crossing96/oncoscreening huggingface dataset:
Comparison of definite chemoradiation therapy with carboplatin/paclitaxel or cisplatin/5-fluoruracil in patients with squamous cell carcinoma of the esophagus.	BACKGROUND: While neoadjuvant chemoradiation therapy (nCRT) with subsequent surgery is the treatment of choice for patients with locally advanced or node-positive squamous cell carcinoma of the esophagus (SCC) suitable for surgery, patients who are unsuitable for surgery or who refuse surgery should be treated with definite chemoradiation therapy (dCRT). Purpose of this study was to compare toxicity and oncologic outcome of dCRT with either cisplatin and 5-fluoruracil (CDDP/5FU) or carboplatin and paclitaxel (Carb/TAX) in patients with SCC. METHODS: Twenty-two patients who received dCRT with carboplatin (AUC2, weekly) and paclitaxel (50 mg per square meter of body-surface area, weekly) were retrospectively compared to 25 patients who were scheduled for dCRT with cisplatin (20 mg/m(2)/d) and 5-fluoruracil (500 mg/m(2)/d) on day 1-5 and day 29-33. For the per-protocol (PP) analysis, PP treatment was defined as complete radiation therapy with at least 54Gy and at least three complete cycles of Carb/TAX or complete radiation therapy with at least 54Gy and at least one complete cycle of CDDP/5FU. While patients who were scheduled for dCRT with Carb/TAX received a significantly higher total radiation dose (median dose 59.4Gy vs. 54Gy, p < 0.001) than patients who were scheduled for dCRT with CDDP/5FU, no significant differences were seen for other parameters (age, sex, TNM-stage, grading and tumor extension). RESULTS: Forty-seven patients (25 patients treated with CDDP/5FU and 22 patients treated with Carb/TAX) were evaluated for the intention-to-treat (ITT) analysis and 41 of 47 patients (23 patients treated with CDDP/5FU and 18 patients treated with Carb/TAX) were evaluated for the PP analysis. Severe myelotoxicity (≥ III°) was seen in 52% (CDDP/5FU) and 55% of patients (Carb/TAX), respectively (p = 1.000). In the univariate binary logistic regression analysis, patients age was the only factor associated with an increased risk of ≥ III° myelotoxicity (hazard ratio 1.145, 95% CI 1.035; 1.266; p = 0.009). Regarding treatment efficiency, no significant differences were seen for overall survival (OS) and freedom from relapse (FFR) between both treatment groups. CONCLUSION: Myelotoxicity and oncologic outcome under dCRT were not different for patients with SCC of the esophagus treated with either CDDP/5FU or Carb/TAX. The putative equivalence of dCRT with Carb/TAX in this setting should be further investigated in prospective trials. However, our data reveal that the risk of significant myelotoxicity increases with patient age and therefore other chemotherapy regimens might be evaluated in elderly patients.	esophagus
Pre-treatment CT radiomics to predict 3-year overall survival following chemoradiotherapy of esophageal cancer.	BACKGROUND: Radiomic features retrieved from standard CT-images have shown prognostic power in several tumor sites. In this study, we investigated the prognostic value of pretreatment CT radiomic features to predict overall survival of esophageal cancer patients after chemoradiotherapy. MATERIAL AND METHODS: Two datasets of independent centers were analyzed, consisting of esophageal cancer patients treated with concurrent chemotherapy (Carboplatin/Paclitaxel) and 41.4Gy radiotherapy, followed by surgery if feasible. In total, 1049 radiomic features were calculated from the primary tumor volume. Recursive feature elimination was performed to select the 40 most relevant predictors. Using these 40 features and six clinical variables as input, two random forest (RF) models predicting 3-year overall survival were developed. RESULTS: In total 165 patients from center 1 and 74 patients from center 2 were used. The radiomics-based RF model yielded an area under the curve (AUC) of 0.69 (95%CI 0.61-0.77), with the top-5 most important features for 3-year survival describing tumor heterogeneity after wavelet filtering. In the validation dataset, the RF model yielded an AUC of 0.61 (95%CI 0.47-0.75). Kaplan Meier plots were significantly different between risk groups in the training dataset (p = .027) and borderline significant in the validation dataset (p = .053). The clinical RF model yielded AUCs of 0.63 (95%CI 0.54-0.71) and 0.62 (95%CI 0.49-0.76) in the training and validation dataset, respectively. Risk groups did not reach a significant correlation with pathological response in the primary tumor. CONCLUSIONS: A RF model predicting 3-year overall survival based on pretreatment CT radiomic features was developed and validated in two independent datasets of esophageal cancer patients. The radiomics model had better prognostic power compared to the model using standard clinical variables.	esophagus
