crossing96/oncoscreening huggingface dataset:
Percutaneous radiologic gastrostomy in patients with malignant pharyngoesophageal obstruction.	OBJECTIVE: Percutaneous endoscopic gastrostomy is widely practiced, but we use interventional radiology techniques to perform percutaneous radiologic gastrostomy in cancer patients with conditions that prevent endoscope insertion due to pharyngoesophageal obstruction. This study retrospectively investigated the effectiveness of percutaneous radiologic gastrostomy at our hospital. METHODS: We investigated the medical records of 105 patients who underwent percutaneous radiologic gastrostomy between 2001 and 2011. The technique used for percutaneous radiologic gastrostomy comprised insufflation to dilate the stomach via a nasogastric tube, followed by fluoroscopically guided puncture and gastrostomy tube placement. In patients for whom a nasogastric tube could not be inserted, the stomach was punctured with a fine needle under ultrasonographic guidance and insufflated via this puncture needle to achieve dilation. RESULTS: Patients comprised 75 men and 30 women (mean age, 63 years). A nasogastric tube was used during percutaneous radiologic gastrostomy in 81 cases, but could not be used in 24. The percutaneous radiologic gastrostomy procedure was successful in all cases. Serious post-percutaneous radiologic gastrostomy complications comprised one case each of decreased hemoglobin requiring blood transfusion, pneumoperitonitis that was treated by a laparotomy and infected fistula requiring tube removal (3/105, 2.9%). Duration of gastrostomy tube placement was 1-731 days, and the outcome was death in 59 cases, hospital transfer in 23, tube removal in 18 and survival with gastrostomy tube in place in 5. CONCLUSIONS: Serious complications requiring treatment occurred in 2.9% of cases in which percutaneous radiologic gastrostomy was performed, with mostly good effectiveness. Percutaneous radiologic gastrostomy is feasible even for patients in whom a nasogastric tube cannot be inserted.	esophagus
A case of oesophageal cancer with low back pain: the accidental finding of skeletal muscle metastasis.	Skeletal muscle metastasis is a very rare event in patients with oesophageal cancer. We herein report and discuss a case of a 65 years old man with history of gastro-esophageal reflux disease referred to our department for pyrosis associated to persistent low back pain. Oesophageal endoscopy and transesophageal endo-sonography showed a tumour localized in the lower third of the esophagus, histologically proved to be adenocarcinoma. Clinical staging procedures detected a two centimetres vascularized nodular lesion placed into right para-vertebral muscles at the level of L4 as the only sign of potential distant disease (versus a differential diagnosis of primitive sarcoma). The muscle lesion was completely removed and confirmed as secondary adenocarcinoma. Due to this evidence a chemotherapy protocol was initiated. After nine months the patient underwent transhiatal oesophagectomy. To the best of our knowledge this is the first reported case of a soft tissue metastasis from oesophageal cancer resected with radical intent.	esophagus
[Effects of esophageal cancer on the nerve fiber growth and guidance].	OBJECTIVE: To establish the co-culture model of cancer cells and nerve, and to study the influence of esophageal cancer on nerve fibers. METHODS: Mouse dorsal root ganglion (DRG) was cultured in sterile conditions by primary isolation. Co-culture model was established using matrigel matrix-embedded DRG and EC109 (esophageal cancer cell line) transfected with green fluorescent protein. Morphological changes of DRG, number and area of neurites were quantified with microscopy and image analysis. Furthermore, the mRNA expression of nerve growth factor(NGF) and brain derived neurotrophic factor(BDNF) was detected by real-time PCR. RESULTS: In mixture cultivation model of EC109 and DRG cells, directional outgrowth of neurite projecting to EC109 was observed, and the length of neurite was markedly longer in proximal field compared to distal field. The number and area of neurite were 87 and 346 μm(2) in proximal field respectively, and 23 and 141 μm(2) in distal field on the 7th day. The expressions of NGF and BDNF were up-regulated in esophageal cancer cells. CONCLUSIONS: The esophageal cancer may play an important role in nerve fiber growth and guidance, which may be associated with the up-regulation of NGF and BDNF expressions.	esophagus
