crossing96/oncoscreening huggingface dataset:
Meta-Analysis of Two Different Methods for Cervical Esophagogastric Anastomosis: Triangulating Versus Circular Stapling.	Background: The standard treatment for esophageal carcinoma is extensive resection of the tumor and esophagogastric anastomosis despite the high incidence of related anastomotic complications, such as stricture and leakage. Thus, the choice of the cervical esophagogastric anastomotic method-triangulating stapling (TS) versus circular stapling (CS)-is a critical decision for the surgeon. Aim: To compare the incidence of major adverse outcomes between TS and CS in patients with resectable thoracic esophageal cancer. Methods: For this meta-analysis, PubMed, Embase, Wiley Online Library, Google Scholar, Wanfang, and China National Knowledge Infrastructure databases were searched for subject-relevant studies by using a rigorous study protocol established according to the recommendations of the Cochrane Handbook. Anastomotic leakage, anastomotic stricture, and postoperative pulmonary complications were the primary endpoints used for comparison. Relative risk (RR) with 95% confidence intervals (CI) were calculated to assess the strength of association. Results: Six studies were selected by our inclusion/exclusion criteria and represented a total of 739 patients in our meta-analysis of TS (n = 376) versus CS (n = 363). The TS group showed a lower incidence of anastomotic stricture (RR: 0.23 [95% CI: 0.08-0.63]; P = .004) and pulmonary complications (RR: 0.57 [95% CI: 0.37-0.87]; P = .01). However, the incidence of anastomotic leakage was similar for the two groups (RR: 0.66 [95% CI: 0.41-1.09]; P = .1). Subgroup analysis of four studies in which the surgical methods were minimally invasive demonstrated the TS group to have a lower incidence of lung complications (RR: 0.55 [95% CI: 0.35-0.87]; P = .01), anastomotic leakage (RR: 0.36 [95% CI: 0.18-0.74]; P = .005), and anastomotic stricture (RR: 0.23 [95% CI: 0.05-0.98]; P = .05). Conclusion: The TS method for cervical esophagogastric anastomosis after esophagectomy had a lower incidence of anastomotic stricture and postoperative lung complications.	esophagus
A Case of Dermatomyositis Along with Esophageal Cancer and Screening of Serum Transcriptional Intermediary Factor 1 Gamma Antibodies in Various Cancer Patients.	BACKGROUND Dermatomyositis (DM) is occasionally associated with malignancy, which is so-called cancer-associated myositis. The cancer screening in patients with dermatomyositis is an important clinical issue. That is because malignant disease underlying dermatomyositis is potentially life-threatening. Transcriptional intermediary factor 1γ (TIF1γ) antibodies (anti-TIF1γ Abs) are one of the myositis-specific autoantibodies, which are investigated as potential predictors of malignancy in patients with dermatomyositis. However, the etiology of anti-TIF1γ Abs generations in various cancer patients is not known. CASE REPORT A 70-year-old male patient was admitted for muscle pain and weakness in both legs. Erythematous on the face, eruption, and a V sign were also observed. Laboratory tests showed the elevation of creatine kinase, myoglobin, and aldolase. He was diagnosed as dermatomyositis. Cancer screening was performed, and esophageal cancer was detected in the lower esophagus. Despite the symptoms of dermatomyositis were improved with steroid, methotrexate, and radical esophagectomy, he died with esophageal cancer 3 years after the onset of dermatomyositis. TIF1γ is frequently overexpressed in cancer tissues. Therefore, some cancer patients without dermatomyositis could be positive for anti-TIF1γ Abs. We retrospectively analyzed anti-TIF1γ Abs in cancer patients (n=131). However, the screening of anti-TIF1γ Abs in cancer patients without dermatomyositis (n=130) showed there were no seropositive patients. Only this cancer-associated myositis patient was positive for anti-TIF1γ Abs. CONCLUSIONS Our result suggested the generation of anti-TIF1γ Abs is specific for cancer associated myositis, not for tumorigenesis.	esophagus
