crossing96/oncoscreening huggingface dataset:
Alcohol dehydrogenase 3 and risk of esophageal and gastric adenocarcinomas.	OBJECTIVES: Alcohol increases esophageal squamous carcinoma risk but has been less consistently associated with esophageal adenocarcinoma. Alcohol dehydrogenase catalyzes the oxidation of approximately 80% of ethanol to acetaldehyde, a carcinogen. The alcohol dehydrogenase gene has several polymorphisms which may lead to faster conversion of ethanol to acetaldehyde, which may increase cancer risk. METHODS: We undertook a study to examine whether a common polymorphism in the alcohol dehydrogenase 3 gene was associated with a higher risk of esophageal adenocarcinoma using data and biological samples collected for the Esophageal and Gastric Cancer Study (n = 114 esophageal and gastric cardia adenocarcinoma, n = 60 non-cardia gastric carcinoma, n = 23 cases of esophageal squamous cell carcinoma and 160 controls). RESULTS: Individuals homozygous for ADH ( 3 ) (1-1) had a higher risk of each tumor type compared to individuals who had ADH ( 3 ) (2-2) or ADH ( 3 ) (1-2) genotype (OR = 1.7, 95% CI = 1.0-2.9 for esophageal and gastric cardia adenocarcinomas; OR = 1.7, 95% CI = 0.7-4.3 for esophageal squamous cell carcinoma; and OR = 2.8, 95% CI = 1.5-5.1 for non-cardia gastric cancer). The elevation in risk from homozygosity of the ADH ( 3 ) (1) allele was seen in drinkers and nondrinkers, although the risk estimate was only significant for drinkers, particularly of liquor. CONCLUSION: These data suggest ADH3 genotype may be associated with risk of esophageal and gastric cardia adenocarcinomas.	esophagus
Metastatic basaloid-squamous cell carcinoma of the esophagus treated by 5-fluorouracil and cisplatin.	Basaloid squamous cell carcinoma (BSC) of the esophagus is a rare malignant disease. We report here a patient with recurrent esophageal BSC, who was successfully treated by systemic chemotherapy containing 5-fluorouracil (5-FU) and cisplatin (CDDP). A 57-year-old woman was diagnosed as having squamous cell carcinoma of the esophagus upon endoscopic examination. Curative esophagectomy with lymph node dissection was performed under the thoracoscope. The pathological diagnosis of the surgical specimen was BSC. Five months after operation, the patient was diagnosed as having a recurrence of the BSC with metastases to the liver and spleen, and a right paraclavicular lymph node. She was given systemic chemotherapy consisting of continuous infusion of 800 mg/d of 5-FU and 3 h infusion of 20 mg/d of CDDP for 5 consecutive days every 4 wk. The metastatic lesions in the spleen and right paraclavicular lymph node disappeared, and the liver metastasis was apparently reduced in size after 2 courses of chemotherapy. The tumor regression was seen over 6 courses, with progression afterwards. Although subsequent treatment with CPT-11 and CDDP was not effective, docetaxel and vinorelbine temporarily controlled the tumor growth for 2 mo. 5-FU and CDDP combination may be useful for the patients with advanced BSC.	esophagus
[Expression of 39 HOX genes in esophageal cancer cell lines].	OBJECTIVE: To identify whether HOX genes can be used as markers of esophageal cancer. METHODS: The expression of 39 HOX genes in esophageal cancer cell lines was examined. Specific primers were designed and RT- PCR was performed for each HOX gene members in above esophageal cancer cell lines, EC109 and CAES. RESULTS: Fifteen out of 39 HOX genes were expressed in esophageal cancer cell lines. They were HOXA2, HOXA7, HOXA9, HOXA10, HOXA13, HOXB7, HOXB9, HOXC4, HOXC5, HOXC6, HOXC8, HOXC9, HOXD9, HOXD10, and HOXD13 respectively. Of them. Eleven genes were overlapped with the ones detected in human esophageal squamous cell carcinoma(ESCC) in our former study. CONCLUSION: This study reconfirms our former that some HOX genes are deregulated expressed in ESCC, which provides more positive evidence for their roles in ESCC.	esophagus
18FDG uptake in oesophageal adenocarcinoma: linking biology and outcome.	PURPOSE: Variable uptake of 18FDG has been noticed in positron emission tomography (PET) studies of patients with oesophageal adenocarcinoma. The aim of the present study was to investigate biological parameters involved in 18FDG uptake in oesophageal adenocarcinoma for selection of patients with increased 18FDG uptake and prediction of prognostic value of 18FDG PET. PATIENTS AND METHODS: Preoperative PET scans were performed in 26 patients with histologically proven oesophageal adenocarcinoma. 