Crypt dysplasia in Barrett's oesophagus shows clonal identity between crypt and surface cells.	Epithelial dysplasia is an important histological diagnosis signifying the presence of pre-invasive disease, usually needing intervention. However, the specific genetic changes responsible for the induction of this phenotypic change are unknown. Moreover, recent reports indicate that the dysplastic phenotype may not be immutable: in basal crypt dysplasia (CD), unequivocal dysplastic changes are seen in the crypts in Barrett's oesophagus and other pre-invasive lesions in the gastrointestinal tract, but the upper crypts and surface epithelium associated with these dysplastic crypts show the definitive morphology of a differentiated epithelium. The genotypic relationship between CD and the differentiated surface epithelium is presently unclear. We obtained 17 examples of CD: the lower and upper crypts and surface epithelium were differentially laser-microdissected from formalin-fixed, paraffin-embedded sections and mutations were sought in tumour suppressor genes frequently associated with progression in Barrett's oesophagus. We found two patients who both showed a c. C238T mutation in the CDKN2A (CDKN2AInk4A) gene and where the precise microanatomical relationships could be discerned: this mutation was present in both the CD at the crypt base and in the upper crypt and surface epithelium. We conclude that, in CD, the dysplastic basal crypt epithelium and the upper crypt and surface epithelium show clonal CDKN2A mutations, thus showing definitively that the surface epithelium is derived from the dysplastic crypt epithelium: the dysplastic phenotype is therefore not fixed and can be reversed. The mechanism of this change is unclear but may be related to the possibility that dysplastic cells can, probably early in their progression, respond to differentiation signals. However, it is also clear that a heavy mutational burden can be borne by crypts in the gastrointestinal tract without the development of phenotypic dysplasia. We are evidently some way from understanding the plasticity and the genotypic correlates of the dysplastic phenotype.	esophagus
Defining the learning curve for robotic-assisted esophagogastrectomy.	"INTRODUCTION: The expansion of robotic-assisted surgery is occurring quickly, though little is generally known about the ""learning curve"" for the technology with utilization for complex esophageal procedures. The purpose of this study is to define the learning curve for robotic-assisted esophagogastrectomy with respect to operative time, conversion rates, and patient safety. METHODS: We have prospectively followed all patients undergoing robotic-assisted esophagogastrectomy and compared operations performed at our institutions by a single surgeon in successive cohorts of 10 patients. Our measures of proficiency included: operative times, conversion rates, and complications. Statistical analyses were undertaken utilizing Spearman regression analysis and Mann-Whitney U test. Significance was accepted with 95 % confidence. RESULTS: Fifty-two patients (41 male: 11 female) of mean age 66.2 ± 8.8 years underwent robotic-assisted esophagogastrectomies for malignant esophageal disease. Neoadjuvant chemoradiation was administered to 30 (61 %) patients. A significant reduction in operative times (p <0.005) following completion of 20 procedures was identified (514 ± 106 vs. 397 ± 71.9). No conversions to open thoracotomy were required. Complication rates were low and not significantly different between any 10-patient cohort; however, no complications occurred in the final 10-patient cohort. There were no in-hospital mortalities. CONCLUSIONS: For surgeons proficient in performing minimally-invasive esophagogastrectomies, the learning curve for a robotic-assisted procedure appears to begin near proficiency after 20 cases. Operative complications and conversions were infrequent and unchanged across successive 10-patient cohorts."	esophagus
Concurrent chemoradiotherapy with a novel fluoropyrimidine, S-1, and cisplatin for locally advanced esophageal cancer: long-term results of a phase II trial.	OBJECTIVES: A phase II study was performed to investigate the safety and efficacy of concurrent chemoradiotherapy (CCRT) combined with an orally active fluoropyrimidine, S-1, plus cisplatin for locally advanced esophageal cancer (LAEC). METHODS: CCRT comprised 2 courses, a 30-Gy radiotherapy over 3 weeks plus daily oral S-1 (80 mg/m(2)/day) for 2 weeks and a 24-hour cisplatin infusion (70 mg/m(2)) on day 8, and an identical course administered after a 2-week break. RESULTS: One hundred and sixteen patients, 12 with stage II, 71 with stage III, and 33 with stage IVa LAEC participated, and 106 of them (91.4%) completed the CCRT course. The most serious toxicity was myelosuppression: grade 3 and 4 neutropenia occurred in 28.4 and 9.5% of patients, respectively. Nonhematologic toxicity was moderate. Complete response rates in patients with stage II, III, and IVa LAEC were 91.7, 67.6, and 36.4%, respectively. The overall median survival time was 2.3 years and that of patients with stage II, III, and IVa cancer was 7.0, 2.6, and 1.3 years, respectively. CONCLUSIONS: CCRT combined with S-1 plus cisplatin showed promising safety and efficacy. Potentially, this combination therapy could become a baseline medication for patients with LAEC.	esophagus