Does brain radiotherapy improve survival in patients with esophageal squamous cell carcinoma with brain metastasis?	BACKGROUND: To investigate the clinical characteristics, influencing factors, and their impact on survival in patients with brain metastases from esophageal squamous cell carcinoma (BM-ESCC). METHODS: A total of 67 patients with patients with newly diagnosed BM-ESCC were retrospectively analyzed from December 2000 to December 2016, in order to examine the correlation between clinicopathological characteristics and brain metastases, and between brain metastases and survival. RESULTS: The number of BM-ESCC was positively correlated with T and N stages (P<0.05). The higher the T and N stages, the higher the incidence. The median survival time was 9.65 months. N stage was an independent risk factor for BM-ESCC. N0 + N1 was associated with a lower risk of brain metastases (P<0.05). Patients with 1 brain metastasis had a significantly longer survival than those with 2 and 3 brain metastases. N stage-stratified analysis revealed that N0 + N1 patients had a longer survival than N2 and N3 patients (P<0.05). Cox regression analysis revealed that mortality in T3 + T4 patients was 2.337 times that of Tis + T1 patients; mortality in N3 patients was 3.486 times that of N0 + N1 patients; and mortality in untreated patients was 2.772 times that of those treated with whole brain radiotherapy. CONCLUSIONS: The number of BM-ESCC is correlated to T and N stages. The higher the N stage, the higher risk of brain metastases. The higher of T and N stages in ESCC, the worse in prognosis. Whole brain radiotherapy could offer greater survival benefits.	esophagus
Current Status of Mucosal Imaging with Narrow-Band Imaging in the Esophagus.	Recent advances in endoscopic imaging of the esophagus have revolutionized the diagnostic capability for detecting premalignant changes and early esophageal malignancy. In this article, we review the practical application of narrow-band imaging focusing on diseases of the esophagus, including Barrett's esophagus, adenocarcinoma, and squamous cell carcinoma.	esophagus
LncRNA TUG1 promotes tumor growth and metastasis of esophageal squamous cell carcinoma by regulating XBP1 via competitively binding to miR-498.	Esophageal squamous cell carcinoma (ESCC) is a major subtype of esophageal cancer with high mortality. Previous reports suggested that lncRNA taurine upregulated gene 1 (TUG1) functioned as an oncogene in numerous cancers. The purpose of this study was to explore the potential mechanism of TUG1 carcinogenesis in ESCC. The expression of TUG1 and miR-498 was measured by a quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation and apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry. Cell migration and invasion were identified through the transwell assay. The interaction between miR-498 and TUG1 or X-box binding protein 1 (XBP1) was predicted by bioinformatics software starBase and verified by luciferase reporter assay. The expression of XBP1 was quantified by qRT-PCR and western blot analysis. Xenograft tumor mouse model was established to determine the function of TUG1 in vivo. TUG1 was upregulated in ESCC tissues and cells, and its high expression was associated with tumor lymph node metastasis and low cumulative survival. TUG1 knockdown inhibited proliferation, migration, and invasion but promoted apoptosis in ESCC cells. It was confirmed that miR-498 was a target of TUG1, and XBP1 was a target of miR-498. The expression of miR-498 was reduced in ESCC tissues while XBP1 expression was notably enhanced. Mechanism analysis manifested that TUG1 regulated proliferation, apoptosis, migration, and invasion by upregulating XBP1 via targeting miR-498 in vitro. Furthermore, knockdown of TUG1 attenuated tumor growth in vivo. TUG1 accelerated tumorigenesis and metastasis by inducing XBP1 expression through directly targeting miR-498 in ESCC.	esophagus
Scheduled intravenous acetaminophen versus nonsteroidal anti-inflammatory drugs (NSAIDs) for better short-term outcomes after esophagectomy for esophageal cancer.	PURPOSE: To evaluate the effect of scheduled intravenous acetaminophen administration versus nonsteroidal anti-inflammatory drugs on postoperative pain and short-term outcomes after esophagectomy. METHODS: The subjects of this study were 150 consecutive patients who underwent esophagectomy for esophageal cancer. Seventy-seven patients received scheduled intravenous acetaminophen and the other 73 received NSAIDs enterally for postoperative pain management. We compared the postoperative pain and short-term outcomes between the groups. Inverse probability of treatment weighting (IPTW) based on propensity scores was used to control for selection bias. RESULTS: The visual analog scale (VAS) of postoperative pain was lower in the acetaminophen group than in the NSAIDs group, based on the mean values of chest VAS on postoperative days (PODs) 0, 4, 5, and 6 and the mean values of abdomen VAS on PODs 4, 5, and 6. The incidence of anastomotic leakage and postoperative delirium was lower in the acetaminophen group than in the NSAIDs group (anastomotic leakage, odds ratio (OR) 0.3, p = 0.01; postoperative delirium, OR 0.19, p < 0.01). CONCLUSION: Scheduled intravenous acetaminophen administration is effective and feasible for the postoperative pain management of patients undergoing esophagectomy and may be associated with a lower incidence of anastomotic leakage and postoperative delirium.	esophagus
