crossing96/oncoscreening huggingface dataset:
Indications, stains and techniques in chromoendoscopy.	Early detection of malignancies within the gastrointestinal tract is essential to improve the prognosis and outcome of affected patients. However, conventional white light endoscopy has a miss rate of up to 25% for gastrointestinal pathology, specifically in the context of small and flat lesions within the colon. Chromoendoscopy and other advanced imaging techniques aim at facilitating the visualization and detection of neoplastic lesions and have been applied throughout the gastrointestinal tract. Chromoendoscopy, particularly in combination with magnifying endoscopy has significantly improved means to detect neoplastic lesions in the gastrointestinal mucosa, particularly in ulcerative colitis and Crohn's colitis. In addition, chromoendoscopy is beneficial in the upper gastrointestinal tract, especially when evaluating Barrett's oesophagus (BO) for the presence of dysplasia. Furthermore, it also improves characterization, differentiation and diagnosis of endoscopically detected suspicious lesions, and helps to delineate the extent of neoplastic lesions that may be amenable to endoscopic resection. This review discusses the dyes, indications and advanced endoscopic imaging methods used in various chromoendoscopic techniques, and presents a critical overview of the existing evidence supporting their use in current practice with a particular emphasis on the role in inflammatory bowel disease and BO.	esophagus
Modified triangulating stapling technique for esophagogastrostomy after esophagectomy for esophageal cancer.	BACKGROUND: Anastomosis performed during esophagectomy for esophageal cancer is usually involves hand-sewn or circular stapled methods. However, these techniques have been reported to be associated with a high frequency of anastomotic complications, including leakage and benign stenosis. Here a novel triangulating stapling technique for esophagogastrostomy after esophagectomy for esophageal cancer and its retrospective investigation are described. METHODS: Forty-eight patients were underwent esophagectomy for esophageal cancer from January 2006 to December 2009 by the same surgeon using the triangulating stapling technique. The short-term outcomes were evaluated retrospectively. This end-to-end anastomosis used three linear staplers in an everted fashion. RESULTS: Patients comprised 36 men and 12 women with a mean age of 59.4 years. Anastomotic leakage occurred in 4 patients (8.3 %), while anastomotic stenosis was observed in 6 (12.5 %). The average number of endoscopic pneumatic dilatations in patients with anastomotic stenosis was 2.4. The median (range) duration of hospital stay was 40.8 (19-154) days. CONCLUSIONS: Our modified triangulating stapling technique for esophagogastrostomy may be a feasible alternative, resulting in a lower frequency of postoperative anastomotic complications.	esophagus
Short DNA sequences and bacterial DNA induce esophageal, gastric, and colorectal cancer cell invasion.	Toll-like receptor 9 (TLR9) recognizes both bacterial and self-DNA and it is abundantly expressed in the gastrointestinal tract. In this study, we investigated the influences of both bacterial DNA and specific short DNA sequences on TLR9-mediated gastrointestinal cancer cell invasion. We assessed the effect of various DNA ligands on cellular invasion and on TLR9 and matrix metalloproteinase expression of three gastrointestinal cancer cell lines. DNA-ligands described in this study include CpG-ODN M362, 9-mer (hairpin), human telomeric sequence h-Tel22 G-quadruplex, and bacterial DNAs from Escherichia coli and Helicobacter pylori. All of the DNAs studied were demonstrated to induce invasion in the studied cells. The DNA-induced invasion was inhibited with a broad-spectrum MMP inhibitor and partly also with chloroquine suggesting that it could be mediated via MMP activation, endosomal signaling, and TLR9. Interestingly, H. pylori DNA was shown to induce a more pronounced invasion in a gastric cancer cell line than in the other cell lines. Our results suggest that bacterial DNA as well as deoxynucleotides having stable secondary structures (i.e. hairpins or G-quadruplex structures) may serve as endogenous, invasion-inducing TLR9-ligands and promote local progression and metastasis of cancers in the alimentary tract.	esophagus
