crossing96/oncoscreening huggingface dataset:
Red and processed meat intake and risk of esophageal adenocarcinoma: a meta-analysis of observational studies.	AIMS: Inconsistent results relating dietary red and processed meat intake and risk of esophageal adenocarcinoma (EAC) have been reported. This article summarizes and quantifies the current evidence in a meta-analysis of observational studies. METHODS: Electronic search of MEDLINE and EMBASE databases was performed to identify peer-reviewed manuscripts up to 31 May 2012. Random-effects models were used to pool study results. RESULTS: Ten manuscripts from 3 cohort studies and 7 case-control studies were identified. The summary relative risks (SRRs) of EAC for highest versus lowest intake categories were 1.31 (95 % confidence intervals [CIs]: 1.05-1.64) for red meat consumption, and 1.41 (95 % CIs 1.09-1.83) for processed meat consumption. Subgroup analyses indicated that these positive relations were seen in case-control studies, but not in cohort studies. Based on dose-response analysis, similar results were found; the SRRs were 1.45(95 % CIs 1.09-1.93) per 100 g/day of red meat intake and 1.37 (95 % CIs 1.03-1.81) per 50 g/day of processed meat intake. CONCLUSIONS: The results of this meta-analysis indicate that consumption of red and processed meat may be associated with increased risk of esophageal adenocarcinoma. More studies, particularly prospective studies, are needed.	esophagus
Mevalonate pathway is a therapeutic target in esophageal squamous cell carcinoma.	Esophageal squamous cell carcinoma (ESCC) is one of the most common lethal tumors in the world. Thus, it is very urgent to develop new therapeutic targets against this disease. The mevalonate (MVA) pathway, paced by its rate-limiting enzyme, hydroxymethylglutaryl coenzyme A reductase, is required for the generation of several fundamental end products including cholesterol and isoprenoids. The function of the MVA pathway in ESCC has not been investigated. In this study, it was found that the MVA pathway was upregulated in ESCC clinical samples. Statin, the inhibitor of the MVA pathway, exerted potent cytotoxicity against human ESCC cells by inhibiting cell growth and proliferation, while it exerted lesser effects on non-tumorigenic SHEE cells. Further study revealed that statin could potently induce cell apoptosis and cell cycle arrest and also dose-dependently inhibit the growth of xenograft tumors in nude mice. With regard to the molecular mechanism, statin treatment was related to decreased extracellular signal-regulated kinase activation and proliferating cell nuclear antigen, cyclin D1 expression, and increased cleavage of poly(ADP-ribose) polymerase. Taken together, our findings suggest that the MVA pathway plays an important role in the progression of ESCC by modulating cell growth and statin might be a potential therapeutic agent in ESCC.	esophagus
[Primary synovial sarcoma of the esophagus].	Synovial sarcomas are uncommon malignant mesenchymal tumors occurring mainly near the joints of the extremities of young adults. Synovial sarcomas are exceedingly rare neoplasms of the digestive tract. We report the first diagnosed case of esophageal synovial sarcoma, highlighting its diagnostic features surgical management and follow-up.	esophagus
STAT3 is involved in esophageal carcinogenesis through regulation of Oct-1.	The transcription factor signal transducer and activator of transcription 3 (STAT3) contributes to cell proliferation, apoptosis and motility in human cancer cells. We aim to elucidate the function of STAT3 in esophageal carcinogenesis process and molecular mechanisms. We showed that hyperactivated STAT3 in esophageal carcinogenesis tissues correlated with the overexpression of octamer transcription factor-1 (Oct-1). High STAT3 phosphorylation correlated with shorter survival compared with low STAT3 phosphorylation. STAT3 and Oct-1 expression levels affected the proliferation and colony formation of Eca-109 esophageal squamous cell carcinoma cells by altering Erk and Akt activation. Nevertheless, STAT3 regulated the migration and invasion of esophageal squamous cell carcinoma cells independent of Oct-1. In conjunction with Oct-1, STAT3 inhibited apoptosis in esophageal squamous cell carcinoma cells. Constitutively activated STAT3 in normal human esophageal epithelium cells (HET-1A) elevated Oct-1 expression,and promoted proliferation and decreased apoptosis. STAT3 activated HET-1A cells to form tumors in vivo, suggesting that overactivated STAT3 is sufficient for carcinogenesis. We further confirmed the colocalization of STAT3 and Oct-1 in the nucleus and found that STAT3 regulates the transcription and expression of Oct-1 by directly targeting its promoter. Activated STAT3 also upregulated many genes associated with Oct-1. Together, our results indicate that STAT3 plays a crucial role in esophageal carcinogenesis by regulating the cell proliferation and apoptosis in conjunction with Oct-1.	esophagus