Generation and Characterization of Patient-Derived Head and Neck, Oral, and Esophageal Cancer Organoids.	Esophageal cancers comprise adenocarcinoma and squamous cell carcinoma, two distinct histologic subtypes. Both are difficult to treat and among the deadliest human malignancies. We describe protocols to initiate, grow, passage, and characterize patient-derived organoids (PDO) of esophageal cancers, as well as squamous cell carcinomas of oral/head-and-neck and anal origin. Formed rapidly (<14 days) from a single-cell suspension embedded in basement membrane matrix, esophageal cancer PDO recapitulate the histology of the original tumors. Additionally, we provide guidelines for morphological analyses and drug testing coupled with functional assessment of cell response to conventional chemotherapeutics and other pharmacological agents in concert with emerging automated imaging platforms. Predicting drug sensitivity and potential therapy resistance mechanisms in a moderate-to-high throughput manner, esophageal cancer PDO are highly translatable in personalized medicine for customized esophageal cancer treatments. © 2020 by John Wiley & Sons, Inc. Basic Protocol 1: Generation of esophageal cancer PDO Basic Protocol 2: Propagation and cryopreservation of esophageal cancer PDO Basic Protocol 3: Imaged-based monitoring of organoid size and growth kinetics Basic Protocol 4: Harvesting esophageal cancer PDO for histological analyses Basic Protocol 5: PDO content analysis by flow cytometry Basic Protocol 6: Evaluation of drug response with determination of the half-inhibitory concentration (IC(50) ) Support Protocol: Production of RN in HEK293T cell conditioned medium.	esophagus
Mean cardiopulmonary dose and vertebral marrow dose differentially predict lineage-specific leukopenia kinetics during radiotherapy for esophageal cancer.	BACKGROUND AND PURPOSE: Lymphopenia is associated with poor outcomes in esophageal cancer (EC) patients undergoing chemoradiotherapy (CRT). We hypothesized that radiation dose to marrow (central) vs. circulating (peripheral) leukocytes (WBCs) may have unique effects on WBC counts and clinical outcomes in EC. MATERIALS AND METHODS: Weekly and 90-day post-CRT blood cell counts were evaluated for 46 patients with stage II-III EC treated with CRT. Thoracic vertebral volume spared (TVS) radiation was extracted from dose volume histograms (DVH). Mean cardiopulmonary dose (mCPD) was calculated as mean dose to the volumetric sum of heart, lungs, and great vessels as a surrogate for circulating blood pool. Linear and logistic regression identified associations between dosimetric variables and hematologic toxicities (HT). Repeated measures ANOVA tested associations between cell count trends and clinical predictors. RESULTS: WBCs and platelets reached nadir at week 6 of CRT. On multivariate analysis, mCPD was associated with lower WBC and neutrophil nadirs (p < 0.05). TVS5-40 Gy were associated with higher lymphocyte nadirs (all p < 0.05). Repeated measures ANOVA revealed an interaction effect of sex on absolute lymphocyte trend as well as age (<67 vs. >67) and diabetes on normalized lymphocyte trend (all p < 0.015). CONCLUSIONS: mCPD and volume of thoracic marrow spared radiation differentially predict lineage-specific leukopenias during CRT for EC. mCPD is significantly associated with lower total WBC and neutrophil nadirs. In contrast, greater thoracic marrow spared radiation is associated with mitigation of lymphopenia during CRT. Clinical factors such as sex, age, and diabetes may be associated with a more rapid decline in hematologic counts during treatment.	esophagus
A genomic biomarker-based model for cancer risk stratification of non-dysplastic Barrett's esophagus patients after extended follow up; results from Dutch surveillance cohorts.	Barrett's esophagus is the only known mucosal precursor for the highly malignant esophageal adenocarcinoma. Malignant degeneration of non-dysplastic Barrett's esophagus occurs in < 0.6% per year in Dutch surveillance cohorts. Therefore, it has been proposed to increase the surveillance intervals from 3 to 5 years, potentially increasing development of advanced stage interval cancers. To prevent such cases robust biomarkers for more optimal stratification over longer follow up periods for non-dysplastic Barrett's patients are required. In this multi-center study, aberrations for chromosomes 7, 17, and structural abnormalities for c-MYC, CDKN2A, TP53, Her-2/neu and 20q assessed by DNA fluorescence in situ hybridization on brush cytology specimens, were used to determine marker scores and to perform clonal diversity measurements, as described previously. In this study, these genetic biomarkers were combined with clinical variables and analyzed to obtain the most efficient cancer prediction model after an extended period of follow-up (median time of 7 years) by applying Cox regression modeling, bootstrapping and leave-one-out analyses. A total of 334 patients with Barrett's esophagus without dysplasia from 6 community hospitals (n = 220) and one academic center (n = 114) were included. The annual progression rate to high grade dysplasia and/or esophageal adenocarcinoma was 1.3%, and to adenocarcinoma alone 0.85%. A prediction model including age, Barrett circumferential length, and a clonicity score over the genomic set including chromosomes 7, 17, 20q and c-MYC, resulted in an area under the curve of 0.88. The sensitivity and specificity of this model were 0.91 and 0.38. The positive and negative predictive values were 0.13 (95% CI 0.09 to 0.19) and 0.97 (95% CI 0.93 to 0.99). We propose the implementation of the model to identify non-dysplastic Barrett's patients, who are required to remain in surveillance programs with 3-yearly surveillance intervals from those that can benefit from less frequent or no surveillance.	esophagus
Trichostatin A augments esophageal squamous cell carcinoma cells migration by inducing acetylation of RelA at K310 leading epithelia-mesenchymal transition.	Protein acetylation modification controlled by acetyltransferases (HATs) and histone deacetylases (HDACs) regulates multiple biologic processes including cell proliferation and migration. HDAC inhibitors (HDACi) are currently used as a promising epigenetic-based therapy for cancer treatment. Of the anticancer activity, accumulating evidence has shown that HDACi can enhance cell migration in subset of cancer cells. Thus, there is a critical need to identify such counter anticancer activity to HDACi in different cancer cell types and elucidate the rational in order to develop appropriate combination therapies in cancer treatment. In seeking to address the effect of HDACi on esophageal squamous cell carcinoma (ESCC) cells migration, trichostatin A (TSA), a canonical HDACi targeting class I and class II HDACs, was used. Here, we report the discovery that TSA augmented ESCC cells migration by increasing the acetylation of nuclear factor-κB/RelA at lysine 310 (K310). To elucidate the mechanism by which TSA promotes the migration of ESCC cells, plasmid of RelA K310R, a mutant precluding acetylation at K310, was transfected into ESCC cells. Blocking acetylation of RelA at K310 significantly arrogated TSA-induced cell migration. Mechanistic investigations revealed that TSA increased the level of acetylated RelA at K310 (RelA K310ac), thereby increasing the level of epithelia-mesenchymal transition (EMT) transcription factor slug mRNA, which in turn induced EMT. Overall, this study indicates that TSA promotes ESCC cells migration by RelA K310ac-slug-EMT pathway. Our findings provide a strategy to eradicate HDACi-induced ESCC cells migration by targeting RelA as a combination therapy with nonspecific HDACi in ESCC treatment.	esophagus
Nutritional management of patients with oesophageal cancer throughout the treatment trajectory: benchmarking against best practice.	PURPOSE: Oesophageal cancer (OC) impacts nutritional status and outcomes. This study aims to benchmark the current nutrition management of patients with OC against best practice recommendations, identify critical points in the treatment trajectory where nutritional status is compromised, service gaps and opportunities for improvement. METHODS: A retrospective audit collected demographic, medical and nutritional data from medical records of patients who received curative treatment for OC at a tertiary referral hospital in Sydney, Australia. RESULTS: Thirty-seven patient records were audited over the time period. Twenty-nine patients underwent nutrition screening on admission to the service. Eighteen out of 25 patients receiving neoadjuvant radiation therapy, all patients during surgical admission, and only 19 patients at postsurgical discharge were seen by a dietitian. All patients received tube feeding post-operatively; however, initiation within 24 h only occurred for 14 patients. Weight significantly declined over the course of treatment (p < 0.001), whilst malnutrition during surgical admission (p = 0.004) and postsurgical discharge (p = 0.038) were both associated with significantly higher unplanned readmissions. CONCLUSIONS: Best practice recommendations were met for aspects of the immediate post-operative period; however, service gaps remain during pre-operative and post-discharge care. Findings from this study indicate that nutritional care is inconsistent across different treatment stages, and malnutrition impacts negatively on unplanned readmission. Research is needed to address evidence-practice gaps, assess appropriateness of recommendations and provide evidence for models of care during multimodality treatments and across different services.	esophagus