Correlation between circulating myeloid-derived suppressor cells and Th17 cells in esophageal cancer.	AIM: To perform a comprehensive investigation into the potential correlation between circulating myeloid-derived suppressor cells (MDSCs) and Th17 cells in esophageal cancer (ECA). METHODS: A total of 31 patients newly diagnosed with ECA and 26 healthy subjects were included in the current study. The frequencies of MDSCs and Th17 cells in peripheral blood were determined by flow cytometry. The mRNA expression of cytokines, arginase 1 (Arg1) and inducible NO synthase (iNOS) in peripheral blood mononuclear cells (PBMCs) and plasma Arg1 were assessed by real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. RESULTS: There was an increased prevalence of MDSCs in the peripheral blood from ECA patients (15.21% ± 2.25%) when compared with healthy control (HC) (1.10% ± 0.12%, P < 0.0001). The plasma levels of Arg1 in ECA patients were significantly higher than those in HC (28.28 ± 4.10 ng/mL vs 9.57 ± 1.51 ng/mL, P = 0.0003). iNOS mRNA levels in the peripheral blood of ECA patients also showed a threefold increase compared with HC (P = 0.0162). The frequencies of Th17 cells (CD4⁺IL-17A⁺) were significantly elevated in ECA patients versus HC (3.50% ± 0.33% vs 1.82% ± 0.19%, P = 0.0001). Increased mRNA expression of IL-17 and ROR-γt was also observed in ECA patients compared with HC (P = 0.0041 and P = 0.0004, respectively), while the mRNA expression of IL-6 and tumor necrosis factor-α (TNF-α) showed significant decreases (P = 0.0049 and P < 0.0001, respectively). No obvious correlations were found between the frequencies of MDSCs and Th17 cells in the peripheral blood from ECA patients(r = -0.1725, P = 0.3534). Arg1 mRNA levels were positively correlated with levels of IL-6 (r = 0.6404, P = 0.0031) and TNF-α (r = 0.7646, P = 0.0001). Similarly, iNOS mRNA levels were also positively correlated with levels of IL-6 (r = 0.6782, P = 0.0007) and TNF-α (r = 0.7633, P < 0.0001). CONCLUSION: This study reveals the relationship between circulating MDSCs and Th17 cells, which may lead to new immunotherapy approaches for ECA based on the associated metabolites and cytokines.	esophagus
Acquired factor V inhibitor developing in a patient with esophageal squamous cell carcinoma.	An 82-year-old man referred to our medical ward because of epistaxis and melena was found to have 12 Bethesda units of factor V inhibitor. He was managed for bleeding with supportive care, followed by corticosteroid therapy. The bleeding completely stopped 1 week after corticosteroid therapy. Medical history revealed dysphagia during the past 6 months and further evaluation brought to light a squamous cell carcinoma (SCC) in the esophagus. This is the first case of an acquired factor V inhibitor developing in a patient with esophageal SCC without any other risk factors such as surgery.	esophagus
Metastatic esophagogastric adenocarcinoma: trends in first-line treatment and predictive factors for the implementation of HER2 testing in clinical practice during the first year after trastuzumab market approval.	"PURPOSE: Little is known about the use of first-line chemotherapy in clinical practice in patients with advanced esophagogastric adenocarcinoma, and no data have been published regarding potential obstacles for the implementation of molecular testing for targeted agents in this patient group. Here, we sought to evaluate factors influencing treatment decisions with special focus on the implementation of HER2 testing during the first year after trastuzumab market approval in Germany. METHODS: A total of 754 patients undergoing treatment decisions for palliative first-line therapy in 2010 were documented using Therapiemonitor(®). Drug use and intensity of first-line treatment were analyzed. Data on HER2 testing and test algorithm are described, and variables influencing HER2 testing were selected using bivariate analysis. Significant factors were included in a multivariate logistic regression analysis. RESULTS: Compared with previous years, treatment intensity has further increased. The use of chemotherapy triplets rose from 10.1 % in 2006 to 60.3 % in 2010. In 2010, 49.1 % of patients were tested for HER2 and in 52.2 % of these patients the currently proposed test algorithm was used. Using multivariate logistic regression analysis age ≥67 years and ""initiating institution: practice"" were found to negatively impact the likelihood of HER2 testing, while treatment goal ""prevention of progression"", multiple metastases and a Karnofsky status >80 % showed positive correlation with HER2 testing. CONCLUSION: The tendency to use more intensive first-line chemotherapy regimens in patients with advanced esophagogastric adenocarcinoma continued in 2010. Only a minority of patients had an access to the appropriate molecular diagnostics and therefore to treatment with trastuzumab. The access was limited due to the preselection following individual, clinical and institutional factors."	esophagus
