crossing96/oncoscreening huggingface dataset:
Initial experience with minimally invasive Ivor Lewis esophagectomy.	BACKGROUND: We have previously reported our experience with minimally invasive esophagectomy. Our standard approach involves laparoscopic and thoracoscopic mobilization of the esophagus with a cervical esophagogastric anastomosis. In the present study we report our early experience with a modification of this technique, in which a high intrathoracic anastomosis is performed. METHODS: From 2002 to 2005, a minimally invasive Ivor Lewis esophagectomy was performed in 50 patients. The planned approach included a totally laparoscopic abdominal procedure and either a minithoracotomy or thoracoscopy. Indications for esophagectomy included short segment Barrett's esophagus with high-grade dysplasia or resectable adenocarcinoma of the gastroesophageal junction (GEJ) with minimal proximal esophageal extension. . RESULTS: The median age was 62.3 years (range, 38 to 79). Twenty-five patients (50%) received either preoperative chemotherapy or chemoradiation. There was one nonemergent conversion to an open procedure during laparoscopy. Planned minithoracotomy was successful in 35 patients; an additional 15 patients had the entire thoracic component performed thoracoscopically. A circular stapled anastomosis was performed in all patients. The operative mortality was 6%. Three patients (6%) developed an anastomotic leak; all were successfully managed nonoperatively. Four patients (8%) developed postoperative pneumonia. There were no recurrent laryngeal nerve injuries. CONCLUSIONS: Minimally invasive Ivor Lewis esophagectomy was technically feasible and resulted in good initial results in our center, which is experienced in minimally invasive and open esophagectomy. This approach minimizes the degree of gastric mobilization, almost eliminates recurrent laryngeal nerve injury and pharyngeal dysfunction, and allows additional gastric resection margin in the case of cardia extension of GEJ tumors.	esophagus
The major 8p22 tumor suppressor DLC1 is frequently silenced by methylation in both endemic and sporadic nasopharyngeal, esophageal, and cervical carcinomas, and inhibits tumor cell colony formation.	Identification of tumor suppressor genes (TSG) silenced by methylation uncovers mechanisms of tumorigenesis and identifies new epigenetic tumor markers for early cancer detection. Both nasopharyngeal carcinoma (NPC) and esophageal carcinoma are major tumors in Southern China and Southeast Asia. Through expression subtraction of NPC, we identified Deleted in Liver Cancer 1 (DLC1)/ARHGAP7 (NM_006094)--an 8p22 TSG as a major downregulated gene. Although expressed in all normal tissues, DLC1 was silenced or downregulated in 11/12 (91%) NPC, 6/15 (40%) esophageal, 5/8 (63%) cervical and 3/9 (33%) breast carcinoma cell lines. No genetic deletion of DLC1 was detected in NPC although a hemizygous deletion at 8p22-11 was found by 1-Mb array-CGH in some cell lines. We then located the functional DLC1 promoter by 5'-RACE and promoter activity assays. This promoter was frequently methylated in all downregulated cell lines and in a large collection of primary tumors including 89% (64/72) NPC (endemic and sporadic types), 51% (48/94) esophageal, 87% (7/8) cervical and 36% (5/14) breast carcinomas, but seldom in paired surgical marginal tissues and not in any normal epithelial tissue. The transcriptional silencing of DLC1 could be reversed by 5-aza-2'-deoxycytidine or genetic double knock-out of DNMT1 and DNMT3B. Furthermore, ectopic expression of DLC1 in NPC and esophageal carcinoma cells strongly inhibited their colony formation. We thus found frequent epigenetic silencing of DLC1 in NPC, esophageal and cervical carcinomas, and a high correlation of methylation with its downregulation, suggesting a predominant role of epigenetic inactivation. DLC1 appears to be a major TSG implicated in the pathogenesis of these tumors, and should be further tested as a molecular biomarker in patients with these cancers.	esophagus