Inhibition of esophageal-carcinoma cell proliferation by genistein via suppression of JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways.	Esophageal carcinoma (EsC) is a clinically challenging neoplastic disease. Genistein, a natural isoflavone product, has anti-tumor properties. Through in vitro and in vivo studies, we found that genistein suppressed EsC cell proliferation in a time- and concentration-dependent manner. In addition, genistein markedly promoted apoptosis and arrested cell cycle at the G0/G1 phase in a concentration-dependent manner. Furthermore, high concentrations of genistein have no adverse effect on normal esophageal epithelial cells. Mechanistically, genistein treatment strikingly reduced the expression of cell cycle-associated genes, and up-regulated the expression of cell apoptosis-related genes in EsC cells. Additionally, genistein dramatically decreased epidermal growth factor receptor (EGFR) expression and attenuated its down-stream signaling molecules STAT3, MDM2, Akt and JAK1/2 phosphorylation, resulting in inhibited nuclear translocation of STAT3 and MDM2, thereby inhibiting the JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways. In xenograft nude mice, genistein administration strikingly impaired tumor growth in a dose-dependent manner. Moreover, similar disturbances in molecular mechanisms were observed in vivo. Taken together, genistein suppressed the JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways by decreasing EGFR expression, leading to cell apoptosis, cell cycle arrest, and proliferation inhibition in EsC cells. Our findings suggest that genistein may be a promising alternative adjuvant therapy for patients with EsC.	esophagus
Constructing a risk prediction model for anastomotic leakage after esophageal cancer resection.	OBJECTIVE: The purpose of this study was to investigate a newly constructed risk prediction model for anastomotic leakage after esophageal cancer resection. METHODS: A retrospective survey of 205 patients who underwent esophageal cancer resection was conducted using a self-designed questionnaire. The influencing factors were explored by single factor analysis, and a logistic regression analysis was performed to construct the prediction equation. A receiver operating characteristic curve was used to evaluate the model. RESULTS: The incidence of anastomotic leakage after esophageal cancer resection was 11.73%. There were five independent risk factors entered into the regression equation. The risk prediction equation was Z = 0.108 × age + 2.011 × preoperative chemotherapy history + 3.007 ×incision redness/exudation + 2.632 × pleural effusion + 1.934 × increased white blood cell count − 12.304. According to the receiver operating characteristic curve test, the area under the curve was 0.946, the sensitivity was 0.833, the specificity was 0.912, and the Youden index was 0.745. CONCLUSION: The risk model of anastomotic leakage after esophageal cancer resection had a good predictive effect that was of significance for guiding clinical observation and early-screening.	esophagus
Transhiatal esophagogastric anastomosis and postoperative monitoring of thoracic esophageal leiomyosarcoma in a dog.	A 12-year-old Maltese dog was referred to the Veterinary Teaching Hospital at Konkuk University because of severe regurgitation. Radiography, ultrasonography, and computed tomography showed a mass in the thoracic esophagus. Localization of the tumor, its extraluminal nature, the positioning and involvement of the stomach, and the lack of diffuse metastasis to the lung were factors considered when developing a surgical plan. A successful surgical procedure was performed. The final diagnosis was leiomyosarcoma. Following surgery, clinical signs were significantly reduced and postoperative complications were not observed. The dog died 25 days after surgery; we suspected that the death was due to postoperative stricture. Key clinical message: Surgical approaches that prioritize maintenance of low tension on the thoracic esophagus are important to prevent arrhythmia, bradycardia, and ventricular premature complex during esophagogastric anastomosis. In dogs with a small esophageal lumen anastomosis may lead to postoperative stricture.	esophagus