Elevated serine protease HtrA1 inhibits cell proliferation, reduces invasion, and induces apoptosis in esophageal squamous cell carcinoma by blocking the nuclear factor-κB signaling pathway.	Emerging evidence has demonstrated that high-temperature requirement protein A1 (HtrA1) appears to be involved in several important biological processes in mammals such as growth, apoptosis, embryogenesis, invasion, metastasis, and cancer and has been verified to be reduced in a variety of human tumors. However, its precise functions and molecular mechanisms in esophageal squamous cell carcinoma (ESCC) remain unclear. Here, we detected HtrA1 level in ESCC tissues and cells and investigated the biological roles of HtrA1 in ESCC. We found that expressions of HtrA1 mRNA and protein in ESCC tissues and cells were significantly lower than those in normal esophageal epithelial tissues and cells (P < 0.05). Expressions of HtrA1 mRNA and protein were closely associated with TNM staging and lymph node metastasis (P < 0.05). Additionally, the survival rate of patients with low HtrA1 level was lower than those patients with high HtrA1 level (P < 0.05). Elevated HtrA1 level markedly inhibited cell proliferation in vitro and in vivo, reduced cell invasion in vitro, and induced cell apoptosis. Notably, HtrA1 overexpression inhibited phosphorylation levels of IκBα and p65 subunit of the NF-κB signaling pathway, but increased total IκBα level, coupled with decreases of Ki-67, Bcl-2, Bcl-xL, cyclin D1, and MMP-9 proteins and increase of caspase-3 activity. Overall, these data suggest that HtrA1 may play critical roles in the tumorgenesis and progression of ESCC, and HtrA1 overexpression exerts its anti-tumor effect by blocking the NF-κB signaling pathway; thus, manipulation of HtrA1 may be an effective molecular target for ESCC treatment.	esophagus
PLC-ε1 gene polymorphisms significantly enhance the risk of esophageal squamous cell carcinoma in individuals with a family history of upper gastrointestinal cancers.	BACKGROUND AND AIMS: Phospholipase C epsilon 1 (PLCε1) may regulate cell growth, differentiation, apoptosis and angiogenesis and play an important role in carcinogenesis and the progression of several cancers. This study was designed to validate the association of the PLCε1 rs2274223 single nucleotide polymorphism (SNP) with esophageal squamous cell carcinoma (ESCC) as identified by genome-wide association studies (GWAS) and further assess whether the rs11599672 SNP could affect an individual's susceptibility to ESCC. METHODS: These two SNPs were genotyped by polymerase chain reaction ligase detection reaction (PCR-LDR) in 527 ESCC patients and 527 controls. RESULTS: Compared with the rs2274223 SNP AA genotype, other genotypes or combined genotypes all enhanced the risk of ESCC. Further analyses showed that AG/GG genotype carriers with a family history of upper gastrointestinal cancers (UGIC) had an increased risk of ESCC than those AA genotype carriers without UGIC family history (OR = 2.10, 95% CI = 1.46-3.10). Overall, rs11599672 SNP had no influence on ESCC susceptibility. However, UGIC family history elevated the risk of ESCC for subjects with the TT genotype (OR = 1.59, 95% CI = 1.13-2.24). CONCLUSIONS: These results highlighted the role of a genetic factor in ESCC and suggested that the PLCε1 rs2274223 SNP might be an effective genetic marker to assess the risk of ESCC in individuals with a UGIC family history from a region of high incidence in northern China.	esophagus
The selective Hsp90 inhibitor BJ-B11 exhibits potent antitumor activity via induction of cell cycle arrest, apoptosis and autophagy in Eca-109 human esophageal squamous carcinoma cells.	BJ-B11 is a selective heat shock protein 90 (Hsp90) inhibitor that has been reported to possess significant antitumor activity in multiple types of cancer cells; however, the mechanism of action needs to be further clarified. We investigated, for the first time, the antitumor activity and the molecular mechanism underlying growth inhibition in Eca-109 cells. The results revealed that BJ-B11 inhibited the proliferation of Eca-109 cells in a time- and concentration-dependent manner, with 50% inhibitory concentration (IC(50)) values of 0.31±0.01 µM after 48-h incubation. BJ-B11 induced concentration-dependent G2/M cell cycle arrest and apoptosis. The cleavage of caspase 3 and PARP signals detected might originate from mitochondrial dysfunction, which was supported by the results of reactive oxygen species (ROS) production, cytochrome c release and the mitochondrial membrane potential (MMP) reduction. The general caspase inhibitor Z-VAD-fmk did not completely abolish BJ-B11-induced cell death. Furthermore, inhibition of the Akt/mTOR/p70S6K signaling pathway might be involved in the process of BJ-B11-induced autophagy, which was characterized by the production of autophagic vacuoles and upregulation of LC3-II protein in a time- and concentration-dependent manner. Meanwhile, the general autophagy inhibitor 3-MA decreased the apoptotic ratio. Furthermore, BJ-B11 induced the polymerization of cytoskeleton β-tubulin and F-actin. Taken together, our results suggest that the growth inhibition of Eca-109 cells induced by BJ-B11 may result from the induction of G2/M cell cycle arrest, apoptosis and autophagy.	esophagus
