and high-resolution contrast-enhanced magnetic resonance imaging has not been reported previously.	esophagus
Alcohol drinking and esophageal squamous cell carcinoma with focus on light-drinkers and never-smokers: a systematic review and meta-analysis.	Quantification of the association between alcohol drinking and risk of esophageal squamous cell carcinoma (ESCC) is an open issue, particularly among light alcohol drinkers, never-smokers, and Asian populations, in which some high-risk polymorphisms in alcohol metabolizing genes are more prevalent. To address these issues, we conducted a systematic review and meta-analysis using 40 case-control and 13 cohort studies that reported on the risk associated with alcohol drinking for at least three levels of consumption. In studies adjusted for age, sex, and tobacco smoking, the relative risk (RR) and 95% confidence interval (CI) for the association between light alcohol drinking (≤ 12.5 g/d) and risk of ESCC was 1.38 (1.14-1.67). The association was slightly stronger in Asian countries than in other populations. The adjusted RRs (95% CIs) were 2.62 (2.07-3.31) for moderate drinking (>12.5-<50 g/d) and 5.54 (3.92-7.28) for high alcohol intake (≥50 g/d); the RRs were slightly higher in non-Asian populations. In prospective studies, the RR (95% CI) was 1.35 (0.92-1.98) for light, 2.15 (1.55-2.98) for moderate, and 3.35 (2.06-5.46) for high alcohol intakes; light drinking showed an association with ESCC in Asia (five studies) but not in other regions (three studies). Among never-smokers (nine studies), the RR (95% CI) was 0.74 (0.47-1.16) for light, 1.54 (1.09-2.17) for moderate, and 3.09 (1.75-5.46) for high intakes. This meta-analysis further corroborates the association of moderate and high alcohol intake with risk of ESCC and provides risk estimates based on multiple prospective studies. Light alcohol intake appears to be associated to ESCC mainly in studies in Asia, which suggests a possible role of genetic susceptibility factors.	esophagus
Alcohol and aldehyde dehydrogenase polymorphisms and a new strategy for prevention and screening for cancer in the upper aerodigestive tract in East Asians.	The ethanol in alcoholic beverages and the acetaldehyde associated with alcohol consumption are Group 1 human carcinogens (WHO, International Agency for Research on Cancer). The combination of alcohol consumption, tobacco smoking, the inactive heterozygous aldehyde dehydrogenase-2 genotype (ALDH2*1/*2) and the less-active homozygous alcohol dehydrogenase-1B genotype (ADH1B*1/*1) increases the risk of squamous cell carcinoma (SCC) in the upper aerodigestive tract (UADT) in a multiplicative fashion in East Asians. In addition to being exposed to locally high levels of ethanol, the UADT is exposed to a very high concentration of acetaldehyde from a variety of sources, including that as an ingredient of alcoholic beverages per se and that found in tobacco smoke; acetaldehyde is also produced by salivary microorganisms and mucosal enzymes and is present as blood acetaldehyde. The inefficient degradation of acetaldehyde by weakly expressed ALDH2 in the UADT may be cri! tical to the local accumulation of acetaldehyde, especially in ALDH2*1/*2 carriers. ADH1B*1/*1 carriers tend to experience less intense alcohol flushing and are highly susceptible to heavy drinking and alcoholism. Heavy drinking by persons with the less-active ADH1B*1/*1 leads to longer exposure of the UADT to salivary ethanol and acetaldehyde. The ALDH2*1/*2 genotype is a very strong predictor of synchronous and metachronous multiple SCCs in the UADT. High red cell mean corpuscular volume (MCV), esophageal dysplasia, and melanosis in the UADT, all of which are frequently found in ALDH2*1/*2 drinkers, are useful for identifying high-risk individuals. We invented a simple flushing questionnaire that enables prediction of the ALDH2 phenotype. New health appraisal models that include ALDH2 genotype, the simple flushing questionnaire, or MCV are powerful tools for devising a new strategy for prevention and screening for UADT cancer in East Asians.	esophagus