Video-Assisted Thoracoscopic Surgery for Esophageal Leiomyoma: A Ten-Year Single-Institution Experience.	OBJECTIVE: This study was a 10-year single-institution experience with surgery for esophageal leiomyomas comparing a minimally invasive approach to thoracotomy. MATERIALS AND METHODS: A retrospective review of patients who underwent resection of esophageal leiomyomas between 2008 and 2017 was conducted. Information on demographic features, symptoms, the operative approach, and complications was recorded. RESULTS: Fifty-six patients were enrolled. Forty patients underwent an open surgical approach, and 16 patients were treated using thoracoscopy. There was no postoperative mortality or esophageal leakage. Five patients required the repair of a mucosal injury during resection. There were no statistically significant differences in operative time, blood loss, chest tube duration, or the length of postoperative stay between the video-assisted thoracoscopic surgery (VATS) group and the thoracotomy group. The mean tumor size in the thoracotomy group was larger than that in the VATS group (3.63 ± 2.15 versus 2.23 ± 1.30, P = .01). CONCLUSIONS: Thoracoscopic enucleation is a safe and effective treatment for esophageal leiomyoma.	esophagus
[Data mining of esophageal squamous cell carcinoma from The Cancer Genome Atlas database].	Objective: To deeply investigate the gene expression profiles of esophageal squamous cell carcinoma (ESCC) and the relationship of gene expression levels with prognosis from The Cancer Genome Atlas (TCGA) database. Methods: RNA-seq V2 data of 11 normal samples and 81 esophageal squamous cell carcinoma patients, and their corresponding clinical data were downloaded from The Cancer Genome Atlas database. Differentially expressed genes between normal and tumor samples were identified by using edgeR package. Gene function enrichment analyses of differentially expressed genes were conducted. A protein-protein interaction network based on differentially expressed genes was constructed by using STRING database and the hub genes were identified based on the created gene co-expression network. In addition, survival analysis was performed. Results: Totally, 2 788 genes were identified as differential expression. Among these, 1 168 genes were up-regulated and 1 620 genes were down-regulated in tumor cases compared with normal samples. Up-regulated genes were enriched in cell cycle, DNA replication and mismatch repair pathways, while down-regulated genes were enriched in metabolic pathways. 707 genes and their 3 428 interactions were identified by protein-protein interaction analysis. Genes with copy number amplifications were considered to interact with other crucial genes. 10 co-expression modules were identified based on the gene co-expression network analysis and the ribosomal protein genes were illustrated to be correlated with tumor locations of ESCC patients (P=0.003). The 3-years survival rates of high and low expression of TNFRSF10B groups were 82.5% and 15.1%, respectively. Similarly, the 3-years survival rates of high and low expression of DDX18 groups were 82.4% and 15.2%, respectively. The survival differences stratified by these two genes were statistically significant (both P<0.1). Conclusions: The analysis results of TCGA database showed that ribosomal protein genes are correlated with tumor locations of ESCC patients. Low expressions of TNFRSF10B and DDX18 are associated with poor prognose of ESCC patients. Consequently, TNFRSF10B and DDX18 may serve as predictive markers for ESCC patients.	esophagus
Immunotherapy for esophageal squamous cell carcinoma: a review.	Cancer vaccines and immune checkpoint inhibitors (ICI) have recently been employed as immunotherapies for esophageal squamous cell carcinoma (ESCC). Cancer vaccines for ESCC have yielded several promising results from investigator-initiated phase I and II clinical trials. Furthermore, a Randomized Controlled Trial as an adjuvant setting after curative surgery is in progress in Japan. On the other hand, ICI, anti-CTLA-4 mAb and anti-PD-1 mAb, have demonstrated tumor shrinkage and improved overall survival in patients with multiple cancer types. For ESCC, several clinical trials using anti-PD-1/anti-PD-L1 mAb are underway with several recent promising results. In this review, cancer vaccines and ICI are discussed as novel therapeutic strategies for ESCC.	esophagus