18FDG uptake was semiquantitatively measured by SUV(BSAg. )Tumour sections were stained by immunohistochemistry for angiogenic markers (VEGF, CD31), glucose transporter-1 (Glut-1), hexokinase (HK) isoforms, for proliferation marker (Ki67), for macrophage marker (CD68) and for apoptosis marker (cleaved caspase-3). Cell densities, differentiation grade, degree of necrosis and mucus, T-stage and tumour size were assessed. In addition follow-up was analysed. RESULTS: No association was found between 18FDG uptake and angiogenic markers. In contrast, a significant correlation was found between 18FDG uptake and Glut-1 expression. No correlations were found between 18FDG uptake and HK isoforms, Ki67 or cleaved caspase-3. Also, no correlations were found between 18FDG uptake and cell density, differentiation grade, CD68, mucus and necrosis. However, there was a significant correlation between 18FDG uptake and tumour size and between 18FDG uptake and tumour recurrence. CONCLUSIONS: Glut-1 expression and tumour size seem parameters associated with 18FDG uptake in patients with biopsy proven oesophageal adenocarcinoma, and may be used to select oesophageal cancer patients in whom 18FDG-PET is of diagnostic value and may predict disease outcome.	esophagus
[Cervical esophagogastrostomy with circular mechanical stapler in the treatment of esophageal carcinoma--report of 346 cases].	OBJECTIVE: To evaluate the efficacy of esophagogastrostomy in the neck using circular mechanical stapler through the esophageal bed. METHODS: From March 1998 to June 2004 subtotal esophagectomy and mechanical anastomosis with stomach in the neck through the esophageal bed was carried out in 346 esophageal cancer patients. RESULTS: In this series, the positive rate of detecting residual cancer cells in the esophageal stump was 1.2% (4/346); anastomotic fistula was observed in 5.5% (19/346) causing one patient died; the overall operative mortality rate was 0.6% (2/346); esophageal anastomotic stricture developed in 3.8% (13/346), which were cured by endoscopic dilatation. CONCLUSION: This modified operation mode has low rate of complication, reducing impairement to pulmonary function due to the transposed thoracic stomach within the mediastinum instead of the thoracic cavity. Using mechanical circular stapler for anastomosis in the neck simplifies the operation and reducing the postoperative risk caused by anastomotic leak.	esophagus
Diagnosis of esophageal adenocarcinoma by serum proteomic pattern.	BACKGROUND: Currently, endoscopic biopsy is the only method used to diagnose esophageal adenocarcinoma. Using surface-enhanced laser desorption/ionization (SELDI) ProteinChip technology, we sought to identify a potentially diagnostic serum protein pattern that can serve as a reliable blood test for the diagnosis of esophageal adenocarcinoma. In addition, we sought to identify potential biomarkers for esophageal adenocarcinoma. METHODS: Whole serum was collected using standard techniques from subjects with a known diagnosis of esophageal adenocarcinoma as well as from subjects without any known esophageal disease. The samples were spotted onto a hydrophobic (H50) and immobilized metal affinity (IMAC30) chip surface and allowed to incubate. All samples were run in duplicate. After several washes, matrix was added and a mass range of 1500 to 30000 daltons was analyzed by SELDI-Time-of-Flight mass spectroscopy. Statistical analysis was performed using Biomarker Pattern Software (Bio-Rad Laboratories, Hercules, CA). RESULTS: For the H50 analysis, 3 peaks were identified that correctly diagnosed 42 of 43 cancers and 10 of 11 normals. For the IMAC30, 4 peaks were identified that correctly diagnosed 50 of 50 cancers and 10 of 10 normals. CONCLUSIONS: Serum proteomic pattern shows great promise in the diagnosis of esophageal adenocarcinoma. This technology may lead to the development of a noninvasive screening test as well as to the identification of potential novel biomarkers for esophageal adenocarcinoma.	esophagus
Activation of the serine/threonine protein kinase Akt during the progression of Barrett neoplasia.	Esophageal adenocarcinoma has demonstrated a rapid increase in incidence over the last 10 years. This increase mirrors a dramatic rise in that of Barrett esophagus, which is associated with esophageal adenocarcinoma in at least 95% of cases. In an attempt to understand the pathogenesis of esophageal adenocarcinoma, attention has turned to the antiapoptotic and oncogenic pathways. Here we demonstrated that Akt was frequently activated in Barrett esophagus-related adenocarcinoma. Remarkably, the levels of Akt activation were associated with tumor progression. After institutional review board ethics approval, 60 archival tissue specimens of esophageal adenocarcinoma arising on a background of Barrett esophagus were selected for immunohistochemical