crossing96/oncoscreening huggingface dataset:
Visualization of the Stomach's Arterial Networks During Esophageal Surgery Using the HyperEye Medical System.	AIM: The present study investigated the visualization of the arterial networks in the stomach (ANS) during gastric tube (GT) creation using indocyanine green fluorescence and the HyperEye Medical System (HEMS), and the feasibility of the HEMS-line-marking method (LMM). PATIENTS AND METHODS: We reviewed 51 consecutive patients who had undergone esophageal surgery with GT reconstruction. Patients for whom the HEMS was deployed after GT creation to confirm the anastomosed area's blood supply formed the control group (n=28). Patients for whom the HEMS was deployed before GT creation to confirm and mark the ANS border comprised the HEMS-LMM group (n=23). RESULTS: The HEMS-LMM visualized the ANS border, and the leakage rate decreased from 17.9% to 4.4% (p=0.204). CONCLUSION: The HEMS-LMM is safe and feasible for visualizing the blood supply border of the right gastroepiploic artery and the ANS before GT creation during esophageal surgery, and it might reduce leakage in esophageal surgery.	esophagus
Four Synchronous Primary Malignancies of the Breast, Lung, Colon and Esophagus.	The literature contains few reports of patients with four more or more synchronous primary malignancies. We report the case of a 74-year-old woman who presented with synchronous primary malignant neoplasms of the breast (metaplastic carcinoma), lung (squamous cell carcinoma), esophagus (adenocarcinoma), and colon (adenocarcinoma). She was treated with multimodality therapy and demonstrated a favorable response at early follow-up. To our knowledge, this combination of synchronous primary malignancies has not been previously reported. The management of patients with multiple synchronous primary malignancies introduces a number of unique challenges which necessitate highly individualized treatment plans that may not strictly adhere to standard practices in the setting of a single malignancy.	esophagus
Plummer-Vinson Syndrome in Children.	OBJECTIVES: Plummer-Vinson syndrome (PVS), also called Kelly-Paterson syndrome, is a rare cause of dysphagia in children. This syndrome associates single or multiple webs in the upper esophagus with frequent iron deficiency. METHODS: We reported 3 pediatric cases of PVS before analyzing all of the cases of PVS in children reported in the PubMed and EMBASE databases. RESULTS: Among 17 reported PVS cases in children, all of the patients experienced iron-deficiency anemia, and no immunological disease was reported. The male/female ratio was 1/1.9, and most cases were observed in adolescents. Conversely to adults, endoscopic dilation was often necessary because dysphagia resisted iron supplementation. A single dilation was usually sufficient. One case of pediatric PVS experienced esophageal cancer in adulthood. CONCLUSIONS: In the case of dysphagia in children, a swallow barium exploration with lateral incidence should look for PVS. Conversely to adults, an endoscopic dilation is frequently necessary to control dysphagia in children.	esophagus
MiR-613: a novel diagnostic and prognostic biomarker for patients with esophageal squamous cell carcinoma.	MicroRNA-613 (miR-613) plays important roles in tumorigenesis and cancer progression. We aimed to evaluate its expression level and potential for diagnosis and prognosis in esophageal squamous cell cancer (ESCC). We examined miR-613 expression in 60 pairs of ESCC cancerous and matched paracancerous tissues, serum samples from 75 ESCC patients and 75 healthy volunteers, and 105 formalin-fixed paraffin-embedded (FFPE) tissue samples using quantitative reverse transcription polymerase chain reaction. Receiver-operating characteristic (ROC) curve analysis, Kaplan-Meier method, and Cox regression were applied to analyze its diagnostic and prognostic value. MiR-613 was significantly decreased in ESCC tissue compared with paracancerous tissue (P < 0.001). Moreover, the expression level of miR-613 was significantly reduced with increased T stage of ESCC. Statistically significant difference between ESCC patients and healthy controls in expression level of miR-613 (0.89 ± 0.73 vs. 1.71 ± 1.03, P < 0.001) was found. The area under the ROC curve (AUC) based on serum miR-613 was 0.767 ± 0.040. We also performed analysis on early-stage patients and revealed that the AUC value was 0.728 ± 0.052 (P < 0.001). The Kaplan-Meier curve revealed that the downregulation of miR-613 was related to worse overall survival (OS) and progression-free survival (PFS) of ESCC patients (P = 0.018 and P = 0.035, respectively). Furthermore, the multivariate analysis identified miR-613 to be an independent prognostic factor for OS and PFS (P = 0.031 and P = 0.006, respectively) In conclusion, miR-613 is significantly reduced in cancerous tissue and serum samples of ESCC patients. It can serve as an ideal indicator for the diagnosis and prognosis of ESCC.	esophagus