Properties of a new mouthrinse for patients receiving radiation therapy.	INTRODUCTION: Patients receiving radiation therapy due to oral cancer develop complications such as hyposalivation, mucositis, oral infections, dental hypersensitivity and caries. Mouthrinses can alleviate some of these problems. AIMS AND OBJECTIVES: To investigate the in vitro antimicrobial properties and cytotoxicity of an experimental mouthrinse. METHODS: The mouthrinse contained 30% hexylene glycol (glycerine), 7% potassium nitrate and 0.025% sodium fluoride. The minimal inhibitory concentration (MIC) of these ingredients and the mixture was determined for C. albicans, S. aureus and S. mutans over 24 hours at different concentrations. The MICs of two commercial mouthrinses, Corsodyl and Plax, were also determined using the same organisms. All mouthrinses were then tested to determine the percentage kill over 1, 2, and 3 minutes. RESULTS: The MICs for hexylene glycol were 10%, 30% and 10% for C. albicans, S. aureus and S. mutons respectively. Potassium nitrate and sodium fluoride had no antimicrobial effects. The MIC of Corsodyl was 0.016 mg/ml for all the test organisms. The MIC for Plax varied from 0.0002 mg/ml to 0.001 mg/ml. The kill rates for all mouthrinses were acceptable, with no statistical differences between them. The experimental mouthrinse was not toxic to human oesophageal SCC cells after 1 minute exposure. At the time of the experiment, the costs of a similar quantity of the experimental mouthrinse, Corsodyl and Plax were R5.24, R30.00 and R10.00 respectively. CONCLUSIONS: The experimental mouthrinse was cost-effective and proved to have an antimicrobial effect and could be used safely to alleviate oral infections, desensitize teeth, improve oral hygiene and control dental caries in cancer patients after radiation therapy.	esophagus
Celecoxib antagonizes the cytotoxicity of cisplatin in human esophageal squamous cell carcinoma cells by reducing intracellular cisplatin accumulation.	High cyclooxygenase 2 (COX-2) expression has been reported to be clinically associated with reduced cisplatin-based therapy efficacy in esophageal cancer. However, the benefit of including COX-2-selective inhibitors in therapeutic regimens remains uncertain. Thus, we sought to determine the effects of COX inhibitors on the cytotoxicity of cisplatin and to further explore the mechanism involved in human esophageal squamous cell carcinoma cells. Among the four tested COX inhibitors [celecoxib, 4-[5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzenesulfonamide (SC-236), nimesulide, and indomethacin], all of which substantially suppressed prostaglandin E(2) production to a similar extent; only the COX-2-selective inhibitors celecoxib and SC-236 antagonized cisplatin-induced cytotoxicity and apoptosis in both cisplatin-resistant cells and their wild-type counterparts. Knockdown of COX-2 by small interference RNA failed to mimic the antagonizing effects of celecoxib and SC-236, implying that their action is COX-2-independent. Further mechanistic analysis revealed that the antagonizing effect of celecoxib and SC-236 on cytotoxic action of cisplatin was associated with decreased whole-cell cisplatin accumulation and DNA platination. Reduced influx, accompanied by the reduction of protein level of copper transporter 1, accounts for decreased intracellular cisplatin accumulation. In addition, combined treatment did not elicit greater antitumor activity than cisplatin or celecoxib monotherapy in vivo in an esophageal cancer xenograft model. Collectively, these data demonstrate that celecoxib antagonizes the cytotoxicity of cisplatin by decreasing intracellular cisplatin and DNA platination. The combination treatment also shows no beneficial effect compared with cisplatin or celecoxib monotherapy in vivo. Therefore, current clinical trials with celecoxib in combination with cisplatin should be approached with caution.	esophagus