staining with phosphorylated Akt (p-Akt) antibody. The slides were scored by 2 independent observers. Approximately 80% of high-grade dysplasia and esophageal adenocarcinoma cases demonstrated strong to moderate Akt activity. Sixty-two percent of Barrett mucosa revealed low Akt activity, the remaining cases being p-Akt negative. None of the low-grade dysplasia cases exhibited strong p-Akt staining, whereas only weak p-Akt activity is seen in a portion of metaplastic Barrett mucosa, Akt is highly activated in high-grade dysplasia and esophageal adenocarcinoma arising from Barrett esophagus. These findings suggest a role of p-Akt in the progression of Barrett esophagus to esophageal adenocarcinoma and provide the rationale for using p-Akt inhibitor API-2/triciribine, which is currently in clinical trial, in the treatment of esophageal adenocarcinoma.	esophagus
Thoracoscopic management of benign tumors of the mid-esophagus: a retrospective study.	Benign esophageal tumors are rare conditions. Traditionally, thoracotomy was the preferred route to approach these lesions. Now, increasingly more surgeons are using minimally invasive techniques to treat these benign mid-esophageal lesions. We present our experiences from a specialised minimally invasive surgery unit. We have managed 12 patients with benign tumors of the mid-esophagus from 1995 to 2007 in our institute. The enucleation was achieved with the patient placed in the prone position and approached via a right thoracoscopy in all cases. Hospital stay was 3-5 days and there were minor postoperative complications in 2 patients. Mortality was nil. There were 10 patients with leiomyoma and 2 with GISTs, as proved by immunohistochemistry. Short and long-term follow up was satisfactory, with none of the patients having recurrences or other problems. Leiomyomas and GISTs, respectively, are the commonest benign tumors of the esophagus. Tumors more than 5 cm have to be enucleated, and thoracotomy has been the traditional approach to these lesions. Thoracoscopy has definite benefits regarding reduced morbidity. The combined modality of peroperative endoscopy is useful in locating the lesion as well as confirming its complete removal. Based on our experience, a right thorax approach and the prone patient position is the ideal for thoracoscopic procedures.	esophagus
Fluorine-18 fluorodeoxyglucose positron emission tomography in the preoperative staging of thoracic oesophageal and gastro-oesophageal junction cancer: a prospective study.	BACKGROUND: The pre-operative staging in oesophageal cancer is often challenging and underestimation of the extent of the disease may lead to unnecessary surgery. AIM: To audit the use and assess the value of fluorine-18 fluorodeoxyglucose positron emission tomography ((18)F FDG-PET) as a staging tool for thoracic oesophageal and gastro-oesophageal junction (GOJ) cancers in our oncological surgical practice. PATIENTS AND METHODS: Over a 3 year period, between 2002 and 2004, 134 patients with thoracic oesophageal or GOJ cancer were referred to our unit for treatment. The standard preoperative staging investigation in all cases was CT (thorax, abdomen and pelvis). A preoperative FDG-PET scan was further requested in 22 patients. The case notes of all the patients that underwent a FDG-PET scan were reviewed and compared with the preoperative imaging, the operative findings and the histopathology of the resected tumours. RESULTS: Eighteen men and 4 women with a median age of 65 (range 43-79) years were studied. After FDG-PET, 13 out of 22 patients (59%) were deemed suitable for tumour resection. Twelve of the 13 patients were fit to undergo surgery. At laparotomy, 2 of those (17%) were found inoperable due to widespread disease. The sensitivity of CT versus FDG-PET to detect infiltrated lymph nodes was 29% (95% CI: 3-70) versus 71% (95% CI: 29-96) (P=0.0412), whereas both tests had 67% specificity (95% CI: 9-99) in detecting lymph nodes. The sensitivity and the specificity of CT versus FDG-PET to detect distant organ metastases (M1b) were 33% (95% CI: 4-77) and 88% (95% CI: 47-99) versus 50% (95% CI: 6-93) and 100% (95% CI: 69-100), respectively (P>0.05). The FDG-PET regarding the N and M status differed from the CT in 11 patients and led to modification of the planned management in 5 of them. CONCLUSIONS: FDG-PET is more accurate than CT in defining N and M status. It can result in a reduction of unnecessary surgery in a significant number of patients. The combined PET-CT scan as a single imaging modality is expected to further improve diagnostic accuracy of FDG-PET.	esophagus