Intervention effects of nedaplatin and cisplatin on proliferation and apoptosis of human tumour cells in vitro.	OBJECTIVE: To study synergistic effects of nedaplatin and cisplatin on three human carcinoma cell lines (esophageal carcinoma cell line Eca-109, ovarian carcinoma Skov-3 and cervical carcinoma Hela). METHODS: Inhibition effects were evaluated by MTT assay and cell apoptosis was detected by flow cytometry. In addition, changes of Ki-67, Bax and Bcl-2 at mRNA and protein levels were quantified by RT-PCR and Western blotting. RESULTS: Growth inhibition in each cell lines was dose-dependent after exposure to nedaplatin or cisplatin alone. The interaction of the two drugs was synergistic at higher concentrations according to the median-effect principle. The inhibition rates with nedaplatin, cisplatin and combined treatment were 41.9±4.1%, 47.4±2.9%, 52.5±0.9%(Eca-109), 39.0±1.26%, 45.0±1.45% , 56.2±1.44% (Skov-3) and 44.8±2.11%, 46.9±0.99%, 56.6±1.83% (Hela) respectively, with increase in apoptosis. Compared with the nedaplatin or cisplatin alone treatment group, the combinative treatment group's Ki-67 and bcl-2 mRNA (protein) expression was decreased while that of Bax mRNA (protein) was increased. CONCLUSION: Compared to the effects of nedaplatin or cisplatin alone at high concentrations, combination of nedaplatin and cisplatin at low concentrations proved to be much more effective for inhibition of proliferation and the induction of apoptosis in the Eca-109, Skov-3 and Hela cell lines.	esophagus
Esophageal leiomyosarcoma: clinical analysis and surgical treatment of 12 cases.	Leiomyosarcoma of the esophagus is a rare malignant tumor with slow growth and late metastasis. The aim of this study was to reassess the clinical characteristics and treatment modality in one of the largest series of esophageal leiomyosarcomas from a single institution. From February 1973 to December 2011, 12 cases of esophageal leiomyosarcoma were identified. The principal symptoms included progressive dysphagia in 11 cases (91.7%), retrosternal/back pain in four (33.3%), weight loss in four (33.3%), upper gastrointestinal hemorrhage in two (16.7%), and emesis in two (16.7%). The average duration of symptoms was 10.6 months. The location of the primary tumor was in the middle thoracic esophagus in five cases, and lower thoracic esophagus in seven cases. Six cases were classified as the polypoid type, five cases as the infiltrative type, and only one case as the intramural type. All 12 of the patients underwent esophagectomies, and radical resections were achieved in these patients. Based on the Kaplan-Meier Method, the 3-, 5-, and 10-year survival rates were 80.0%, 58.3%, and 31.1%, respectively, with a median survival of 63 months. Five-year survival rates for patients with polypoid or intramural tumors (n = 7) was 83.3%, and for patients with infiltrative tumor (n = 5) it was 25.0%. One of the patients had tumor resected four times and survived for 161 months. In conclusion, patients presenting with esophageal leiomyosarcomas have an excellent prognosis, and radical resection may achieve acceptable results.	esophagus
Effect of estrogen on growth and apoptosis in esophageal adenocarcinoma cells.	The epidemiology of esophageal adenocarcinoma demonstrates a strong gender bias with a sex ratio of 8-9:1 in favor of males. A potential explanation for this is that estrogen might protect against esophageal adenocarcinoma. Estrogen has previously been shown to stimulate apoptosis in esophageal squamous cancer cells. However, the effect of estrogen on esophageal adenocarcinoma cells has not been determined. We used immunoblotting analysis to determine the expression of estrogen receptors, cell adhesion marker E-cadherin, and proliferation marker Ki-67 in cell lines derived from esophageal adenocarcinoma (OE-19, OE-33) and Barrett's esophagus (QhTRT, ChTRT, GihTRT). Estrogen and selective estrogen receptor modulator (SERM)-dependent effects on cell growth were determined by the CellTiter-96 Aqueous Proliferation Assay. Apoptosis was determined by Annexin V/Propidium Iodide cell labeling and flow cytometry. We detected that physiological and supra-physiological concentrations of 17β-estradiol and SERM decreased cell growth in esophageal adenocarcinoma cells. In Barrett's esophagus cells (QhTRT, ChTRT), decreased growth was also detected in response to estrogen/SERM. The level of estrogen receptor expression in the cell lines correlated with the level of anti-growth effects induced by the receptor agonists. Flow cytometry analysis confirmed estrogen/SERM stimulated apoptosis in esophageal adenocarcinoma cells. Estrogen/SERM treatments were associated with a decrease in the expression of Ki-67 and an increase in E-cadherin expression in esophageal adenocarcinoma cells. This study suggests that esophageal adenocarcinoma and Barrett's esophagus cells respond to treatment with selective estrogen receptor ligands, resulting in decreased cell growth and apoptosis. Further research to explore potential therapeutic applications is warranted.	esophagus