Molecular characterization of antitumor effects of the rhizome extract from Curcuma zedoaria on human esophageal carcinoma cells.	Curcuma zedoaria has been used as a traditional agent against malignant diseases. To elucidate detailed mechanisms producing such an activity, characterization and determination of molecular mechanisms of its antitumor effects was conducted. Inhibiting activities against cell proliferation, invasion and colony formation, and expression levels of corresponding molecules were investigated using human esophageal cancer TE-8 cells treated with the rhizome extract from C. zedoaria. Antitumor effect of the extract administered orally was also examined in tumor-bearing mice. The extract possessed strong anti-proliferation and invasion activities against TE-8 cells. Further, upregulated PTEN and downregulated phosphorylated Akt, mTOR and STAT3 expressions in the cells were induced shortly after treatment with the extract, followed by attenuation of FGFR1 and MMP-2, activation of caspase-9, caspase-3 and PARP, and suppression of Bcl-2 expressions, which led the cells to apoptotic cell death. Furthermore, tumor formation in mice was significantly suppressed through the oral administration of the extract. Taken together, these results suggest that the C. zedoaria extract could be a promising agent against esophageal cancer.	esophagus
Prognostic significance of FAM3C in esophageal squamous cell carcinoma.	BACKGROUND: Family with sequence similarity 3, member C (FAM3C) has been identified as a novel regulator in epithelial-mesenchymal transition (EMT) and metastatic progression. However, the role of FAM3C in esophageal squamous cell carcinoma (ESCC) remains unexplored. The purpose of present study is to illustrate the role of FAM3C in predicting outcomes of patients with ESCC. METHODS: FAM3C expression was measured in ESCC tissues and the matched adjacent nontumorous tissues by quantitative real-time RT-PCR and Western blot analysis. The relationship between FAM3C expression and prognosis of ESCC patients was further evaluated by univariate and multivariate regression analyses. Univariate and multivariate analyses of the prognostic factors were performed using Cox proportional hazards model. RESULTS: The FAM3C mRNA expression was remarkably upregulated in ESCC compared with their nontumor counterparts (P < 0.001). In addition, high expression of FAM3C was significantly associated with pT stage (P = 0.014) , pN stage (P = 0.026) and TNM stage (P = 0.003). Kaplan-Meier analysis showed that the 7-year overall survival rate in the group with high expression of FAM3C was poorer than that in low expression group (32.0 versus 70.9 %; P < 0.001). Univariate and multivariate analyses demonstrated that FAM3C was an independent risk factor for overall survival. Moreover, Stratified analysis revealed that FAM3C expression could differentiate the prognosis of patients in early clinical stage (TNM stage I-II). CONCLUSIONS: FAM3C expression was dramatically increased in ESCC and might serve as a valuable prognostic indicator for ESCC patients after surgery.	esophagus
Use of FDG-PET to detect a chronic odontogenic infection as a possible source of the brain abscess.	This study describes the use of (18)F-fluoro-2-deoxyglucose positron emission tomography (FDG-PET) to detect a chronic odontogenic infection as the possible origin of a brain abscess (BA). A 74-year-old man with esophageal carcinoma was referred to our department to determine the origin of a BA in his oral cavity. He had no acute odontogenic infections. The BA was drained, and bacteria of the Staphylococcus milleri group were detected. Whole body FDG-PET revealed that the only sites of definite uptake of FDG were the esophageal carcinoma and the left upper maxillary region (SUVmax: 4.5). These findings suggested that the BA may have originated from a chronic periodontal infection. Six teeth with progressive chronic periodontal disease were extracted to remove the possible source of BA. These findings excluded the possibility of direct spread of bacteria from the odontogenic infectious lesion to the intracranial cavity. After extraction, there was no relapse of BA.	esophagus