Activation of histamine H(4) receptor suppresses the proliferation and invasion of esophageal squamous cell carcinoma via both metabolism and non-metabolism signaling pathways.	Although dysregulation of histamine H(4) receptor (H4R) has widely and frequently been documented in digestive carcinomas and correlates with the malignancy and proliferation of these tumors, the existence of H4R and its pathophysiological function in esophageal squamous cell carcinoma (ESCC) remains unknown. In our present study, we explored the expression and function of H4R in human ESCC samples and cell lines. H4R was overexpressed in poorly differentiated ESCC samples and cell lines and correlated with the median survival of ESCC patients. H4R activation not only significantly blocked cell proliferation, cell cycle, and invasion but also inhibited the growth of TE-2 xenografts and increased the survival of xenograft-bearing mice. According to the mechanistic experiments, both metabolism (acetyl-coenzyme A synthetase 2 (ACSS2))- and non-metabolism (mitogen-activated protein kinase (MAPK))-related pathways were involved in the effect of H4R activation on suppressing tumor proliferation and invasion. Based on these findings, H4R was overexpressed in esophageal cancer and exerted antitumor effects on ESCC proliferation and invasion, suggesting that H4R may be a novel potential target of therapies for ESCC. KEY MESSAGES: The function of H4R in ESCC and the underlying mechanisms were investigated. H4R expression was correlated with ESCC cell differentiation and patients' survival. Both metabolism (ACSS2) and non-metabolism (MAPK)-related pathways were involved. This study provided new insight into the relationship between H4R and ESCC. H4R may be a novel potential therapeutic target for ESCC.	esophagus
Endoscopic Treatment of Early-Stage Esophageal Cancer.	PURPOSE OF REVIEW: Esophageal cancer is a leading cause of global cancer-related mortality. Here, we discuss the major endoscopic treatment modalities for management of early esophageal cancer (EEC). RECENT FINDINGS: Advances in endoscopic imaging and therapy have shifted the paradigm of managing early esophageal cancers. Though esophagectomy remains the preferred management for advanced cancers, guidelines now recommend endoscopic resection followed by ablative therapy for early (Tis and T1a) cancers. Available data suggests endoscopic treatment is comparable to surgery with regard to overall and cancer-specific survival with lower procedural morbidity and mortality. Endoscopic modalities are emerging as frontline treatment options for patients with early esophageal cancers. Accurate clinical staging with assessment of disease extent, tumor grade, and risk of nodal metastases is crucial when determining eligibility for endoscopic management of EEC. High-quality routine surveillance endoscopy is critical in patients who have undergone resection and/or ablation.	esophagus
Failure pattern of elective nodal irradiation for esophageal squamous cell cancer treated with neoadjuvant chemoradiotherapy.	OBJECTIVE: To analyze the failure pattern and clinical efficacy of elective nodal irradiation in patients with esophageal squamous cell carcinoma who received neoadjuvant chemoradiotherapy. METHODS: We retrospectively analyzed 173 esophageal squamous cell carcinoma patients who received neoadjuvant chemoradiotherapy including elective nodal irradiation from 2002 to 2015. Failure pattern, survival and recurrence sites were analyzed. For patients with regional recurrences, the recurrence sites were analyzed in relation to an imaginary field of involved field irradiation. RESULTS: After a median follow-up of 55.5 months, 58 patients (33.5%) developed recurrences. Among 22 patients with regional recurrences, infield failure occurred in 19 patients (86.4%) and outfield failure occurred in 3 patients (13.6%), of whom only 1 patient had an outfield failure without synchronous distant metastasis. Compared with the involved field irradiation field, 6 patients' failure sites (27.3%) were located in the involved field irradiation field and 13 patients' failure sites (59.1%) were out of the involved field irradiation field but within the elective nodal irradiation field. CONCLUSIONS: Since only a minority of patients had outfield regional recurrences, neoadjuvant chemoradiotherapy with elective nodal irradiation yields satisfactory infield control. More than half of the regional recurrences occurred within the elective nodal irradiation field but out of the involved field irradiation field. Prospective evaluation of whether elective nodal irradiation could lead to an improved survival outcome is necessary.	esophagus