DNA Nanostructure-based Interfacial engineering for PCR-free ultrasensitive electrochemical analysis of microRNA.	MicroRNAs (miRNAs) have been identified as promising cancer biomarkers due to their stable presence in serum. As an alternative to PCR-based homogenous assays, surface-based electrochemical biosensors offer great opportunities for low-cost, point-of-care tests (POCTs) of disease-associated miRNAs. Nevertheless, the sensitivity of miRNA sensors is often limited by mass transport and crowding effects at the water-electrode interface. To address such challenges, we herein report a DNA nanostructure-based interfacial engineering approach to enhance binding recognition at the gold electrode surface and drastically improve the detection sensitivity. By employing this novel strategy, we can directly detect as few as attomolar (<1, 000 copies) miRNAs with high single-base discrimination ability. Given that this ultrasensitive electrochemical miRNA sensor (EMRS) is highly reproducible and essentially free of prior target labeling and PCR amplification, we also demonstrate its application by analyzing miRNA expression levels in clinical samples from esophageal squamous cell carcinoma (ESCC) patients.	esophagus
Transferrin conjugation does not increase the efficiency of liposomal Foscan during in vitro photodynamic therapy of oesophageal cancer.	Photodynamic therapy (PDT) is based on the delivery of photocytotoxic agents to a target tissue, followed by irradiation. In order to increase the efficiency of PDT in oesophageal cancer therapy, polyethylene glycol (PEG)-grafted, transferrin (Tf)-conjugated liposome formulations of 5,10,15,20-tetra(m-hydroxyphenyl)chlorin (Foscan), a second-generation photosensitiser, were prepared. Expression of transferrin receptors (CD71) in the oesophageal cancer cell line, OE21, was confirmed by immunoblot and confocal laser scanning microscopy. The anti-proliferative effect of Foscan liposomes was evaluated and compared with plain formulations (i.e., without Tf) as well as with free drug. In addition, the intracellular accumulation was studied using high content analysis. Surprisingly, delivering Foscan by transferrin-conjugated PEG-liposomes to oesophageal cancer cells did not improve the photocytotoxicity or the intracellular accumulation of Foscan when compared to unmodified liposomes or indeed free photosensitiser. Tf-targeted drugs and drug delivery systems have shown improved the therapy of many cancers. Our study, however, did not corroborate these findings. If this is due to the tumour type, the choice of in vitro model or the delivery systems remains to be confirmed.	esophagus
Identifying patients with undetected gastro-oesophageal cancer in primary care: External validation of QCancer® (Gastro-Oesophageal).	OBJECTIVE: To evaluate the performance of QCancer® (Gastro-Oesophageal) for predicting the risk of undiagnosed gastro-oesophageal cancer in an independent UK cohort of patients from general practice records. DESIGN: Open cohort study to validate QCancer® (Gastro-Oesophageal) prediction model. Three hundred sixty-five practices from the United Kingdom contributing to The Health Improvement Network database. 2.1 million patients registered with a general practice surgery between 01 January 2000 and 30 June 2008, aged 30-84years (3.7 million person years) with 1766 gastro-oesophageal cancer cases. The outcome, gastro-oesophageal cancer was defined as incident diagnosis of gastro-oesophageal cancer during the 2years after study entry. RESULTS: The results from this independent and external validation of QCancer® (Gastro-Oesophageal) demonstrated good performance data on a large cohort of general practice patients. QCancer® (Gastro-Oesophageal) had very good discrimination with c-statistics of 0.93 and 0.94 for women and men respectively. QCancer® (Gastro-Oesophageal) was well calibrated across all tenths of risk and over all age ranges with predicted risks closely matching observed risks. QCancer® (Gastro-Oesophageal) explained 74.4% and 75.6% of the variation in men and women respectively. CONCLUSIONS: QCancer® (Gastro-Oesophageal) is a useful tool to identify undiagnosed gastro-oesophageal cancer in primary care in the United Kingdom.	esophagus