Obesity and the Incidence of Upper Gastrointestinal Cancers: An Ecological Approach to Examine Differences across Age and Sex.	BACKGROUND: Esophageal and gastric cancers differ in their epidemiology but have several risk factors in common. The aim of this study was to assess age and sex differences in the burden of esophageal and gastric cancers in the context of the global obesity epidemic. METHODS: Data from 50 countries were obtained from Cancer Incidence in Five Continents Volume X and GLOBOCAN 2012. Age-specific and age-standardized incidence rates of esophageal adenocarcinoma and squamous cell carcinoma (ESCC), as well as cardia (CGC) and noncardia (NCGC) gastric cancer, were estimated. Countries were grouped and analyzed according to their obesity prevalence. RESULTS: A gradient across quartiles of obesity prevalence was found for esophageal adenocarcinoma, with the highest incidence rates in high prevalence countries (ASR 3.0 vs. 0.8 per 100,000 in highest vs. lowest obesity quartiles, males). In contrast, for ESCC as well as for CGC and NCGC the reverse was true, with the highest rates observed in countries with the lowest obesity prevalence (ESCC, 2.2 vs. 11.5; CGC, 2.8 vs. 7.8; NCGC, 3.9 vs. 17.4 in highest vs. lowest obesity quartiles, males). Although for esophageal adenocarcinoma, sex and age differences in incidence were most pronounced in countries with a high prevalence of obesity, these differences were much smaller for the other cancer sites assessed. CONCLUSIONS: Variation in obesity prevalence may partly explain age and sex differences in the incidence of esophageal adenocarcinomas. IMPACT: Ecologic studies can help assess relationships between risk factors and cancer, and generate new hypotheses that may be pursued through more directed research.	esophagus
[Current Status and Future Prospects of Chemoradiotherapy for Esophageal Cancer].	Chemoradiotherapy is a very important factor and one of the 2 pillars of esophageal cancer treatment. Although esophagectomy is the standard treatment for clinical stage Ⅰ(T1N0M0)esophageal cancer, chemoradiotherapy is reported to be effective. Currently, a phaseⅢ clinical trial is underway to compare patients who undergo esophagectomy and those who receive radical chemoradiotherapy. Esophagectomy after neoadjuvant chemotherapy is the standard treatment for clinical stageⅡ/Ⅲ(except for T4) esophageal cancer, whereas chemoradiotherapy is regarded as the standard treatment for patients who wish to preserve their esophagus, those who refuse surgery, and those with inoperable disease. Chemoradiotherapy, rather than surgical treatment, is usually selected for clinical stageⅣ (T4/M1LYM) esophageal cancer. While curability increases with chemoradiotherapy, late adverse events such as cardiopulmonary toxicity and safety problems with salvage treatment of cases with residual tumor or recurrent cancer have been observed. New irradiation techniques using radiation technology are being developed, such as intensity-modulated radiation therapy (IMRT). These innovations are expected to improve treatment results by avoiding irradiation of at-risk organs, without reducing the target radiation volume. New treatments, including salvage protocols, introduction of new radiotherapy equipment such as IMRT, and new drugs, are being developed, and further advances are anticipated.	esophagus
Different accuracy of endosonographic tumor staging after neoadjuvant chemotherapy and chemoradiotherapy in esophageal cancer.	BACKGROUND: Treatment response to neoadjuvant therapy is histologically associated with more or less intensive inflammation and fibrosis. In consequence, accuracy of endosonographic TN-tumor staging after neoadjuvant treatment is hampered. We analyzed whether the kind of treatment chosen [chemoradiotherapy (CRT) or chemotherapy (CT)] differently influences the accuracy of endoscopic ultrasound after neoadjuvant therapy in esophageal cancer. METHODS: We performed serial endoscopic ultrasound examinations in 18 patients after neoadjuvant CRT and 30 patients after neoadjuvant CT. TN-stage was classified according to the standard parameter. Histological examination of the surgical resection specimen served as gold standard. RESULTS: The most frequent error was overstaging, especially in patients with complete tumor response or minimal residual disease. Accuracy of T-staging was significantly worse after CRT (0.16) than after CT (0.43), obviously due to difficulty in distinguishing residual tumor from treatment-associated fibrosis and inflammation. Accuracy of N-staging was also hampered, but to a less extent (sensitivity/specificity 0.85/0.36 after CRT, and 0.5/0.42 after CT). CONCLUSIONS: Accuracy of endosonographic TN-tumor staging is significantly more hampered by neoadjuvant CRT than after CT. However, endoscopic ultrasound is insufficient for TN-staging irrespective of the kind of neoadjuvant therapy performed.	esophagus