Thoracic duct injury following esophagectomy in carcinoma of the esophagus: ligation by the abdominal approach.	BACKGROUND: Thoracic duct injury (TDI) is a potentially lethal complication of esophagectomy. There is no consensus regarding when and how to intervene in these injuries. Both thoracic and abdominal approaches have been used. METHODS: Esophagectomies performed for cancer of the esophagus (n = 104) from October 2003 to July 2011 were analyzed for TDI. Diagnosis, histological type, stage, and location of tumor, neoadjuvant therapy, trans-thoracic or trans-hiatal procedure performed, nature and amount of drain output, and levels of triglyceride in the effluent were analyzed. Management of these injuries and morbidity and mortality associated with the approach taken were reviewed. RESULTS: We observed chylothorax in 9 patients. All nine patients had undergone trans-hiatal esophagectomy. All patients eventually required surgical intervention. Mass ligation of the thoracic duct was performed via the thoracic route in three patients and via the trans-abdominal approach in six others. Thoracic duct ligation was successful in all patients. One patient required a second laparotomy and repeat ligation of the duct. There were two postoperative deaths; both these patients had ligation by the thoracic route. CONCLUSIONS: Trans-abdominal ligation of the thoracic duct in patients with chylothorax after esophagectomy is technically easy and safe. It may be preferred over the trans-thoracic approach, especially after an initial trans-hiatal esophagectomy.	esophagus
Iterated combination-based paired permutation tests to determine shape effects of chemotherapy in patients with esophageal cancer.	The nonparametric combination of dependent permutation tests method is a useful general tool when a testing problem can be broken down into a set of different k > 1 partial tests. These partial tests, after adjustment of p-values to control for multiplicity, can be marginally analyzed, but jointly considered they can provide information on an overall hypothesis, which might represent the true goal of the testing problem. On the one hand, independence among the partial tests is usually an unrealistic assumption; on the other, even when the underlying dependence relations are known quite often they are difficult to cope with properly. Therefore this combination must be achieved nonparametrically, by implicitly taking into account the dependence structure of tests without explicitly describing it. An important property of the tests based on nonparametric combination methodology, when the number of response variables is high compared to the sample sizes, consists in the finite sample consistency. A practical problem involves choosing the most suitable combining function for each specific testing problem given that the final result can be affected by this crucial choice. The purpose of this article is to present an nonparametric combination solution based on the iterated combination of partial tests, evaluate its power behavior using a Monte Carlo simulation study and apply it to a real medical problem, namely the evaluation of the effects of chemotherapy on the shape of esophageal tumors. R code has been implemented to carry out the analyses.	esophagus
Decreased expression and aberrant methylation of Raf kinase inhibitory protein gene in esophageal squamous cell carcinoma.	Raf kinase inhibitory protein (RKIP) gene is considered to be a suppressor of metastasis involved in various carcinomas. In the present study, we observed that promoter methylation repressed the expression of RKIP in TE-13 cell line. 5-Aza treatment and stable transfection of RKIP resulted in a significant inhibition of TE-13 cell proliferation. The promoter hypermethylation of RKIP was found to occur in dysplastic tissues and a close correlation was noted between RKIP methylation and the loss of mRNA and protein expression of the gene in ESCC specimens. In summary, RKIP may act as a tumor suppressor gene in esophageal cancer.	esophagus