Preoperative chemotherapy for resectable thoracic esophageal cancer.	BACKGROUND: Surgery has been the treatment of choice for localized esophageal cancer. A number of studies have investigated whether preoperative chemotherapy followed by surgery leads to an improvement in cure rates but the individual reports have been conflicting. An explicit systematic update of the role of preoperative chemotherapy in the treatment of resectable thoracic esophageal cancer is, therefore, warranted. OBJECTIVES: The objective of this review is to determine the role of preoperative chemotherapy on patients with resectable thoracic esophageal carcinomas. SEARCH STRATEGY: Trials were identified by searching the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (1966 to 2006), EMBASE (1988 to 2006) and CANCERLIT (1993 to 2002). There were no language restrictions. SELECTION CRITERIA: All trials of patients with potentially resectable carcinomas of the esophagus (of any histologic type) who were randomised to having either chemotherapy or no chemotherapy before surgery. DATA COLLECTION AND ANALYSIS: The primary outcome was survival, which was assessed using hazard ratios. This is an amendment to the original review which used relative risks to assess survival at yearly intervals. Hazard ratios (HR) have now been introduced to summarise the complete survival experience in a single analysis. The risk ratio (relative risk; RR) was used to compare rates of resections, tumour recurrences and treatment morbidity and mortality. MAIN RESULTS: There were eleven randomised trials involving 2019 patients. Eight trials (1729 patients) reported sufficient detail on survival to be included in a meta-analysis for the primary outcome. There was some evidence to suggest that preoperative chemotherapy improves survival, but this was inconclusive (HR 0.88; 95% CI 0.75 to 1.04). There was no evidence to suggest that the overall rate of resections (RR 0.96, 95% CI 0.92 to 1.01) or the rate of complete resections (R0) (RR 1.05; 95% CI 0.97 to 1.15) differ between the preoperative chemotherapy arm and surgery alone. There is no evidence that tumour recurrence (RR 0.81, 95% CI 0.54 to 1.22) or non-fatal complication rates (RR 0.90; 95% CI 0.76 to 1.06) differ for preoperative chemotherapy compared to surgery alone. Trials reported risks of toxicity with chemotherapy that ranged from 11% to 90%. AUTHORS' CONCLUSIONS: In summary, preoperative chemotherapy plus surgery may offer a survival advantage compared to surgery alone for resectable thoracic esophageal cancer, but the evidence is inconclusive. There is some evidence of toxicity and preoperative mortality associated with chemotherapy.	esophagus
Expression profile of metastasis-associated genes in esophageal squamous cell carcinoma.	The differentially expressed genes between esophageal squamous cell carcinoma (ESCC) with or without lymphatic metastasis were investigated by gene chip, and the lymphatic metastasis-associated genes were screened out. Expression array was used to detect the mRNA from both the primary carcinoma and the corresponding esophageal epithelium in 15 cases of human ESCC. The lymphatic metastasis-associated genes were screened by bioinformatics between ESCC with or without lymphatic metastasis. The results showed that 43 (4.85 %) genes significantly differed between the ESCC with and without lymphatic metastasis (P<0.05), of which 18 (2.03 %)were upregulated and 25 (2.82 %) down-regulated. The up-regulated genes were involved in cell adhesion molecules and cell membrane receptors and the down-regulated genes were mostly cell cycle regulators and intracellular signaling molecules. It was suggested that lymphatic metastasis-associated genes were screened by gene chip, which was helpful to understand the molecular mechanism of ESCC lymphatic metastasis and lymphatic metastasis-associated genes might be used as diagnostic markers and therapeutic targets for lymphatic metastasis.	esophagus
Minimally invasive esophagectomy for cancer: prospective evaluation of laparoscopic gastric mobilization.	BACKGROUND: Esophagectomy carries high morbidity, mainly respiratory. Minimally invasive surgery has been demonstrated to improve postoperative outcome in digestive surgery, without impairment of oncological results. A prospective study was conducted to evaluate feasibility, postoperative outcome, and mid-term oncological results of minimally invasive esophagectomy (MIE) in cancer. METHODS: From July 2001 to August 2005, 25 patients underwent esophagectomy with laparoscopic gastric mobilization (LGM) for epidermoid carcinoma (n=15) or adenocarcinoma (n=10). Tumors were located on the cardia (n=6), on the lower third (n=14), or on the median third (n=5) of the esophagus. Following LGM, transthoracic esophagectomy was performed. RESULTS: Complete LGM was achieved in all patients but 1. Mean operative time for LGM was 191+/-49 minutes. Fifteen patients (60%) developed complications, mainly respiratory. Anastomotic leakage occurred in 2 patients, with a favorable outcome. Pylorospasm (n=1) was the only intra-abdominal complication. Median hospital stay was 18 days. Two patients died (8%). Twenty-three patients underwent R0 resection. A mean of 12+/-4 lymph nodes (range 4-19 nodes) were analyzed. With a mean follow-up of 14 months (1-46 months), actuarial survival at 1 and 2 years was, respectively, 73% and 56%. CONCLUSION: Esophagectomy with LGM is feasible with few specific complications. However, no decrease in morbidity and hospital stay could be observed. Mid-term oncological results seem comparable to those of conventional surgery. Further studies are required to evaluate the extent of lymphadenectomy and the oncologic safety of MIE.	esophagus