[Clinical effect of lower tidal volume combine with lung recruitment maneuver on ARDS for post operative esophageal carcinoma surgery patients].	OBJECTIVE: To study clinical effectiveness and possible side effects of lower tidal volume combine with lung recruitment on acute respiratory distress syndrome (ARDS) for post operative esophageal carcinoma surgery patients. METHODS: Twenty six hypoxemie post operative esophageal carcinoma surgery patients from Cancer Hospital and Peking Union Medical College Hospital were included from 1st January 2007 to 30th September 2009. There were 20 male and 6 female with an average age of 65.5 years (51 - 76 years). Circulation was stable among them. They could not weaned from mechanical ventilation due to ARDS. Bedside monitoring included noninvasive continuous artery blood pressure (NBP), pulse oximetry saturation (SPO2). Patients were ventilated on volume control mode. Tidal volumes set to 6 ml/kg. Recruitment maneuvers were conducted by stepwise rising of positive end expiratory pressure (PEEP) level. PEEP, fraction of inspired oxygen (FiO2), static compliance of lung (CLS) and arterial blood gas analysis (ABG) before and at 30 min after each of twice applying recruitment maneuvers were measured. RESULTS: Fifty-two recruitments were completed on these 26 cases. PaO2/FiO2 improved significantly in 26 cases. The level of FiO2 were significantly lowered, CLS were increased significantly 30 min after each of twice applying recruitment maneuvers in all 26 cases. No complication was encountered. All patients were discharged successfully. CONCLUSION: Hypoxemia of ARDS following esophageal carcinoma surgery can be improved by lower tidal volume combine with lung recruitment maneuver.	esophagus
A prospective cohort study on overweight, smoking, alcohol consumption, and risk of Barrett's esophagus.	BACKGROUND: Barrett's esophagus (BE) is a precursor lesion of esophageal adenocarcinoma. Besides gastroesophageal reflux, possible risk factors for BE include overweight, cigarette smoking, and alcohol consumption. Our objective was to study these associations by using prospective data. METHODS: The prospective Netherlands Cohort Study, initiated in 1986, consists of 120,852 men and women, aged 55 to 69 years at baseline. At baseline, all subjects completed a questionnaire on dietary habits and lifestyle. After 16.3 years of follow-up, 370 BE cases with specialized intestinal metaplasia and 3,866 subcohort members were available for case-cohort analysis. Cox proportional hazards models were used to calculate incidence rate ratios (RR) and 95% CIs. RESULTS: Body mass index (BMI) at baseline was associated with risk of BE in women [multivariable adjusted RR per 1 kg/m(2), 1.07 (1.03-1.11)] but not in men [RR per 1 kg/m(2), 0.99 (0.93-1.05)]. The association in women was not specifically due to abdominal overweight. Former cigarette smokers were at increased risk of BE (RR = 1.33, 95% CI: 1.00-1.77), but current smokers were not. Smoking duration showed a positive association with BE risk (P(trend) = 0.03). For alcohol consumption, the RR per 10 g ethanol/d was 0.95 (0.87-1.03). CONCLUSIONS: Increased BMI was a risk factor for BE in women but not in men. Several aspects of cigarette smoking were positively associated with BE risk. Alcohol consumption was not associated with an increased risk of BE. IMPACT: Future research should focus on risk factors both for development and for progression of BE to esophageal adenocarcinoma.	esophagus
Primary epithelioid hemangioendothelioma of the kidney and penis.	Epithelioid hemangioendothelioma (EHE) is a rare vascular tumor of low malignant potential most commonly found in the lung, liver, and soft tissues. Here we describe the very rare presentations of primary EHE in the kidney and on the penis. One patient is a 59-year-old man with a renal lesion found incidentally on surveillance radiography, and the other is a 26-year-old man with an asymptomatic subdermal glanular lesion. Both were treated surgically via open partial nephrectomy and partial penectomy, respectively. Surgery is standard treatment, and close clinical follow up is necessary due to the unpredictable nature of EHE.	esophagus
CpG island methylator phenotype of cell-cycle regulators associated with TNM stage and poor prognosis in patients with oesophageal squamous cell carcinoma.	