Low-dose hyperthermia enhances the antitumor effects of chemotherapy in squamous cell carcinoma.	Esophageal squamous cell carcinoma is a highly aggressive neoplasm and the sixth leading cause of global cancer-related death; the 5-year survival rate for esophageal cancer is only about 20%-25% for all stages. Therefore, improving the therapeutic effect is important. This study assessed whether low-dose hyperthermia (LDH) enhances the antitumor effects of chemotherapy. The antitumor effect of chemotherapy with/without LDH in the squamous cell carcinoma cell line SCCVII was evaluated. A comprehensive analysis was performed with real-time polymerase chain reaction (PCR) to study the hyperthermia-induced changes in the gene expression of SCCVII cell lines. In addition, the cytotoxic and apoptotic changes in the cells treated with LDH combined with/without 5-fluorouracil (5-FU) were measured. LDH combined with 5-FU (10 nM) strongly inhibited the cell growth of SCCVII, with flow cytometry showing an increased population of apoptotic cells. PCR showed that LDH promoted a 25.22-fold increase of p53 mRNA and 18.08-fold increase of Bax mRNA in vitro. MDR1 expression was decreased to 28.7% after LDH. This treatment can result in much higher efficacy of antitumor drugs. After LDH, the expressions of TS decreased to 12.06%, OPRT increased by 4.17-fold, and DPD did not change (1.03-fold). This transformations will induce susceptibility to 5-FU. LDH may be a useful enhancer of chemotherapy drugs for squamous cell carcinoma.	esophagus
Exosome-mediated transfer of lncRNA PART1 induces gefitinib resistance in esophageal squamous cell carcinoma via functioning as a competing endogenous RNA.	BACKGROUND: Currently, resistance to tyrosine kinase inhibitors, such as gefitinib, has become a major obstacle in improving the clinical outcome of patients with metastatic and advanced-stage esophageal squamous cell carcinoma (ESCC). While cell behavior can be modulated by long non-coding RNAs (lncRNAs), the roles of lncRNAs within extracellular vesicles (exosomes) are largely unknown. Therefore, we investigated the involvement and regulatory functions of potential lncRNAs enclosed in exosomes during formation of chemoresistance in human ESCC. METHODS: Gefitinib-resistant cell lines were established by continuously grafting TE1 and KYSE-450 cells into gefitinib-containing culture medium. LncRNA microarray assay followed by RT-qPCR were used to verify the differential expression of lncRNA Prostate Androgen-Regulated Transcript 1 (PART1) between gefitinib resistant and parental cell lines. RNA fluorescence in situ hybridization (FISH) was used to investigate whether extracellular PART1 could be incorporated into exosomes and transmitted to recipient cells. Subsequently, a series of in vitro assays and a xenograft tumor model were used to observe the functions of lncRNA PART1 in ESCC cells. A signal transduction reporter array, bioinformatics analysis, western blotting, and immunofluorescence were carried out to verify the regulation of PART1 and its downstream Bcl-2 signaling pathway. RESULTS: lncRNA PART1 was upregulated in gefitinib-resistant cells when compared to parental ESCC cells. It was found that STAT1 can bind to the promoter region of lncRNA PART1, resulting in its activation. Knockdown of lncRNA PART1 potently promoted the gefitinib-induced cell death, while elevated PART1 promoted gefitinib resistance by competitively binding to miR-129 to facilitate Bcl-2 expression in ESCC cells. In addition, extracellular PART1 could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating gefitinib resistance. Clinically, high levels of serum lncRNA PART1 in exosome were associated with poor response to gefitinib treatment in ESCC patients. CONCLUSIONS: LncRNA PART1 promotes gefitinib resistance by regulating miR-129/Bcl-2 pathway, and may serve as a therapeutic target for ESCC patients.	esophagus
Lymph node regression and survival following neoadjuvant chemotherapy in oesophageal adenocarcinoma.	BACKGROUND: The aim was to define the pathological response in lymph nodes following neoadjuvant chemotherapy for oesophageal adenocarcinoma and to quantify any associated survival benefit. METHODS: Lymph nodes retrieved at oesophagectomy were examined retrospectively by two pathologists for evidence of a response to chemotherapy. Patients were classified as lymph node-negative (either negative nodes with no evidence of previous tumour involvement or negative with evidence of complete regression) or positive (allocated a lymph node regression score based on the proportion of fibrosis to residual tumour). Lymph node responders (score 1, complete response; 2, less than 10 per cent remaining tumour; 3, 10-50 per cent remaining tumour) and non-responders (score 4, more than 50 per cent viable tumour; 5, no response) were compared in survival analyses using Kaplan-Meier and Cox regression analysis. RESULTS: Among 377 patients, 256 had neoadjuvant chemotherapy. Overall, 68 of 256 patients (26·6 per cent) had a lymph node response and 115 (44·9 per cent) did not. The remaining 73 patients (28·5 per cent) had negative lymph nodes with no evidence of regression. Some patients had a lymph node response in the absence of a response in the primary tumour (27 of 99, 27 per cent). Lymph node responders had a significant survival benefit (P < 0·001), even when stratified by patients with or without a response in the primary tumour. On multivariable analysis, lymph node responders had decreased overall (hazard ratio 0·53, 95 per cent c.i. 0·36 to 0·78) and disease-specific (HR 0·42, 0·27 to 0·66) mortality, and experienced reduced local and systemic recurrence. CONCLUSION: Lymph node regression is a strong prognostic factor and may be more important than response in the primary tumour.	esophagus