Novel functional variants locus in PLCE1 and susceptibility to esophageal squamous cell carcinoma: based on published genome-wide association studies in a central Chinese population.	"A novel functional single nucleotide polymorphism (SNP) rs2274223 located in the phospholipase C epsilon 1 (PLCE1) gene was found to be associated with the risk of esophageal squamous cell carcinoma (ESCC) by three large-scale genome-wide association studies (GWAS) in Chinese populations. In the present study, we validated this finding and also explored the risk of ESCC associated with other two unreported potentially functional SNPs (rs17417407 G>T and rs2274224 C>G) of PLCE1 in a population-based case-control study to investigate the association between these three potentially functional SNPs in PLCE1 and susceptibility to ESCC. A total of 381 ESCC cases and 420 controls matched by age and sex were recruited and successfully genotyped for three SNPs (rs17417407, rs2274223 and rs2274224) of the PLCE1 in a central Chinese population. SNP rs2274223 was independently associated with increased risk of ESCC (adjusted odds ratio [OR], 2.80; 95% confidence interval [95% CI], 1.45-5.39 for GG vs. AA), and SNP rs2274224 was found to be associated with decreased risk of ESCC (adjusted OR, 0.65; 95% CI, 0.46-0.91 for CG vs. CC). The combined effects of risk alleles for three SNPs (rs17417407T, rs2274223G and rs2274224G) were found to be associated with elevated risk of ESCC in a dose-dependent effect manner (Ptrend=0.005). The Grs17417407Ars2274223Crs2274224 haplotype decreased the risk of ESCC (adjusted OR, 0.76; 95% CI, 0.62-0.93), meanwhile the Grs17417407Grs2274223Crs2274224 and Trs17417407Grs2274223Crs2274224 haplotypes could increase the risk of ESCC (adjusted OR, 1.75; 95% CI, 1.33-2.18 and OR, 2.51; 95% CI, 1.15-2.49). Gene-environment interaction analysis presented a best model consisted of four factors (rs2274223, rs2274224, family history, and smoking) with testing balance accuracy (TBA): 0.66 and cross validation consistency (CVC): 7/10, which could increase the esophageal cancer risk in the ""high risk group"" with 3.67-fold (OR: 3.67, 95% CI: 2.74-4.92), compared to the ""low risk group"". Our results further confirmed that genetic variations in PLCE1 may contribute to ESCC risk associated with tobacco exposure in a central Chinese population. Further functional studies are needed to validate our results."	esophagus
Oncogene GAEC1 regulates CAPN10 expression which predicts survival in esophageal squamous cell carcinoma.	AIM: To identify the downstream regulated genes of GAEC1 oncogene in esophageal squamous cell carcinoma and their clinicopathological significance. METHODS: The anti-proliferative effect of knocking down the expression of GAEC1 oncogene was studied by using the RNA interference (RNAi) approach through transfecting the GAEC1-overexpressed esophageal carcinoma cell line KYSE150 with the pSilencer vector cloned with a GAEC1-targeted sequence, followed by MTS cell proliferation assay and cell cycle analysis using flow cytometry. RNA was then extracted from the parental, pSilencer-GAEC1-targeted sequence transfected and pSilencer negative control vector transfected KYSE150 cells for further analysis of different patterns in gene expression. Genes differentially expressed with suppressed GAEC1 expression were then determined using Human Genome U133 Plus 2.0 cDNA microarray analysis by comparing with the parental cells and normalized with the pSilencer negative control vector transfected cells. The most prominently regulated genes were then studied by immunohistochemical staining using tissue microarrays to determine their clinicopathological correlations in esophageal squamous cell carcinoma by statistical analyses. RESULTS: The RNAi approach of knocking down gene expression showed the effective suppression of GAEC1 expression in esophageal squamous cell carcinoma cell line KYSE150 that resulted in the inhibition of cell proliferation and increase of apoptotic population. cDNA microarray analysis for identifying differentially expressed genes detected the greatest levels of downregulation of calpain 10 (CAPN10) and upregulation of trinucleotide repeat containing 6C (TNRC6C) transcripts when GAEC1 expression was suppressed. At the tissue level, the high level expression of calpain 10 protein was significantly associated with longer patient survival (month) of esophageal squamous cell carcinoma compared to the patients with low level of calpain 10 expression (37.73 ± 16.33 vs 12.62 ± 12.44, P = 0.032). No significant correction was observed among the TNRC6C protein expression level and the clinocopathologcial features of esophageal squamous cell carcinoma. CONCLUSION: GAEC1 regulates the expression of CAPN10 and TNRC6C downstream. Calpain 10 expression is a potential prognostic marker in patients with esophageal squamous cell carcinoma.	esophagus