AIMS: CpG island methylator phenotype (CIMP) involves the targeting of multiple genes by promoter hypermethylation, and the cell-cycle regulatory proteins often change in human neoplasms. To gain insight into the role of epigenetic aberration of cell-cycle regulator genes in oesophagus squamous cell carcinoma (ESCC), the authors determined the hypermethylation profile in ESCC. METHODS: The promoter methylation status of nine cell-cycle regulator genes was examined in 50 ESCC, 50 dysplastic tissues and 50 normal epithelial tissues by methylation-specific PCR. RESULTS: The frequency of promoter methylation was 52% for p14, 44% for p15, 50% for p16, 56% for p21, 38% for p27, 8% for p53, 42% for p57, 36% for p73, and 44% for RB1 of 50 ESCC. CIMP+ was detected in 54% (27/50) of ESCC and 8% (4/50) of dysplastic tissues; no CIMP+ was present in normal epithelial tissues (p<0.001). The results show that promoter methylation of p14, p15, p16, p21, p27, p57 and p73 was far more common in ESCC samples with CIMP+ than those with CIMP-. A significant difference between CIMP status and TNM stage and metastasis was found in ESCC (p<0.05). Patients with ESCC with CIMP+ had poorer 4-year survival than those with CIMP-. CONCLUSIONS: The results suggest that CIMP of a subset of cell-cycle regulatory genes has an important role in the pathogenesis and progression of ESCC.	esophagus
Genetic pathways of multiple esophageal squamous cell carcinomas.	Whether multiple esophageal squamous cell carcinomas (SCCs) in a patient develop through an identical genetic pathway is still unclear. We examined multiple esophageal SCCs for alterations of p53, p16, IRF and mitochondrial DNA (mtDNA) and microsatellite instability (MSI). Thirty patients with multiple superficial esophageal SCCs, 23 with double lesions and 7 with triple lesions, were enrolled. Loss of heterozygosity (LOH) of p53 (TP53), p16 (D9S171), IRF (IRF) and other microsatellite loci including D1S191, D17S858, D18S58 and D18S61 of the tumors was examined by microsatellite assay. Mutations of p16 and mtDNA were examined with PCR single-strand conformation polymorphism (SSCP) analysis. LOH of p53, p16 and IRF were detected in 16 of 50 (32%), 5 of 38 (13%) and 5 of 48 (10%) tumors, respectively. Mutations of p16 were detected in 4 of 67 (6%) tumors. Six of 67 (9%) tumors had mtDNA alterations and none of the tumors showed high-frequency MSI. All 30 patients showed one or more gene alterations in one or more genetic loci. Discordant genetic patterns among individual lesions within a patient were observed in 28 of the 30 (93%) patients. The most discordant locus was TP53, present in 11 of 29 (38%) informative cases, followed by D18S61, present in 11 of 30 (37%) informative cases. These results suggest that the genetic pathways of multiple esophageal SCCs may differ even within the same patient.	esophagus
Interobserver variability in the diagnosis of crypt dysplasia in Barrett esophagus.	Recent morphologic and molecular evidence suggests that dysplasia in Barrett esophagus (BE) begins in the bases of the crypts [crypt dysplasia (CD)] and progresses with time to involve the upper portions of the crypts and surface epithelium. The aim of this study was to evaluate the criteria and reproducibility of diagnosing CD among 6 gastrointestinal pathologists, all with research interest in BE. Six gastrointestinal pathologists evaluated 2 clinical study sets, the first consisting of 40 BE cases [BE: 10, CD: 9, low-grade dysplasia (LGD): 10, high-grade dysplasia (HGD); 9, and intramucosal adenocarcinoma; 2] and the second consisting of 63 cases (BE: 16, CD: 15, LGD: 15, HGD: 15, and intramucosal adenocarcinoma: 2), at least 4 months apart. In between evaluations, all of the pathologists met at 1 hospital (consensus conference) to review the areas of disagreement and establish more objective criteria. Overall, the level of agreement for all cases was moderate (κ=0.44), and the level of agreement did not change significantly after evaluation of the second study set. The highest levels of agreement were obtained for lesions at the low and high end of the spectrum (BE without dysplasia and HGD). Overall, the degree of agreement for CD was moderate after both the first and second study set review (κ=0.44 and 0.46, respectively). However, the degree of agreement for CD was higher than that obtained for LGD in both study sets. In the first study set, 4 or more pathologists agreed with the original CD diagnosis in 78% of cases, and this value did not change significantly after review of the second study set. The observers agreed that characteristic features of CD include the presence of unequivocal dysplastic cells, similar in appearance to traditional LGD, involving any part, or all of the length, of the crypt in the absence of intercrypt surface epithelial involvement. Rare cases of CD may show high-grade cytologic features composed of markedly enlarged nuclei with increased nuclear/cytoplasmic ratio, eosinophilic cytoplasm, irregular nuclear membranes, and loss of polarity. The findings in this study suggest that CD can be diagnosed reliably with a moderate level of interobserver agreement. Long-term and multi-institutional studies should be carried out to further determine the biological and clinical significance and natural history of CD in patients with BE.	esophagus