[Establishment of a human esophageal carcinoma transplantation model with MUC1 high expression in nude mice].	BACKGROUND & OBJECTIVE: Mucin-1 (MUC1), a tumor-associated antigen, is an optional molecular target for antitumor immunotherapy protocols. This study was to establish a subcutaneous human esophageal cancer transplantation model with MUC1 high expression in nude mice that closely resembles the biological features of human esophageal cancer, and provide a in vivo model for MUC1-targeting immunotherapy of esophageal cancer. METHODS: Human esophageal carcinoma cell line EC-109 with MUC1 high expression was cultured, and subcutaneously transplanted into BALB/c athymic nude mice (4-5 weeks old). The growth status of transplanted tumor was observed. These subcutaneous tumors were examined histologically. The expression of proliferating cell nuclear antigen (PCNA) was detected by immunohistochemistry. Cell cycle and MUC1 expression of the transplanted tumor cells were analyzed by flow cytometry. RESULTS: Human esophageal carcinoma transplantation models with MUC1 high expression were successfully established in 6 of the 7 nude mice. The histological and biological characteristics of subcutaneous transplanted tumors were similar to those of human esophageal carcinoma. The mean PCNA label index of subcutaneous transplanted tumor cells was (63.5+/-3.6)%. The mean S-phase fraction of cell cycle was (37.6+/-3.7)%. The positive rate of MUC1 in subcutaneous transplanted tumor cells was 97.5%. CONCLUSION: Human esophageal carcinoma transplantation model with MUC1 high expression in nude mice is similar to human malignant tumors in biological characteristics, and can be used to investigate the biological characteristics of esophageal carcinoma, as well as provides an applicable animal model for research on MUC1-targeting immunotherapy of esophageal cancer.	esophagus
Towards the molecular characterization of disease: comparison of molecular and histological analysis of esophageal epithelia.	Reliable quantification of gene expression offers the possibility of more accurate and prognostically relevant characterization of tissues than potentially subjective interpretations of histopathologists. We measured the expression of 18 selected genes and compared them to histological features in a spectrum of esophageal disease to evaluate the feasibility of molecular characterization of normal and pathologic esophageal epithelia. Esophageal tissue biopsies from 82 patients with foregut symptoms were laser capture microdissected, and the expression levels of 18 selected genes were measured by quantitative real-time polymerase chain reaction. Linear discriminant analysis, which uses combinations of genes to distinguish between histological groups, was performed to compare gene expression and the following five histological groups: (1) normal squamous epithelium (n = 35), (2) reflux esophagitis (n = 13), (3) non-dysplastic Barrett's (n = 33), (4) dysplastic Barrett's (n = 16), (5) adenocarcinoma (n = 31). A panel of seven genes had 90-94% predictive power to distinguish non-dysplastic and dysplastic Barrett's esophagus. Clustering analysis revealed structure in gene expression values even in the absence of histology. Expression levels in 17 genes differed significantly across histological groups. Classification based on gene expression agreed with histopathological assessment in the following percentage of cases: normal squamous epithelium = 53%, reflux esophagitis = 31%, non-dysplastic Barrett's = 76%, dysplastic Barrett's = 40%, and adenocarcinoma = 59%. Interestingly, predictive power improved markedly when inflammatory and dysplastic tissues were removed (77-94%). Gene expression classification agrees well with histopathological examination. When differences occur, it is unclear whether this effect is due to intraobserver variability in pathological diagnosis or to a genuine difference between gene expression and histopathology.	esophagus
Increased phosphorylation of p70 S6 kinase is associated with HPV16 infection in cervical cancer and esophageal cancer.	HPV16 E6 interacts with and degrades tumour suppressor protein TSC2 leading to the phosphorylation of p70 S6 kinase. We studied the association of S6 kinase phosphorylation and HPV16 infection in cervical cancer and esophageal cancer. Immunohistochemistry was used to assess phosphorylated S6 kinase (Thr 389) and phosphorylated S6 (Ser235/236) in 140 cervical cancer and 161 esophageal cancer specimens. Immunohistochemical staining for pS6 kinase and pS6 was significantly more frequent in the HPV16-infected cervical cancer specimens than the HPV16-negative specimens. In contrast, the expression of S6 kinase was similar in both HPV16-positive and -negative samples. The phosphorylation of Akt, the key regulator of S6 kinase, was also detected. Our analysis showed that Akt phosphorylation was unaffected by HPV16 infection. These results together with our previous study suggest that HPV16 modifies S6 kinase activation via mechanism, which activates S6 kinase downstream of Akt function.	esophagus
