crossing96/oncoscreening huggingface dataset:
Expression, tissue distribution and function of miR-21 in esophageal squamous cell carcinoma.	"OBJECTIVE: MiR-21 is an oncomir expressed by malignant cells and/or tumor microenvironment components. In this study we focused on understanding the effects of stromal miR-21 on esophageal malignant cells. DESIGN: MiR-21 expression was evaluated in formalin-fixed paraffin-embedded samples from patients with esophageal squamous-cell carcinoma (SCC) by quantitative RT-PCR. MiR-21 tissue distribution was visualized with in situ hybridization. A co-culture system of normal fibroblasts and esophageal cancer cells was used to determine the effects of fibroblasts on miR-21 expression levels, and on SCC cell migration and invasion. RESULTS: MiR-21 was overexpressed in SCCs, when compared to the adjacent non-tumor tissues (P = 0.0007), and was mainly localized in the cytoplasm of stromal cells adjacent to malignant cells. Accordingly, miR-21 expression was increased in tumors with high versus low stromal content (P = 0.04). When co-cultured with normal fibroblasts, miR-21 expression was elevated in SCC cells (KYSE-30), while its expression was restricted to fibroblasts when co-cultured with adenocarcinoma cells (OE-33 and FLO-1). MiR-21 was detected in conditioned media of cancer cell lines, illustrating the release of this miRNA into the environment. Co-culturing with normal fibroblasts or addition of fibroblast conditioned media caused a significant increase in cell migration and invasion potency of KYSE-30 cells (P<0.0001). In addition, co-culturing cancer cells with fibroblasts and expression of miR-21 induced the expression of the cancer associated fibroblast (CAF) marker S100A4. CONCLUSIONS: MiR-21 expression is mostly confined to the SCC stroma and its release from fibroblasts influences the migration and invasion capacity of SCC cells. Moreover, miR-21 may be an important factor in ""activating"" fibroblasts to CAFs. These findings provide new insights into the role of CAFs and the extracellular matrix in tumor microenvironment formation and in tumor cell maintenance, and suggest miR-21 may contribute to cellular crosstalk in the tumor microenvironment."	esophagus
Stomal recurrence: salvage surgery and reconstruction utilizing microvascular free tissue transfer.	BACKGROUND: Stomal recurrence in patients after laryngectomy has a poor prognosis. Studies performed using sternal resection with pectoralis flap reconstruction report <25% 2-year survival. The purpose of this study was to ascertain whether the use of larger resection with free flap reconstruction improves survival. METHODS: Thirteen cases of stomal recurrence that underwent extended sternal resection and free flap reconstruction were identified and classified according to Sisson criteria. Postoperative morbidity, mortality, and survival were assessed. RESULTS: Median survival was 10 months in patients with Sisson types I and II, with 37.5% 1-year and 25% 2-year survival. Median survival was 6 months in patients with Sisson types III and IV, with 40% 1-year and 0% 2-year survival. There were 2 perioperative deaths and a major morbidity rate of 45%. CONCLUSION: Salvage surgery using free flap reconstruction did not show improved survival rates compared with previously described techniques.	esophagus
Esophageal-subarachnoid fistula: a case of spontaneous tension pneumocephalus in the setting of esophageal cancer.	BACKGROUND: Pneumocephalus occurs as a result of traumatic or iatrogenic violation of the dura. Tension pneumocephalus, whereby air continues to accumulate with no mechanism for escape, can cause significant morbidity and mortality. METHODS: This case report reviews the underlying pathophysiology, clinical presentation, diagnosis, and management of tension pneumocephalus. RESULTS: We present the case of a 68-year-old man who presented to the Emergency Department with headache thought to be the result of a newfound intracranial mass. After admission, he became obtunded and was found to have tension pneumocephalus requiring emergent evacuation. A cervical esophagus carcinoma caused an esophageal-subarachnoid fistula that resulted in tension pneumocephalus after a retching episode. CONCLUSION: This case illustrates the importance of considering alternative sources of pneumocephalus in the absence of more typical differential diagnosis.	esophagus
Relevance of [18F]fluorodeoxyglucose positron emission tomography-positive lymph nodes after neoadjuvant chemotherapy for squamous cell oesophageal cancer.	BACKGROUND: Several studies have examined the clinical significance of metabolic response in primary tumours by [(18) F]fluorodeoxyglucose positron emission tomography ((18) F-FDG-PET) in patients with oesophageal cancer who undergo neoadjuvant therapy. The relevance of the metabolic response in lymph nodes is unclear. METHODS: Consecutive patients with oesophageal cancer who underwent neoadjuvant chemotherapy followed by surgery were studied. (18) F-FDG-PET was performed before and 2-3 weeks after completion of neoadjuvant chemotherapy, assessing FDG uptake in primary tumours and lymph nodes considered to be metastatic. RESULTS: Before therapy, 156 (73·9 per cent) of 211 patients had PET-positive nodes, of whom 89 (57.1 per cent) had no evidence of metabolic activity in these lymph nodes following chemotherapy. There was a significant relationship between post-treatment lymph node status assessed by FDG-PET and numbers of pathologically confirmed metastatic lymph nodes. Patients with post-treatment PET-positive nodes had shorter survival than those without (5-year survival rate 25 versus 62·6 per cent; P < 0·001). There was no difference in survival between patients with PET-positive nodes before but not after therapy and patients who had PET-negative nodes throughout (5-year survival rate 59 versus 71 per cent respectively; P = 0·207). Multivariable analysis identified post-treatment nodal status assessed by FDG-PET and tumour depth as independent prognostic factors. CONCLUSION: Identification of PET-positive lymph nodes after completion of chemotherapy is a predictor of poor prognosis of patients with oesophageal cancer scheduled for surgery. FDG-PET lymph node status after neoadjuvant chemotherapy is more important than that before chemotherapy.	esophagus
Preoperative level of serum amyloid A is superior to C-reactive protein in the prognosis of esophageal squamous cell carcinoma.	Preoperative elevations in the levels of serum amyloid A (SAA) or C-reactive protein (CRP) have been reported to be prognostic indicators in several malignancies. The aim of this study is to evaluate the serum levels of SAA and CRP in the prognosis of esophageal squamous cell carcinoma (ESCC). In total, 252 patients with ESCC who had undergone surgery with curative-intent were retrospectively recruited. The specificity, sensitivity, and prognostic value of SAA or CRP levels were measured as the area under the receiver operating characteristic (ROC) curve (AUC). The clinical value of SAA and CRP levels as prognostic indicators was evaluated using Cox's proportional hazards model. The 1-, 3-, and 5-year overall survival (OS) rates for the entire cohort of patients with ESCC were 71.0%, 61.0%, and 43.0%, respectively. The correlation between the levels of SAA and CRP was significant (r(2) = 0. 685, P < 0.001). The ROC analysis showed that the levels of CRP were associated with a significantly lower overall accuracy than were the SAA levels (AUC, 0.615 vs. 0.880; P < 0.001). For the complete cohort, the median OS was 52.0 months longer in patients with low preoperative serum levels of SAA (72.0 months) compared with patients who had high SAA levels (20.0 months, P < 0.001). The median OS among patients with low CRP levels was also longer compared with the patients who had high CRP levels (72.0 vs. 51.0 months, respectively; P < 0.001). Subgroup analyses showed that the preoperative elevated levels of SAA could find significant differences in OS for stage I, stage II, and stage III (P < 0.001, P = 0.001, and P < 0.001, respectively), whereas the increased levels of CRP could only find a difference in OS for stage II cancers. After a multivariate analysis, preoperative elevated level of SAA was found to be an independently and significant prognostic factor (P < 0.001). Our study indicates that the preoperative levels of SAA and CRP can act as prognostic factors, and that elevated levels of these proteins are associated with negative effects on the survival of patients with ESCC. SAA showed a higher prognostic value than CRP in both cohort and subgroup analysis.	esophagus
Anticancer effects of suberoylanilide hydroxamic acid in esophageal squamous cancer cells in vitro and in vivo.	The effects of suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, have not been studied in esophageal squamous cell cancer (ESCC). Cell viability assay; flow cytometry for cell cycle and annexin V apoptosis assays; assays for cell migration, invasion, and adhesion to extracellular matrix (ECM); and immunoblotting and immunofluorescence staining were performed in three ESCC cell lines. Tumor xenograft with semiquantitative immunohistochemistry was used to study the effects of SAHA in vivo. SAHA effectively inhibited growth of ESCC cells with half-inhibitory concentrations (IC50 ) ranging from 2.6 to 6.5 μmol/L. SAHA restored acetylation of histone 3 lysine 9 (H3K9Ac) and histone 4 lysine 12 (H4K12Ac) with an induction of G1 or G2 cell cycle arrest and apoptosis. Expression of cell