Ursodeoxycholic acid amides as novel glucocorticoid receptor modulators.	Ursodeoxycholic acid (UDCA) is used for the treatment of hepatic inflammatory diseases. Recent studies have shown that UDCA's biological effects are partly glucocorticoid receptor (GR) mediated. UDCA derivatives were synthesized and screened for ability to induce GR translocation in a high content analysis assay using the esophageal cancer SKGT-4 cell line. UDCA derivatives induced GR translocation in a time dependent manner with equal efficacy to that of dexamethasone (Dex) and with greatly increased potency relative to UDCA. The cyclopropylamide 1a suppressed TNF-α induced NF-κB activity and it induced GRE transactivation. 1a was unable to displace Dex from the GR ligand binding domain (LBD) in a competition experiment but was capable of coactivator recruitment in a time-resolved fluorescence energy transfer assay (TR-FRET). This represents a novel mechanism of action for a GR modulator. These derivatives could result in a new class of GR modulators.	esophagus
EGFR overexpression induces activation of telomerase via PI3K/AKT-mediated phosphorylation and transcriptional regulation through Hif1-alpha in a cellular model of oral-esophageal carcinogenesis.	Telomerase plays an important role during immortalization and malignant transformation as crucial steps in the development of human cancer. In a cellular model of oral-esophageal carcinogenesis, recapitulating the human disease, immortalization occurred independent of the activation of telomerase but through the recombination-based alternative lengthening of telomeres (ALT). In this stepwise model, additional overexpression of EGFR led to in vitro transformation and activation of telomerase with homogeneous telomere elongation in already immortalized oral squamous epithelial cells (OKF6-D1_dnp53). More interestingly, EGFR overexpression activated the PI3K/AKT pathway. This strongly suggested a role for telomerase in tumor progression in addition to just elongating telomeres and inferring an immortalized state. Therefore, we sought to identify the regulatory mechanisms involved in this activation of telomerase and in vitro transformation induced by EGFR. In the present study we demonstrate that telomerase expression and activity are induced through both direct phosphorylation of hTERT by phospho-AKT as well as PI3K-dependent transcriptional regulation involving Hif1-alpha as a key transcription factor. Furthermore, EGFR overexpression enhanced cell cycle progression and proliferation via phosphorylation and translocation of p21. Whereas immortalization was induced by ALT, in vitro transformation was associated with telomerase activation, supporting an additional role for telomerase in tumor progression besides elongating telomeres.	esophagus
Decoy receptor 3 expression in esophageal squamous cell carcinoma: correlation with tumour invasion and metastasis.	OBJECTIVE: Decoy receptor 3 (DcR3) is a soluble receptor, which can bind to and inactivate the apoptosis-inducing ligands. We studied a possible association between DcR3 expression and clinicopathologic features in patients with esophageal squamous cell carcinoma (ESCC). METHODS: The mRNA expression of DcR3 was examined by RT-PCR in 109 primary ESCC patients. For the 52 pairs of DcR3 positive tissues, the protein expression was determined by immunohistochemistry. RESULTS: There was a strong correlation among DcR3 mRNA expression and tumor invasion (P=0.01) and lymph node metastasis (P=0.036). We also found that there was a correlation between DcR3 overexpression with lymph node metastasis (P=0.014) in 52 pairs of DCR3 mRNA positive tissues. CONCLUSIONS: Our finding suggested that the overexpression of DcR3 is significantly related with ESCC clinical staging. DcR3 might be a candidate as a tumor specific biomarker for ESCC.	esophagus