RRIG1 mediates effects of retinoic acid receptor beta2 on tumor cell growth and gene expression through binding to and inhibition of RhoA.	The expression of retinoic acid receptor beta2 (RAR-beta2) is frequently lost in various cancers and their premalignant lesions. However, the restoration of RAR-beta2 expression inhibits tumor cell growth and suppresses cancer development. To understand the molecular mechanisms responsible for this RAR-beta2-mediated antitumor activity, we did restriction fragment differential display-PCR and cloned a novel retinoid receptor-induced gene 1 (RRIG1), which is differentially expressed in RAR-beta2-positive and RAR-beta2-negative tumor cells. RRIG1 cDNA contains 2,851 bp and encodes a protein with 276 amino acids; the gene is localized at chromosome 9q34. Expressed in a broad range of normal tissues, RRIG1 is also lost in various cancer specimens. RRIG1 mediates the effect of RAR-beta2 on cell growth and gene expression (e.g., extracellular signal-regulated kinase 1/2 and cyclooxygenase-2). The RRIG1 protein is expressed in the cell membrane and binds to and inhibits the activity of a small GTPase RhoA. Whereas induction of RRIG1 expression inhibits RhoA activation and f-actin formation and consequently reduces colony formation, invasion, and proliferation of esophageal cancer cells, antisense RRIG1 increases RhoA activity and f-actin formation and thus induces the colony formation, invasion, and proliferation of these cells. Our findings therefore show a novel molecular pathway involving RAR-beta2 regulation of RRIG1 expression and RRIG1-RhoA interaction. An understanding of this pathway may translate into better control of human cancer.	esophagus
Synergistic function of Smad4 and PTEN in suppressing forestomach squamous cell carcinoma in the mouse.	The genetic bases underlying esophageal tumorigenesis are poorly understood. Our previous studies have shown that coordinated deletion of the Smad4 and PTEN genes results in accelerated hair loss and skin tumor formation in mice. Herein, we exemplify that the concomitant inactivation of Smad4 and PTEN accelerates spontaneous forestomach carcinogenesis at complete penetrance during the first 2 months of age. All of the forestomach tumors were invasive squamous cell carcinomas (SCCs), which recapitulated the natural history and pathologic features of human esophageal SCCs. A small population of the SCC lesions was accompanied by adenocarcinomas at the adjacent submucosa region in the double mutant mice. The rapid progression of forestomach tumor formation in the Smad4 and PTEN double knockout mice corresponded to a dramatic increase in esophageal and forestomach epithelial proliferation. The decreased expression of p27, p21, and p16 together with the overexpression of cyclin D1 contributed cooperatively to the accelerated forestomach tumorigenesis in the double mutant mice. Our results point strongly to the crucial relevance of synergy between Smad4 and PTEN to suppress forestomach tumorigenesis through the cooperative induction of cell cycle inhibitors.	esophagus
Molecular dissection of 17q12 amplicon in upper gastrointestinal adenocarcinomas.	DNA amplification at 17q is frequently detected in upper gastrointestinal adenocarcinomas (UGC; stomach and esophagus). In this study, we did fluorescence in situ hybridization on a tissue microarray that contained 304 UGCs and 89 normal stomach samples using a approximately 168-kb BAC clone (CTD-2019C10) that maps to 17q12-q21.1. This 168-kb region contains the following genes: PPP1R1B/DARPP-32, STARD3, TCAP, PNMT, PERLD1, ERBB2, C17orf37, and GRB7 as well as the first two exons of ZNFN1A3. DNA amplification (> or =5 signals) was detected in 85 of 282 (30%) of UGCs, and high-level amplification (> or =10 signals) was seen in 28 of 282 (10%) of all tumors. Adenocarcinomas of gastroesophageal junction and lower esophagus had the highest frequency of amplification (45%) compared with stomach tumors (27%; P = 0.04). On the other hand, 38% of tumors with intestinal-type morphology had amplification compared with 26% of diffuse-type tumors (P = 0.02). We further did quantitative real-time reverse transcription-PCR on 74 frozen tissue samples from UGCs for 11 genes located within or adjacent to the