cycle checkpoint regulatory proteins including cyclin-dependent kinases (CDKs) and cyclins was decreased, whereas expression of cell cycle suppressors, p21, p27, and Rb was increased in ESCC cells after SAHA treatment. SAHA inhibited migration, invasion, and ECM adhesion in ESCC cells with an induction of E-cadherin expression. SAHA significantly inhibited growth of ESCC tumors with increased expression of p21, p27, Rb, and E-cadherin while decreasing expression of CDK4 and cyclin D1 within the murine tumors. In conclusion, SAHA had antigrowth activity against ESCC cells in vitro and in vivo while inhibiting cell migration, cell invasion, and ECM adhesion, suggesting its potential as an epigenetic therapeutic agent for ESCC.	esophagus
Clinical tools do not predict pathological complete response in patients with esophageal squamous cell cancer treated with definitive chemoradiotherapy.	Chemoradiotherapy for locally advanced esophageal squamous cell carcinoma is associated with high rates of pathological complete response. A pathological complete response is recognized to be an important predictor of improved survival, to the extent that observation rather than surgery is advocated by some in patients with presumed pathological complete response based on their clinical response. The goal of this study was to look at the ability of clinical variables to predict pathological complete response after chemoradiotherapy for locally advanced esophageal squamous cell carcinoma. We reviewed retrospectively patients with locally advanced esophageal squamous cell carcinoma who underwent chemoradiotherapy followed by surgery and compared those with pathological complete response to patients with residual disease. Between January 1996 and December 2010, 116 patients met inclusion criteria. Fifty-six percent of patients had a pathological complete response and a median survival of 128.1 months versus 28.4 months in patients with residual disease. When compared with patients with residual disease, patients with a pathological complete response had a lower post-neoadjuvant positron emission tomography (PET) maximum standardized uptake value (SUVmax), a larger decrease in PET SUVmax, a less thick tumor on post-chemoradiotherapy computed tomography and a higher rate of normal appearing post-chemoradiotherapy endoscopy with benign biopsy of the tumor bed. However, none of these characteristics alone was able to correctly identify patients with a pathological complete response, and none has significant specificity. Although the rate of pathological complete response after chemoradiotherapy is high in patients with esophageal squamous cell carcinoma, the ability of identifying patients with pathological complete response is limited. A reduction of the PET SUVmax by >70%, a normal appearing endoscopic examination, and no residual disease on biopsy all were seen in >65% of the patients with a pathological complete response. Even if these findings were unable to confirm the absence of residual disease in the primary tumor, they can help guide expectant management in high-risk patients.	esophagus
Blockage of Nrf2 suppresses the migration and invasion of esophageal squamous cell carcinoma cells in hypoxic microenvironment.	Nuclear factor erythroid-2-related factor 2 (Nrf2) is a critical cell protector by inducing phase two detoxifying and anti-oxidant enzymes in normal cells. But recently, numerous evidence show Nrf2 may play the same beneficial roles toward the cancer cells. Nrf2 is found upexpressed in lots of cancers and promote the proliferation and drug resistance. But studies about the role of Nrf2 in the metastases are few. It has been testified that the tumor cells are under hypoxic conditions. As an important anti-oxidant element, the expression of Nrf2 may be upregulated, which in turn promotes the tumor invasion and metastases in the hypoxic microenvironment. Our team found the expression of Nrf2 correlated with the lymph node metastasis of esophageal squamous cell carcinoma by pathological sections of esophageal carcinoma patients. Further, the mechanism beneath it was studied in this paper. It was hypothesized that the hypoxia microenvironment transformed Nrf2 a friend to a foe. First, Eca-109 cells were treated with different concentration of CoCl2 . Western blot and quantitative reverse transcription-polymerase chain reaction showed that with the increase of the concentration of CoCl2 , the expression levels of Nrf2 and hypoxia-inducible factor-1 (HIF-1) alpha were upregulated simultaneously. By analyzing the data, a significant correlation between Nrf2 and HIF-1 alpha in the protein levels was found. Further, blockage of Nrf2 mediated by shRNA suppressed the expression of HIF-1 alpha, hemeoxygenase-1 (HO-1), and matrix metalloproteinase 2 but enhanced the expression of E-cadherin. In addition, the results of wound healing and invasion assay-verified blockage of Nrf2 suppressed the migration and invasion. So it was suggested that blockage of Nrf2 repressed the migration and invasion of esophageal squamous cell carcinoma cells in the hypoxic microenvironment. HIF-1 alpha might be one of the downstream genes of Nrf2 regulated through Nrf2/HO-1 axis in the CoCl2 model. Nrf2 inhibition suppressed matrix metalloproteinase 2 and enhanced E-cadherin partly through HIF-1 alpha way.	esophagus