Leptin synergistically enhances the anti-apoptotic and growth-promoting effects of acid in OE33 oesophageal adenocarcinoma cells in culture.	Obesity and gastro-oesophageal reflux are the main predisposing factors for oesophageal adenocarcinoma. We have examined the effects of transient acid exposure and leptin on OE33 oesophageal adenocarcinoma cells. Leptin and acid individually stimulated proliferation and inhibited apoptosis and the combination was synergistic. Leptin receptor protein levels were unchanged by acid exposure. The COX-2 inhibitor NS 398 blocked the effects of acid and leptin but while both acid and leptin individually significantly increased PGE2 production and COX-2 mRNA levels, the combination was not more effective than either stimulant alone. Leptin synergistically enhanced acid-stimulated EGFR and ERK phosphorylation but did not further increase JNK or p38 MAP kinase phosphorylation. Specific EGFR and ERK inhibitors reduced the effects of leptin and acid alone and in combination. The combination of increased circulating leptin levels in obesity and transient reflux of gastric acid may promote oesophageal carcinogenesis by increasing proliferation and inhibiting apoptosis.	esophagus
Early squamous cell carcinoma of the oesophagus: the Japanese viewpoint.	In Japan, more than 90% of oesophageal malignancies are squamous cell carcinomas, and superficial and early carcinomas now account for about 40% and 20%, respectively, of all oesophageal carcinomas. Definition of early carcinoma has changed on the basis of new data. As of 2007, early carcinoma is defined as intramucosal carcinoma with or without metastasis. In the subclassification based on depth of cancer invasion, m1 and m2 carcinomas have no metastasis and are considered curable by endoscopic mucosal resection alone, whereas < 10% of m3 carcinomas and about 20% of sm1 carcinomas have lymph node metastasis. The relationship between various pathological findings and the incidence of lymph node metastasis has been reviewed. High-grade squamous dysplasia (squamous cell carcinoma in situ in Japan) requires surgical or endoscopic removal. Very minute carcinomas have recently been detected by magnifying endoscopy and/or narrowband imaging. Endocytoscopy could replace biopsy histopathological examination for diagnosis of oesophageal squamous cell carcinoma, and endocytoscopic diagnosis and endoscopic therapy may be performed simultaneously. As a result of advances in the development of endoscopes, pathologists are now expected to diagnose very minute lesions, < 1 mm in size, in the oesophagus.	esophagus
Effects of phenylethyl isothiocyanate on early molecular events in N-nitrosomethylbenzylamine-induced cytotoxicity in rat esophagus.	There is little information on early molecular events in the development of N-nitrosomethylbenzylamine (NMBA)-induced rat esophageal tumorigenesis and of the effects of chemopreventive agents on these events. In this study, we identified genes in rat esophagus that were differentially expressed in response to short-term NMBA treatment and modulated by cotreatment with phenylethyl isothiocyanate (PEITC). Rats were fed AIN-76A diet or AIN-76A diet containing PEITC for 3 weeks. During the 3rd week of dietary treatment, they were administered three s.c. doses of NMBA (0.5 mg/kg body weight). Rats were sacrificed 24 h after the last treatment; esophagi were excised and processed for histologic grading, microarray and real-time PCR analysis. Histopathologic analysis showed that treatment of rats with PEITC had a protective effect on NMBA-induced preneoplastic lesions in the rat esophagus. We identified 2,261 genes that were differentially expressed in the NMBA-treated versus control esophagi and 1,936 genes in the PEITC + NMBA versus NMBA-treated esophagi. The intersection of these two sets resulted in the identification of 1,323 genes in NMBA-treated esophagus, the vast majority of which were modulated by PEITC to near-normal levels of expression. Measured changes in the expression levels of eight selected genes were validated using real-time PCR. Results from 12 microarrays indicated that PEITC treatment had a genome-wide modulating effect on NMBA-induced gene expression. Samples obtained from animals treated with PEITC alone or cotreated with PEITC + NMBA were more similar to controls than to samples treated with NMBA alone.	esophagus