boundaries of this approximately 168-kb genomic region. These genes include all 9 genes that are fully or partially located inside the CTD-2019C10 clone as well as 2 additional adjacent genes (NEUROD and TOP2A). Overexpression of PPP1R1B/DARPP-32, TCAP, and TOP2A was seen in approximately half of the tumors, whereas STARD3 and ZNFN1A3 were rarely overexpressed (12%). Interestingly, there was a statistical correlation between expression of all 8 genes that map between PPP1R1B/DARPP-32 and GRB7, whereas expression of NEUROD, ZNFN1A3, and TOP2A that are partially inside or adjacent to the boundaries of the CTD-2019C10 clone did not correlate with the expression of any of these 8 genes. These data show a transcriptionally active oncogenomic region bounded by PPP1R1B/DARPP-32 and GRB7 in UGCs and provide further insight into expression levels of several critical genes.	esophagus
Gastroesophageal junction adenocarcinoma: what are the factors influencing long-term survival?	The incidence of gastroesophageal junction adenocarcinoma is increasing. About 30% of the tumors cannot be completely resected, and 40% of the patients relapse after complete resection. There is much controversy over the role of neoadjuvant therapy, the approach route, lymphadenectomy, and the extent of esophageal resection. The aim of our study was to report our experience in the treatment of gastroesophageal junction adenocarcinoma. From January 1987 until February 2005, 157 patients (125 men, 32 women), mean age 72.1 +/- 3.2 years, came for observation. One hundred sixteen patients underwent curative intervention. Mean operative time was 185 +/- 45 minutes. Mean postoperative hospital stay was 16.4 +/- 6.1 days. Postoperative complications were observed in 25 patients (21.6%); 6 patients (5.2%) died during the postoperative period. Overall survival was 36.2% and 27.6% at 3- and 5-year follow-up, respectively. Five-year survival rate was significantly lesser in R1/R2 versus R0 resections (0% versus 33.7%), N+ versus N- patients (11.3% versus 53.3%), and worsened with progression of pT histological staging (T1, 100%; T2, 24.1%; T3, 15.1%; T4, 0%). Determining prognostic factors are the radicality of resection, lymph nodal invasion, and histological staging.	esophagus
Overexpression of vascular endothelial growth factor-C correlates with lymph node micrometastasis in submucosal esophageal cancer.	Lymph node metastasis, including lymph node micrometastasis (LMM), is one of the most important prognostic factors in esophageal squamous cell carcinoma (ESCC). Vascular endothelial growth factor C (VEGF-C) plays a key role in the process of lymphangiogenesis. We examined VEGF-C expression and tumor microvessel density of the primary tumors in ESCC and analyzed relationships between VEGF-C expression and clinicopathologic findings including LMM in submucosal ESCC. The subjects were 87 patients with submucosal ESCC. Immunohistochemical staining of VEGF-C and CD34 was performed with primary tumors, and staining of cytokeratin was performed with dissected lymph nodes. Microvessel density was calculated from CD34 expression, and LMM was detected by cytokeratin staining. VEGF-C overexpression significantly correlated with depth of tumor invasion, lymphatic invasion, and lymph node metastasis (P < 0.05, P < 0.0001, and P < 0.0001, respectively). High microvessel density also correlated with lymphatic invasion and lymph node metastasis (P < 0.005 and P < 0.05, respectively). LMM was detected in 8 cases and 14 lymph nodes by cytokeratin staining. VEGF-C overexpression and high microvessel density were found in tumors with lymph node metastasis and/or LMM, compared with tumors without nodal metastasis or LMM (P < 0.0001 and P < 0.01, respectively). The present findings indicate that in ESCC with submucosal invasion, VEGF-C overexpression of the primary tumor is a strong high risk factor for lymph node metastasis, including LMM.	esophagus
[Estimation of morbidity risk in aged patients undergoing resections of esophagus carcinoma and gastric cardiac carcinoma using physiological and operative severity score].	