The effect of IGF-I receptor blockade for human esophageal squamous cell carcinoma and adenocarcinoma.	Insulin-like growth factor-I receptor (IGF-IR) signaling is required for carcinogenicity and tumor development, and this pathway has not been well studied in human esophageal carcinomas. Esophageal cancer is one of the human cancers with the worst prognosis and has two main histologies: squamous cell carcinomas (ESCC) and adenocarcinoma (EAC). Previously, we have reported that detection of the IGF axis may be useful for the prediction of recurrence and poor prognosis of ESCC. We have also shown the successful therapy for several gastrointestinal cancers using recombinant adenoviruses expressing dominant negative IGF-IR (ad-IGF-IR/dn). The aim of this study is to develop potential targeted therapeutics to IGF-IR and to assess the effect of IGF-IR blockade in both of these types of esophageal cancer. We determined immunohistochemical expression of IGF-IR in a tissue microarray. We then assessed the effect of IGF-IR blockade on signal transduction, proliferation, apoptosis, and motility. Ad-IGF-IR/dn, a tyrosine kinase inhibitor, BMS-536924, and adenovirus expressing shRNA for IGF-IR were used. IGF-IR expression was common in both tumor types but not in normal tissues. IGF-IR was detected in metastatic sites at similar levels compared to the primary site. IGF-IR inhibition suppressed proliferation and colony formation in both cancers. IGF-IR blockades up-regulated both stress- and chemotherapy-induced apoptosis and reduced migration. Although IGF-IR/dn blocked ligand-induced activation of Akt-1 mainly, BMS-536924 effectively blocked both activation of Akt and MAPK. The IGF axis might play a key role in tumor progression of esophageal carcinomas. The IGF-IR targeting strategies might thus be useful anticancer therapeutics for human esophageal malignancies.	esophagus
p53 immunohistochemical expression and patient prognosis in esophageal squamous cell carcinoma.	It is generally accepted that overexpression of p53 protein is associated with poor prognosis in gastric, lung, and other types of cancer. However, the prognostic significance of p53 aberrations in esophageal cancer remains unclear. This is the largest study (n = 266) examining clinical and prognostic features of p53 immunohistochemical expression in esophageal squamous cell carcinoma. In 139 (52%) esophageal tumors, nuclear immunoreactivity for p53 protein was detected. p53 aberrant expression was not associated with sex, age, preoperative treatment, TNM stage, or histological grade. Furthermore, p53 expression did not correlate with disease-free survival (P = 0.73) or overall survival (P = 0.62). In addition, no significant modification effect by any of the covariates in the survival analysis was observed (all P > 0.15). In conclusion, our large-scale study demonstrates that p53 expression has no impact on the prognosis of esophageal squamous cell carcinoma.	esophagus
Differential expression of miR-195 in esophageal squamous cell carcinoma and miR-195 expression inhibits tumor cell proliferation and invasion by targeting of Cdc42.	MicroRNAs (miRNA) have played an important role in carcinogenesis. In this study, Agilent miRNA microarray was used to identify differentially expressed miRNAs in esophageal squamous cell carcinoma (ESCC) tissues and miR-195 was downregulated in ESCC compared with normal esophageal tissues. Moreover, Cdc42 was confirmed as target gene of miR-195. Ectopic expression of miR-195 in ESCC cells significantly downregulated Cdc42 by directly binding its 3' untranslated regions, and induced G1 cell cycle arrest, leading to a significant decrease in cell growth, migration, and invasion in vitro. Therefore, our findings demonstrated that miR-195 may act as a tumor suppressor in ESCC by targeting Cdc42.	esophagus