[Effect of HMGB1 on the VEGF-C expression and proliferation of esophageal squamous cancer cells].	OBJECTIVE: To explore the effect of HMGB1 on the VEGF-C expression and proliferation of esophageal squamous cancer cells as well as its possible mechanism. METHODS: A cassette encoding siRNA targeting HMGB1 mediated by rAAV was constructed, the rAAV-siHMGB1-hrGFP, and a vector encoding siRNA mismatching HMGB1 was constructed, the rAAV-miHMGB1-hrGFP. This experiment in vitro included three groups, namely, the blank control group (group A) of KYSE150 cells transfected by rAAV-hrGFP, negative mismatch control group (group B) of KYSE150 cells transfected with rAAV-miHMGB1-hrGFP, and RNA interference group (group C) of KYSE150 cells transfected with rAAV-siHMGB1-hrGFP. We examined the expression of HMGB1 mRNA and protein in the three group cells by real-time PCR and Western blot after 24 h and 48 h, respectively. Then, VEGF-C expression and cell proliferation in the three group cells with or without sRAGE, as an inhibitor of RAGE signal pathway, were assayed by ELISA and MTT after 24 h. RESULTS: The expression of HMGB1 mRNA and protein in KYSE150 cells in vitro in the group C transfected with rAAV-siHMGB1-hrGFP at the final concentration of 2×10(6) v.g/cell was significantly lower than that of the group A or B after 24 h and 48 h (P < 0.01). The VEGF-C expression of KYSE150 cells was (502.43 ± 13.10) pg/ml in the group C, significantly reduced in comparison with that of the group A (686.40 ± 10.94) pg/ml or group B (682.31 ± 9.61) pg/ml after 24 h (P < 0.05). At the same time, the proliferation of KYSE150 cells in the group C was significantly inhibited compared with that of groups A and B after 24 h (P < 0.01). Moreover, sRAGE at the final concentration of 0.2 µg/ml inhibited the VEGF-C expression and proliferation of KYSE150 cells compared with the corresponding group without sRAGE after 24 h (P < 0.01 or P < 0.05). However, there was no significant difference of the VEGF-C expression and proliferation of KYSE150 cells with sRAGE in the group C compared with that of cells with sRAGE of the group A or group B after 24 h (P > 0.05). CONCLUSIONS: In esophageal squamous cell carcinoma, HMGB1 can promote the VEGF-C expression and proliferation of the cancer cells through RAGE signal pathway, and HMGB1-RAGE may become a potential target for cell proliferation and lymph node metastasis of this cancer.	esophagus
An Asian population-based survival analysis of patients with distal esophageal and gastric cardia adenocarcinomas.	BACKGROUND: Gastroesophageal junction adenocarcinomas include adenocarcinomas of the distal esophagus (DE) and gastric cardia (GC). It is controversial whether these tumors are the same entity and whether they have the same survival rates. Patients with DE and GC adenocarcinomas have a similar survival rate in the US; however, data are lacking in Asian countries. Therefore, we conducted a retrospective study to understand the implications of the tumor location in the survival of Asian patients. METHODS: A total of 209 patients with pathologically confirmed DE and GC adenocarcinomas, from 2005 to 2007, were included in the study. We identified patients with adenocarcinomas of the DE (DE group, n = 91) and GC (GC group) (n = 118). We performed an unadjusted survival analysis using the Kaplan-Meier method, and used a Cox proportional hazards regression model to adjust for potential confounding covariates. RESULTS: We found no significant difference between the overall survival of the DE and GC groups. The 3-year survival rates were 44.8% and 53.0%, respectively, and the 5-year survival rates were 27.9% and 30.2%, respectively (P = 0.162). We found no significant difference in early staging, advanced staging, different T staging, and different N staging, between the groups. Both advanced post-operative N staging and advanced AJCC staging had a significant adverse effect on survival. CONCLUSIONS: Patients with DE and GC adenocarcinomas have similar survival rates in the Asian population. Both post-operative N staging and AJCC staging are prognostic factors.	esophagus
Laparoscopic Nissen fundoplication post-oesophageal stenting: an unusual case.	Laparoscopic Nissen fundoplication post-oesophageal stenting is uncommon and yet to be reported. We report the case of a 57-year-old palliative lady who underwent surgery for symptomatic relief of severe gastrooesophageal reflux post-oesophageal stenting. Surgery was carried out successfully with no complications. On the evening post-surgery she was able to lie supine for the first time in months without symptoms of reflux. In conclusion, surgery is still valuable and may play an important role, even in a palliative setting.	esophagus