Molecular effects of Lapatinib in the treatment of HER2 overexpressing oesophago-gastric adenocarcinoma.	BACKGROUND: Lapatinib, a dual EGFR and HER2 inhibitor has shown disappointing results in clinical trials of metastatic oesophago-gastric adenocarcinomas (OGAs), and in vitro studies suggest that MET, IGFR, and HER3 confer resistance. This trial applied Lapatinib in the curative neoadjuvant setting and investigated the feasibility and utility of additional endoscopy and biopsy for assessment of resistance mechanisms ex vivo and in vivo. METHODS: Patients with HER2 overexpressing OGA were treated for 10 days with Lapatinib monotherapy, and then in combination with three cycles of Oxaliplatin and Capecitabine before surgery. Endoscopic samples were taken for molecular analysis at: baseline including for ex vivo culture +/- Lapatinib to predict in vivo response, post-Lapatinib monotherapy and at surgery. Immunohistochemistry (IHC) and proteomic analysis was performed to assess cell kinetics and signalling activity. RESULTS: The trial closed early (n=10) due to an anastomotic leak in two patients for which a causative effect of Lapatinib could not be excluded. The reduction in Phosphorylated-HER2 (P-HER2) and P-EGFR in the ex vivo-treated biopsy demonstrated good correlation with the in vivo response at day 10. Proteomic analysis pre and post-Lapatinib demonstrated target inhibition (P-ERBB2, P-EGFR, P-PI3K, P-AKT, and P-ERK) that persisted until surgery. There was also significant correlation between the activation of MET with the level of P-Erk (P=0.0005) and P-PI3K : T-PI3K (total PI3K) ratio (P=0.0037). There was no significant correlation between the activation status of IGFR and HER3 with downstream signalling molecules. CONCLUSIONS: Additional endoscopy and biopsy sampling for multiple biomarker endpoints was feasible and confirmed in vitro data that MET is likely to be a significant mechanism of Lapatinib resistance in vivo.	esophagus
Aberrant hypermethylation of RASSF2 in tumors and peripheral blood DNA as a biomarker for malignant progression and poor prognosis of esophageal squamous cell carcinoma.	As a tumor suppressor gene, RAS-association domain family 2 (RASSF2) is inactivated by promoter hypermethylation in different tumor cell lines and primary tumors. However, the role of RASSF2 in esophageal squamous cell carcinoma (ESCC) has remained uninvestigated. The aims of this study were to determine the role and methylation status of RASSF2 in esophageal cancer cell lines, ESCC tissues and white blood cells, and to evaluate the potential prognostic role of RASSF2 in ESCC. In the present study, we found frequent silencing of RASSF2 and up-regulation of the gene by 5-Aza-dC treatment in esophageal cancer cell lines. Aberrant methylation of the CpG sites close to the transcription start site induced silencing of RASSF2 expression and in vitro methylation of RASSF2 led to a significant decrease in luciferase activity. The results were further verified in clinical specimens and aberrant methylation of the CpG sites close to the transcription start site of RASSF2 was found in ESCC tumor tissues and peripheral white blood cells. Furthermore, RASSF2 hypermethylation was associated with lower level of RASSF2 expression. ESCC patients in stage III and IV, with negative expression or hypermethylation of the CpG sites close to the transcription start of RASSF2 demonstrated poor patient survival. Taken together, our results suggest that RASSF2 may function as a tumor suppressor gene that is inactivated through hypermethylation of CpG sites close to the transcription start site in ESCC and its expression or methylation may have prognostic implications for ESCC patients.	esophagus