High expression of transient potential receptor C6 correlated with poor prognosis in patients with esophageal squamous cell carcinoma.	TRPC6 plays a crucial role in the tumor progression of various cancers. The relation between the expression of TRPC6 and clinical prognosis has not been studied yet. Our study was to elucidate the role of TRPC6 in predicting outcomes of patients with esophageal squamous cell carcinoma (ESCC). Fresh frozen samples were collected immediately from 172 patients with ESCC after surgical resection from 2003 to 2008 at Sun Yat-sen University Cancer Center, including 45 pairs of tumor tissues and nontumor tissues. TRPC6 expression was measured by quantitative real-time PCR and Western blotting analyses. TRPC6 mRNA and protein were up-regulated in ESCC tissues when compared with the paired nontumor tissues. High expression of TRPC6 mRNA was associated with the higher pT status (P = 0.016) and pathological staging (P = 0.040). The 5-year disease-specific survival in the high expression of TRPC6 mRNA group (>188.98, n = 81) is poorer than that in low-level expression group (≤188.98, n = 91) (42.1 vs. 62.7 %, P = 0.004). Stratified analysis according to the pathological stage revealed its discernibility on DSS was only pronounced in patients with pStage III (P = 0.015). Cox multivariate analysis revealed that pN category (P < 0.001; Relative risk, 2.897, 95 % CI 1.830-4.585) and the expression of TRPC6 mRNA (P = 0.006; Relative risk, 1.863, 95 % CI 1.196-2.902) were independent prognostic factors. TRPC6 mRNA overexpression correlated with poor prognosis in patients with ESCC and might serve as a novel prognostic biomarker for resected ESCC patients in advanced stage.	esophagus
Site-specific cancer risk in the Baltic cohort of Chernobyl cleanup workers, 1986-2007.	OBJECTIVE: To assess site-specific cancer risk in the Baltic cohort of Chernobyl cleanup workers, 1986-2007. METHODS: The Baltic cohort includes 17,040 men from Estonia, Latvia and Lithuania who participated in the environmental cleanup after the accident at the Chernobyl Nuclear Power Station in 1986-1991 and who were followed up for cancer incidence until the end of 2007. Cancer cases diagnosed in the cohort and in the male population of each country were identified from the respective national cancer registers. The proportional incidence ratio (PIR) with 95% confidence interval (CI) was used to estimate the site-specific cancer risk in the cohort. For comparison and as it was possible, the site-specific standardised incidence ratio (SIR) was calculated for the Estonian sub-cohort, which was not feasible for the other countries. RESULTS: Overall, 756 cancer cases were reported during 1986-2007. A higher proportion of thyroid cancers in relation to the male population was found (PIR=2.76; 95%CI 1.63-4.36), especially among those who started their mission shortly after the accident, in April-May 1986 (PIR=6.38; 95%CI 2.34-13.89). Also, an excess of oesophageal cancers was noted (PIR=1.52; 95% CI 1.06-2.11). No increased PIRs for leukaemia or radiation-related cancer sites combined were observed. PIRs and SIRs for the Estonian sub-cohort demonstrated the same site-specific cancer risk pattern. CONCLUSION: Consistent evidence of an increase in radiation-related cancers in the Baltic cohort was not observed with the possible exception of thyroid cancer, where conclusions are hampered by known medical examination including thyroid screening among cleanup workers.	esophagus
Association between microsomal epoxide hydrolase 1 polymorphisms and susceptibility to esophageal cancer: a meta-analysis.	