Impact of postoperative morbidity on long-term survival after oesophagectomy.	BACKGROUND: Oesophageal malignancy is a disease with a poor prognosis. Oesophagectomy is the mainstay of curative treatment but associated with substantial morbidity and mortality. Although mortality rates have improved, the incidence of perioperative morbidity remains high. This study assessed the impact of postoperative morbidity on long-term outcomes. METHODS: A prospective database was designed for patients undergoing oesophagectomy for malignancy from 1998 to 2011. An observational cohort study was performed with these data, assessing intraoperative technical complications, postoperative morbidity and effects on overall survival. RESULTS: Some 618 patients were included, with a median follow-up of 51 months for survivors. The overall complication rate was 64·6 per cent (399 of 618), with technical complications in 124 patients (20·1 per cent) and medical complications in 339 (54·9 per cent). Technical complications were associated with longer duration of surgery (308 min versus 293 min in those with no technical complications; P = 0·017), greater operative blood loss (448 versus 389 ml respectively; P = 0·035) and longer length of stay (22 versus 13 days; P < 0·001). Medical complications were associated with greater intraoperative blood loss (418 ml versus 380 ml in those with no medical complications; P = 0·013) and greater length of stay (16 versus 12 days respectively; P < 0·001). Median overall and disease-free survival were 41 and 43 months. After controlling for age, tumour stage, resection margin, length of tumour, adjuvant therapy, procedure type and co-morbidities, there was no effect of postoperative complications on disease-specific survival. CONCLUSION: Technical and medical complications following oesophagectomy were associated with greater intraoperative blood loss and a longer duration of inpatient stay, but did not predict disease-specific survival.	esophagus
PITX2: a promising predictive biomarker of patients' prognosis and chemoradioresistance in esophageal squamous cell carcinoma.	The paired-like homeodomain transcription factor 2 (PITX2), a downstream effector of wnt/β-catenin signaling, is well known to play critical role during normal embryonic development. However, the possible involvement of PITX2 in human tumorigenesis remains unclear. In this study, we extend its function in human esophageal squamous cell carcinoma (ESCC). The real-time PCR, Western blotting and immunohistochemistry (IHC) methods were applied to examine expression pattern of PITX2 in two different cohorts of ESCC cases treated with definitive chemoradiotherapy (CRT). Receiver operating characteristic (ROC) curve analysis was used to determine the cutoff point for PITX2 high expression in the training cohort. The ROC-derived cutoff point was then subjected to analyze the association of PITX2 expression with patients' survival and clinical characteristics in training and validation cohort, respectively. The expression level of PITX2 was significantly higher in ESCCs than that in normal esophageal mucosa. There was a positive correlation between PITX2 expression and clinical aggressiveness of ESCC. Importantly, high expression of PITX2 was observed more frequently in CRT resistant group than that in CRT effective group (p < 0.05). Furthermore, high expression of PITX2 was associated with poor disease-specific survival (p < 0.05) in ESCC. Then, the MTS, clonogenic survival fraction and cell apoptosis experiments showed that knockdown of PITX2 substantially increased ESCC cells sensitivity to ionizing radiation (IR) or cisplatin in vitro. Thus, the expression of PITX2, as detected by IHC, may be a useful tool for predicting CRT resistance and serves as an independent molecular marker for poor prognosis of ESCC patients treated with definite CRT.	esophagus
[A case of esophageal endocrine cell carcinoma with multiple liver metastases that had a complete response to multidisciplinary therapy].	A 71-year-old man was admitted to our hospital because of dysphagia, and primary endocrine cell carcinoma of the esophagus with multiple liver metastases was diagnosed. After 6 courses of CPT-11+CDDP combination chemotherapy, the liver metastases disappeared, although the esophageal squamous cell carcinoma component remained. Radiation therapy was added to treat the residual esophageal tumor, and a complete response was obtained. This case seems to suggest that multidisciplinary therapy, including chemotherapy, may be effective for treating esophageal endocrine cell carcinoma with other types of organ metastasis.	esophagus