Impact of esophagectomy for cancer on patients' occupational status.	BACKGROUND: The aim of our study was to investigate the impact of esophagectomy for cancer on patients' occupational status. METHODS: All 109 consecutive patients presenting with esophageal cancer to the Surgical Oncology Unit of the Veneto Institute of Oncology Padua (Italy) between November 1, 2009 and March 15, 2012, were included in the study. Information on occupational status at diagnosis and at 1 year after esophagectomy was retrieved. Health-related quality of life was evaluated at discharge after surgery using selected aspects of the EORTC QLQ-C30 questionnaire. Non parametric statistics were used. RESULTS: Sixty-one patients (49.6%) were active workers at diagnosis and 50 of them (82.0%) underwent esophagectomy. Eighteen active workers (18/50, 36.0%) quit their job within one year from esophagectomy. They received jejunostomy more often than patients still working after surgery (50.0% vs. 18.8%, respectively; p = 0.03) and reported lower social functioning at discharge (mean ± SD 63.6 ± 16.4 vs. 80.2 ± 25.6 in others, p = 0.02). Multivariable analysis identified jejunostomy as independent predictor of job-quitting at 1 year after esophagectomy (p = 0.03; OR 4.75, 95% C.I. 1.11-20.39) but not social functioning at discharge (p = 0.21). CONCLUSIONS: Patients should be informed that they may experience social and work disability due to cancer treatment and adequate interventions of return-to-work support should be provided. Adequate welfare strategy should be implemented for esophageal cancer survivors, enhancing their role competences and contributing to precision care medicine.	esophagus
Upregulated KLK10 inhibits esophageal cancer proliferation and enhances cisplatin sensitivity in vitro.	The kallikrein-related peptidase 10 (KLK10) gene has tumor-suppressive function in various types of human cancer. However, previous studies showed that KLK10 also acts as an oncogene and is upregulated in gastrointestinal tumors. The role of KLK10 in human esophageal cancer (EC) remains unclear. In the present study, the expression of KLK10 in human esophageal and non-esophageal cancer tissues was investigated by immunohistochemistry. Quantitative RT-PCR and western blot analysis were utilized to detect KLK10 mRNA and protein expression in human esophageal cancer cell lines (TE-1 and Eca-109). Small interference RNA was utilized to specifically knockdown KLK10 expression in Eca-109 and TE-1 cells. Cell proliferation, cell cycle analysis as well as CDDP-dependent apoptosis were determined using a CCK-8 assay and flow cytometry. The results showed that, KLK10 was positive in 67 out of 83 (80.72%) human EC and positive in 3 out of 11 (27.27%) normal tissues (P=0.001). The present study indicated that KLK10 potentially plays a crucial role in Eca-109 cell growth. Additionally, the downregulation of KLK10 induced S-phase arrest and promoted cisplatin-induced apoptosis. The resutls of the present study suggested that KLK10 is a promising novel marker for the diagnostic and therapeutic target of esophageal cancer.	esophagus
Visceral obesity stimulates anaphase bridge formation and spindle assembly checkpoint dysregulation in radioresistant oesophageal adenocarcinoma.	PURPOSE: Oesophageal adenocarcinoma is an exemplar model of obesity-associated cancer. Locally advanced disease is treated with neoadjuvant chemoradiotherapy, and survival rates are highest in patients demonstrating a pathological response following neoadjuvant therapy. Given that 55 % of oesophageal adenocarcinoma patients are obese, uncovering the effect of adipose tissue on radioresponse is clinically relevant. This study investigates if adipose tissue activates genomic instability events in radioresponsive (OE33P) and radioresistant (OE33R) oesophageal cancer cell lines and tumour samples. METHODS: OE33R and OE33P were cultured with adipose-conditioned media derived from oesophageal adenocarcinoma patients (n = 10). Anaphase bridges, a marker of genomic instability, were enumerated in both cell lines following treatment with adipose media, and normalised to cell number. Genomic instability is regulated by the spindle assembly complex. Expression of two spindle assembly complex genes (MAD2L2, BUB1B) was assessed using qPCR, and validated in patient tumour specimens from viscerally obese (n = 46) and nonobese patients (n = 41). RESULTS: Adipose-conditioned media increased anaphase bridging in OE33R (p < 0.0001), with a threefold increase in OE33R compared to OE33P (p < 0.01). Levels of anaphase bridges in OE33R cells correlated with visceral obesity status as measured by waist circumference (R = 0.709, p = 0.03) and visceral fat area (R = 0.794, p = 0.006). Adipose tissue altered expression of MAD2L2 in vitro. In vivo, MAD2L2 expression was higher in viscerally obese oesophageal adenocarcinoma patients compared with nonobese patients (p < 0.05). CONCLUSIONS: Anaphase bridge levels are influenced by obesity and radiosensitivity status in oesophageal adenocarcinoma. Furthermore, visceral adipose-conditioned media stimulates dysregulation of the spindle assembly complex in oesophageal adenocarcinoma patients.	esophagus