A highly integrated precision nanomedicine strategy to target esophageal squamous cell cancer molecularly and physically.	The prognosis of esophageal squamous cell carcinoma is poor. We hereby presented a highly integrated and clinically relevant precision nanomedicine strategy to target ESCC molecularly and physically for significant improvement of the treatment efficacy. We firstly identified PI3K overexpression in patient samples and its relation to poor patient survival. With our highly versatile tumor-targeted drug delivery platform (DCM), we were able to load a potent but toxic docetaxel (DTX) and a PI3K inhibitor (AZD8186) with favorable physical properties. The combination of the DTX-DCM and AZD8186-DCM showed a highly efficacious and synergistic anti-tumor effect and decreased hematotoxicity. A pro-apoptotic protein, Bax was significantly upregulated in ESCC cells treated with combination therapy compared to that with monotherapy. This study utilized a highly integrated precision nano-medicine strategy that combines the identification of cancer molecular target from human patients, precision drug delivery and effective combination therapy for the development of better ESCC treatment.	esophagus
Gastroesophageal reflux and Barrett's esophagus: a pathway to esophageal adenocarcinoma.	The incidence of esophageal adenocarcinoma (EAC) has increased significantly in Western countries. The rising prevalence of gastroesophageal reflux disease (GERD) and obesity has played a major role in the increasing numbers of EAC. Approximately 10-15% of patients with GERD will develop Barrett's esophagus (BE). This metaplastic transformation is due to the chronic injury produced by repeated reflux episodes and involves genetic mutations that can lead to a malignant transformation. Ultimately, the development of EAC is characterized by the sequence BE metaplasia-dysplasia-invasive carcinoma.	esophagus
[Mechanisms of the suppression of proliferation and invasion ability mediated by microRNA-147b in esophageal squamous cell carcinoma].	Objective: To explore the expression of microRNA(miR)-147b in esophageal squamous cell carcinoma (ESCC) and its regulatory roles in cell proliferation, cell cycle and invasion as well as its molecular mechanisms. Methods: Real-time quantitative PCR (qPCR) was used to investigate the expression of miR-147b in ESCC tissues and cells. Negative control (NC) and miR-147b inhibitor were transfected into ESCC EC1 and EC9706 cells, which were divided into two groups: NC group and miR-147b inhibitor group, and qPCR was employed to detect the miR-147 level and CCK-8. Flow cytometry and Transwell chamber were utilized to investigate the effects of miR-147b downregulation on cell proliferation, cell cycle and invasion in ESCC cells. Besides, target genes of miR-147b was confirmed by double luciferase reporter assay. Subsequently, qPCR and Western blot were used to examine the effects of miR-147b downregulation on NDUFA4 expression, and NDUFA4 expression and its correlation with miR-147b were investigated in ESCC tissues. Results: Relative level of miR-147b in ESCC tissues (3.03±0.27) and cells were markedly higher than that in para-carcinoma tissues (1.00±0.01) and normal esophageal epithelial cell, and the differences had statistical significance (P<0.01), and its high expression was closely associated with clinical staging, invasion depth, histological grading and lymph node metastasis(P<0.05). Importantly, clinical staging, lymph node metastasis and miR-147b may be an independent prognostic factor in ESCC. Moreover, miR-147b downregulation dramatically suppressed cell proliferation, arrested cell cycle in G0/G1 phase and reduced invasion ability in ESCC cells. Most importantly, NDUFA4 was a direct target gene of miR-147b, and miR-147b inhibitor evidently upregulated the expression of NDUFA4. Furthermore, NDUFA4 displayed low expression in ESCC tissues and its expression exhibited negative correlation with miR-147b expression. Conclusions: The downregulation of miR-147b expression significantly suppresses the proliferation and invasion abilities as well as alters cell cycle distribution in ESCC.	esophagus