Microsomal epoxide hydrolase 1 (EPHX1) plays an important role in the detoxification of carcinogenic polycyclic aromatic hydrocarbons. EPHX1 Tyr113His and His139Arg polymorphisms have been reported to have some impacts on the EPHX1 activity. Previous case-control studies assessing the associations between EPHX1 polymorphisms and esophageal cancer risk reported conflicting results. To quantitatively summarize the associations of EPHX1 Tyr113His and His139Arg polymorphisms with esophageal cancer risk, a systemic review and meta-analysis of published studies were performed. Published literatures from PubMed, Embase, and China National Knowledge Infrastructure databases were searched. The strength of the associations between EPHX1 polymorphisms and esophageal cancer risk was estimated by the pooled odds ratios (ORs) with its 95 % confidence interval (95 %CI). This meta-analysis yielded nine case-control studies, which included nine studies for Tyr113His polymorphism (1,291 cases and 2,120 controls) and seven studies for His139Arg polymorphism (899 cases and 1,615 controls). Overall, meta-analysis showed that EPHX1 Tyr113His polymorphism was not associated with esophageal cancer risk under all genetic models. Meta-analysis of these seven studies for EPHX1 His139Arg polymorphism showed that EPHX1 His139Arg polymorphism was also not associated with esophageal cancer risk under all genetic models. However, subgroup analysis by ethnicity further showed that there was an obvious association between EPHX1 His139Arg polymorphism and decreased risk of esophageal cancer in Caucasians (ArgArg versus HisArg/HisHis: OR = 0.52, 95 %CI 0.27-0.97, P = 0.041). This meta-analysis suggests that EPHX1 His139Arg polymorphism is associated with decreased risk of esophageal cancer in Caucasians. In addition, more studies with large samples are needed to get a more precise estimation on the associations mentioned above.	esophagus
Clinical outcomes of basaloid squamous cell carcinoma of the esophagus: a retrospective analysis of 142 cases.	BACKGROUND: Basaloid squamous cell carcinoma of the esophagus (BSCCE) is a rare and distinctive tumor with no standard treatment. This study aimed to explore treatment in relation to prognosis of the disease. METHODS: A total of 142 patients with BSCCE that underwent treatment in our hospital from March 1999 to July 2010 were retrospectively analyzed. All patients received surgery, 42 postoperative radiotherapy and 28 patients chemotherapy. RESULTS: There were 26 patients included in stage I, 60 in stage II, 53 in stage III and 3 in stage IV. The clinical symptoms and macroscopic performances of BSCCE did not differ from those of typical esophageal squamous cell carcinoma. Among 118 patients receiving endoscopic biopsy, only 12 were diagnosed with BSCCE. The median survival time (MST) of the entire group was 32 months, with 1-, 3- and 5-year overall survival (OS) of 81.4%, 46.8% and 31.0%, respectively. The 5-year OS of stage I and II patients was significantly longer than that of stages III/IV, at 60.3%, 36.1% and 10.9%, respectively (p<0.001, p=0.001). The MST and 5-year OS were 59.0 months and 47.4% in patients with tumors located in the lower thoracic esophagus, and 27.0 months and 18.1% in those with lesions in the upper/middle esophagus (p=0.002). However, the survival was not significantly improved in patients undegoing adjunctive therapy. Multivariate analysis showed TNM stage and tumor location to be independent prognostic factors. Furthermore, distant metastasis was the most frequent failure pattern, with a median recurrence time of 10 months. CONCLUSION: BSCCE is an aggressive disease with rapid progression and a propensity for distant metastasis. It is difficult to make a definitive diagnosis via preoperative biopsy. Multidisciplinary therapy including radical esophagectomy with extended lymphadenectomy should be recommended, while the effectiveness of radiochemotherapy requires further validation for BSCCE.	esophagus
Acylglycerol kinase augments JAK2/STAT3 signaling in esophageal squamous cells.	JAK2 activity is tightly controlled through a self-inhibitory effect via its JAK homology domain 2 (JH2), which restricts the strength and duration of JAK2/STAT3 signaling under physiological conditions. Although multiple mutations within JAK2, which abrogate the function of JH2 and sustain JAK2 activation, are widely observed in hematological malignancies, comparable mutations have not been detected in solid tumors. How solid tumor cells override the autoinhibitory effect of the JH2 domain to maintain constitutive activation of JAK2/STAT3 signaling remains puzzling. Herein, we demonstrate that AGK directly interacted with the JH2 domain to relieve inhibition of JAK2 and activate JAK2/STAT3 signaling. Overexpression of AGK sustained constitutive JAK2/STAT3 activation, consequently promoting the cancer stem cell population and augmenting the tumorigenicity of esophageal squamous cell carcinoma (ESCC) cells both in vivo and in vitro. Furthermore, AGK levels significantly correlated with increased STAT3 phosphorylation, poorer disease-free survival, and shorter overall survival in primary ESCC. More importantly, AGK expression was significantly correlated with JAK2/STAT3 hyperactivation in ESCC, as well as in lung and breast cancer. These findings uncover a mechanism for constitutive activation of JAK2/STAT3 signaling in solid tumors and may represent a prognostic biomarker and therapeutic target.	esophagus