Volumetric-modulated arc therapy vs. c-IMRT in esophageal cancer: a treatment planning comparison.	AIM: To compare the volumetric-modulated arc therapy (VMAT) plans with conventional sliding window intensity-modulated radiotherapy (c-IMRT) plans in esophageal cancer (EC). METHODS: Twenty patients with EC were selected, including 5 cases located in the cervical, the upper, the middle and the lower thorax, respectively. Five plans were generated with the eclipse planning system: three using c-IMRT with 5 fields (5F), 7 fields (7F) and 9 fields (9F), and two using VMAT with a single arc (1A) and double arcs (2A). The treatment plans were designed to deliver a dose of 60 Gy to the planning target volume (PTV) with the same constrains in a 2.0 Gy daily fraction, 5 d a week. Plans were normalized to 95% of the PTV that received 100% of the prescribed dose. We examined the dose-volume histogram parameters of PTV and the organs at risk (OAR) such as lungs, spinal cord and heart. Monitor units (MU) and normal tissue complication probability (NTCP) of OAR were also reported. RESULTS: Both c-IMRT and VMAT plans resulted in abundant dose coverage of PTV for EC of different locations. The dose conformity to PTV was improved as the number of field in c-IMRT or rotating arc in VMAT was increased. The doses to PTV and OAR in VMAT plans were not statistically different in comparison with c-IMRT plans, with the following exceptions: in cervical and upper thoracic EC, the conformity index (CI) was higher in VMAT (1A 0.78 and 2A 0.8) than in c-IMRT (5F 0.62, 7F 0.66 and 9F 0.73) and homogeneity was slightly better in c-IMRT (7F 1.09 and 9F 1.07) than in VMAT (1A 1.1 and 2A 1.09). Lung V30 was lower in VMAT (1A 12.52 and 2A 12.29) than in c-IMRT (7F 14.35 and 9F 14.81). The humeral head doses were significantly increased in VMAT as against c-IMRT. In the middle and lower thoracic EC, CI in VMAT (1A 0.76 and 2A 0.74) was higher than in c-IMRT (5F 0.63 Gy and 7F 0.67 Gy), and homogeneity was almost similar between VMAT and c-IMRT. V20 (2A 21.49 Gy vs. 7F 24.59 Gy and 9F 24.16 Gy) and V30 (2A 9.73 Gy vs. 5F 12.61 Gy, 7F 11.5 Gy and 9F 11.37 Gy) of lungs in VMAT were lower than in c-IMRT, but low doses to lungs (V5 and V10) were increased. V30 (1A 48.12 Gy vs. 5F 59.2 Gy, 7F 58.59 Gy and 9F 57.2 Gy), V40 and V50 of heart in VMAT was lower than in c-IMRT. MUs in VMAT plans were significantly reduced in comparison with c-IMRT, maximum doses to the spinal cord and mean doses of lungs were similar between the two techniques. NTCP of spinal cord was 0 for all cases. NTCP of lungs and heart in VMAT were lower than in c-IMRT. The advantage of VMAT plan was enhanced by doubling the arc. CONCLUSION: Compared with c-IMRT, VMAT, especially the 2A, slightly improves the OAR dose sparing, such as lungs and heart, and reduces NTCP and MU with a better PTV coverage.	esophagus
The role of radiation therapy in resected T2 N0 esophageal cancer: a population-based analysis.	BACKGROUND: The prognosis of even early-stage esophageal cancer is poor. Because there is not a consensus on how to manage T2 N0 disease, we examined survival after resection of T2 N0 esophageal cancer, with or without radiation therapy. METHODS: Patients who underwent resection for T2 N0 squamous cell carcinoma or adenocarcinoma of the mid or distal esophagus, with or without radiation therapy, were identified using the Surveillance, Epidemiology and End Results cancer registry from 1998 to 2008. The 5-year cancer-specific survival (CSS) and overall survival (OS) after resection alone and combined resection with radiation therapy were compared using the Kaplan-Meier approach, risk-adjusted Cox proportional hazard models, and competing risk models. RESULTS: The 5-year OS of 490 T2 N0 patients was 40.3% (95% confidence interval [CI], 35.2% to 45.4%). Surgical resection alone was used in 267 patients (54%) and combined therapy in 223 (46%). The 5-year OS was 38.6% (95% CI, 31.7% to 45.5%) in patients undergoing resection only and 42.3% (95% CI, 34.7% to 49.6%) for combined therapy (p = 0.48). No difference in OS was found, even after risk adjustment (hazard ratio [HR], 1.14; 95% CI, 0.87 to 1.48; p = 0.35). However, in landmark studies with left truncation for 3 and 6 months, resection only showed better OS than combined therapy (HR, 1.33; 95% CI, 1.01 to 1.75; p = 0.04 vs HR, 1.36; 95% CI, 1.01 to 1.83; p = 0.04, respectively). No such difference for CSS was detected, even for the landmark study after 6 months (HR, 1.16; 95% CI, 0.98 to 1.39, p = 0.09). CONCLUSIONS: Combining radiation therapy with esophagectomy did not result in improved outcomes compared with esophagectomy alone for patients with T2 N0 esophageal cancer in the Surveillance, Epidemiology and End Results database.	esophagus