OBJECTIVE: To test the clinical validity of physiological and operative severity score for the enumeration of mortality and morbidity (POSSUM) in aged patients undergoing resections of esophagus carcinoma and gastric cardiac carcinoma. METHODS: POSSUM was used in 167 aged patients undergoing esophagus carcinoma and gastric cardiac carcinoma resection. The physiological score and the operative severity score were compared between the groups with and without postoperative complications. The morbidity rates were calculated. Observed morbidity rates were compared with the rates predicted by POSSUM. RESULTS: Seventy-six of the 167 patients suffered from postoperative complications. The physiological score of the group with complications was 16.75 +/- 0.4, significantly higher than that of the group without complications (15.4 +/- 0.3, P < 0.0017). The number of the patients with complications predicted by POSSUM was 70, not significantly different from the observed number of the patients with complications (78, P = 0.378). There were 94 person-times of complications in these 78 patients, 12 being with hypertension, 37 with arrhythmia; 5 with asthma; 3 with febrile; 2 with pneumonia; 1 with atelectasis; 1 with respiratory failure; 3 with wound infection; 3 with wound liquefaction; 2 with anastomotic leakage; 6 with phlebitis; 2 with pneumothorax; 2 with acute dilatation of stomach; 1 with chylothorax; 2 with hemorrhage; 1 with cardiac failure; 1 with infectious shock; 2 with empyema; 2 with deep vein thrombo-embolism; 1 with pulmonary infarction; 1 with cerebral infarction; 1 with urinary infection; and 1 with psychiatric symptom. CONCLUSION: The POSSUM makes satisfactory prediction of postoperative morbidity in aged patients undergoing esophagus carcinoma and gastric cardiac carcinoma resection. Intensive monitoring and organ supporting therapy after the operation according to the score is of great benefit to decrease the post-operative complications.	esophagus
[Surgical anatomy of the colic vessels in Chinese and its influence on the operation of esophageal replacement with colon].	OBJECTIVE: To investigate the configuration of colic vessels in Chinese and its influence on the operation of esophageal replacement with colon (ERC). METHODS: The origin, trend, branching, configuration, and distribution of the colic vessels, the intensity of the colic arterial impulse, the integrity of the marginal artery at the splenic flexure and hepatic flexure of colon were observed during the operation of ERC among 582 patients undergoing ERC, 402 males mad 180 females, aged 2 approximately 74, from 22 provinces, municipality, and autonomous regions. RESULTS: The left colic artery (LCA) stemmed from the inferior mesenteric artery (IMA) in 97.3% of the patients, with an absence rate of 0.7%. The middle colic artery (MCA) stemmed from the superior mesenteric artery (SMA) in 77.8% of the patients with an absence rate of 8.2%. Accessory middle colic artery (acMCA), originating from the right colic artery, could be seen in 6.2% of the patients 39.7% of the right colic artery (RCA) stemmed from the SMA by itself, 23.0% of the RMA stemmed together with MCA, and 28.0% of the RCA stemmed together with the ileocolic artery. The absence rate of RCA was 9.8%. The intactness rate of marginal artery was 96.8% at the splenic flexure of colon, and was 88.7% at the hepatic flexure. The Rolan arch was seen in only 7.6% of the patients. CONCLUSION: The configuration of colic vessels in Chinese was basically similar to those of the results of autopsies carried out abroad. The optimal supply artery of colic segment during ERC is LCA, followed by LCA. Attention should be paid to the integrity of marginal arteries and veins in the patients with history of epigastric operation.	esophagus
Age effects and temporal trends in adenocarcinoma of the esophagus and gastric cardia (United States).	A number of hypotheses have been advanced to explain the rapid increase of the incidence of esophageal adenocarcinoma in the US. A major problem in identifying and understanding the nature of this increase is the difficulty in untangling age effects from temporal trends due to cohort and period effects. To address this problem, we have developed multi-stage carcinogenesis models that describe the age-specific incidence of adenocarcinoma of the esophagus and of the gastric cardia with separate adjustments for temporal trends. These models explicitly incorporate important features of the cancers, such as the metaplastic conversion of normal esophagus to Barrett's esophagus (BE). We fit these models separately to the incidence of adenocarcinoma of the esophagus and of the gastric cardia reported in the Surveillance Epidemiology and End Results (SEER) registry over the period 1973-2000. We conclude that the incidence of both cancers is consistent with a sequence that posits a tissue conversion step in the target organ followed by a multi-stage process with three rate-limiting events, the first two leading to an initiated cell that can expand clonally into a premalignant lesion, and the third converting an initiated cell into a malignant cell. Temporal trends in the incidence of both cancers are dominated by dramatically increasing period effects.	esophagus