Notch-1-mediated esophageal carcinoma EC-9706 cell invasion and metastasis by inducing epithelial-mesenchymal transition through Snail.	Notch has recently been shown to promote epithelial-to-mesenchymal transition (EMT) by involving in the EMT process that occurs during tumor progression and converts polarized epithelial cells into motile, invasive cells. However, it is still unclear whether the Notch signaling pathway is associated with the regulation of EMT in esophageal carcinoma. The present study explored Notch-1-mediated esophageal carcinoma EC-9706 cell invasion and metastasis by inducing epithelial–mesenchymal transition through Snail. The results demonstrated that the inhibition of Notch-1 expression in the esophageal carcinoma cell line EC-9706 could suppress the occurrence of EMT and at the same time could decrease the invasion and metastasis ability of the EC-9706 cells, indicative of its role in EMT. Snail is a transcriptional repressor of E-cadherin. We found that with the inhibition of Notch-1 expression in the esophageal carcinoma cell line EC-9706, the expression of Snail also decreased. Mechanistic studies showed that the up-expression of Snail in the EC-9706 cells restored the suppression of EMT regulated by Notch-1 inhibition, suggesting the role of Snail in Notch-1-mediated EMT. At the same time, the up-expression of Snail in the EC-9706 cells could also rescue the invasion and metastasis ability inhibited by Notch-1 siRNA. Taken together, our results had revealed that Notch-1 could participate in the invasion and metastasis of esophageal carcinoma through EMT via Snail. This study indicated that Notch-1 might be a useful target for esophageal carcinoma prevention and therapy.	esophagus
[Clinical target volume delineation for radiotherapy of the esophagus].	The dense lymphatic network of the esophagus facilitates tumour spreading along the cephalo-caudal axis and to locoregional lymph nodes. A better understanding of microscopic invasion by tumour cells, based on histological analysis of surgical specimens and analysis of recurrence sites, has justified a reduction in radiotherapy target volumes. The delineation of the clinical target volume (CTV) depends on tumour characteristics (site, histology) and on its spread as assessed on endoscopic ultrasonography and ((18)F)-fluorodeoxyglucose positron-emission tomography (FDG-PET). We propose that positive and negative predictive values for FDG-PET should be used to adapt the CTV according to the risk of nodal involvement.	esophagus
Multiple cutaneous nodules presenting as metastatic squamous cell carcinoma of the esophagus.	A 62-year-old man with weight loss and dysphagia developed 3 cutaneous nodules. Fine needle aspirate of one of the nodules identified squamous cell carcinoma, which was found to be a metastasis from esophageal cancer.	esophagus
Aortoesophageal fistula--rare complication after esophagogastrectomy, due to cancer.	The paper contains a description of the case--63 year old patient with surgery due locally advanced cancer of the gastric cardia. In 28 postoperative day symptoms of GI bleeding occurred. Despite the endoscopic attempts undertaken to stop bleeding, the patient died in the course of hemorrhagic shock. Posed by the post-mortem consider: aorto-esophageal fistula, is a rare complication in surgery of the esophagus. The rapidly increasing symptoms and deterioration of the patient, in most cases, despite the measures taken, ending in death of the patient. In the literature, there are few reports of this complication. There is also no clear guidelines on how to proceed. Reminder of the possibility of bad promising complications and the analysis carried out on the basis of this case and the available literature can be helpful for specializing in surgery of the digestive tract.	esophagus
Peroxiredoxin 1 is a tumor-associated antigen in esophageal squamous cell carcinoma.	Peroxiredoxin 1 (Prdx1) is an antioxidant and plays an important role in H2O2-mediated cell signaling. We previously found that the expression level of Prdx1 was elevated in esophagus squamous cell carcinoma (ESCC) tissue using a proteomics approach. Since overexpressed protein can induce an autoimmune response, to further examine whether serum from ESCC patients exhibits immunoreactivity against Prdx1, autoantibody responses to Prdx1 were evaluated by ELISA, western blotting and indirect immunofluorescence assay in sera from patients with ESCC and normal individuals. Immunohistochemical study with tissue array slides and western blot analysis with cancer cell lines were also performed to analyze the protein expression profiles of Prdx1 in ESCC tissues and cancer cell lines. The results demonstrated that the positive rate of autoantibody against Prdx1 in ESCC sera was 13.2% (9/68), whereas this rate was 0% (0/89) in normal individuals. Data also showed that expression of Prdx1 was significantly increased in ESCC tissues when compared to expression in paired adjacent normal tissues (P<0.05). The data indicate that Prdx1 may contribute to malignant transformation of the esophagus, and may be used as a biomarker in the immunodiagnosis of ESCC.	esophagus