crossing96/oncoscreening huggingface dataset:
Vagal-sparing esophagectomy: the ideal operation for intramucosal adenocarcinoma and barrett with high-grade dysplasia.	OBJECTIVE: Our aim was to compare outcome of vagal-sparing esophagectomy with transhiatal and en bloc esophagectomy in patients with intramucosal adenocarcinoma or high-grade dysplasia. SUMMARY BACKGROUND DATA: Intramucosal adenocarcinoma and high grade dysplasia have a low likelihood of lymphatic or systemic metastases and esophagectomy is curative in most patients. However, traditional esophagectomy is associated with significant morbidity and altered gastrointestinal function. A vagal-sparing esophagectomy offers the advantages of complete disease removal with the potential for reduced morbidity and a better functional outcome. METHOD: Retrospective review of outcome in patients with intramucosal adenocarcinoma or high grade dysplasia that had a vagal-sparing (n=49), transhiatal (n=39) or en bloc (n=21) esophagectomy. RESULTS: The length of hospital stay and the incidence of major complications was significantly reduced with a vagal-sparing esophagectomy compared with a transhiatal or en bloc resection. Further, postvagotomy dumping and diarrhea symptoms were significantly less common, and weight was better maintained postoperatively with a vagal-sparing esophagectomy. Recurrent cancer has developed in only 1 patient. CONCLUSION: Survival with intramucosal adenocarcinoma or Barrett's with high-grade dysplasia is independent of the type of resection. A vagal-sparing esophagectomy is associated with significantly less perioperative morbidity and a shorter hospital stay than a transhiatal or en bloc esophagectomy. Further, late morbidity including weight loss, dumping, and diarrhea are significantly less likely after a vagal-sparing approach. Consequently a vagal-sparing esophagectomy is the preferred procedure for patients with intramucosal adenocarcinoma or high grade dysplasia.	esophagus
Risk of mortality and cancer incidence in Barrett's esophagus.	BACKGROUND: There are very few prospective follow-up studies of Barrett esophagus (BE) cohorts assessing the risk of extraesophageal cancer incidence or mortality. Such studies are necessary in order to understand the overall risks of cancer and death experienced by patients with BE. METHODS: A cohort of 502 patients with BE were identified at Leeds General Infirmary, England. Mortality and cancer incidence information were provided by the Office for National Statistics. Standardized mortality ratios (SMR) and standardized incidence ratios (SIR) were calculated using indirect standardization. RESULTS: All-cause mortality was found to be elevated in patients with BE [SMR, 1.21; 95% confidence interval (95% CI), 1.06, 1.37] and remained so after esophageal cancers were excluded (SMR, 1.16; 95% CI, 1.01-1.32). Increased mortality risks were also found for malignant neoplasms of the esophagus (SMR, 7.26; 95% CI, 3.87-12.42) and diseases of the digestive system (SMR, 2.03; 95% CI, 1.11-3.40). The remaining disease categories produced no altered risk estimates. Circulatory disease mortality was borderline statistically significant (SMR, 1.24; 95% CI, 1.00-1.52; P = 0.053) for those with a specialized intestinal metaplasia diagnosis of BE. In the cancer incidence analyses, esophageal malignancies (SIR, 8.66; 95% CI, 4.73-14.53) and esophageal adenocarcinomas (SIR, 14.29; 95% CI, 7.13-22.56) were found to be increased in BE. All remaining analyses provided unaltered risks, including that of colorectal cancer. CONCLUSIONS: This study has shown evidence of an increased risk of esophageal cancer incidence and mortality in BE. It has also shown that those who have a histologic BE diagnosis may also have an increased risk of circulatory disease mortality.	esophagus
Establishment and characterization of a new xenograft-derived human esophageal squamous cell carcinoma cell line HKESC-4 of Chinese origin.	A new human esophageal cancer cell line, HKESC-4, was established from a nude-mouse xenograft of a moderately differentiated esophageal squamous cell carcinoma (ESCC) developed from a 65-year-old Hong Kong Chinese man. The cellular characteristics (morphological, electron microscopic, and immunohistochemical studies), tumorigenicity in athymic nude mice, cytogenetic features, and DNA ploidy of the cell line were investigated. The cell line was maintained in vitro for 17 months and passaged 80 times. HKESC-4 grew as a monolayer, with a doubling time of 63 hours. The epithelial nature of HKESC-4 included the presence of cytokeratin intermediate filaments, as shown by antibodies (AE1/AF3, CAM5.2, and MAK 6), and the presence of the tonofilaments, as seen under electron microscopy. HKESC-4 was tumorigenic in nude mice and had DNA aneuploidy. The cytogenetic abnormalities of HKESC-4 included -1, -2, -3, -4, -5, -6, -7, -8, -9, -10, -11, -12, -15, -16, -17, -18, -19, +20, -21, -22, +del(11)(p11), +i(11)(q10), and +21 marker chromosomes. Comparative genomic hybridization analysis demonstrated chromosomal gains at 1p36.13, 3q23 approximately q28, 5p15.33 approximately p15.1, 6p25.1 approximately p22.3, 7p21.3 approximately p11.2, 7q11.21 approximately q21.13, 8q23.3 approximately q23.3, 11p11.2, 11q12.1 approximately q13.2, 14q21.3 approximately q32.2, 17p13.3, 18p11.32 approximately p11.31, and 20p13 approximately p12.2 and chromosomal losses at 1q12, 2p25.1 approximately p24.3, 13p13 approximately p11.2, 21p, 22p13 approximately p11.2, and Y. The newly established cell line HKESC-4 promises to be a useful tool in future studies of molecular pathogenesis and therapeutics in ESCC.	esophagus
Pharmacological characterization of MP-412 (AV-412), a dual epidermal growth factor receptor and ErbB2 tyrosine kinase inhibitor.	Epidermal growth factor receptor (EGFR) and ErbB2 are currently recognized as validated target molecules in cancer treatment strategies. MP-412 (AV-412) is a potent dual inhibitor of EGFR and ErbB2 tyrosine kinases, including the mutant EGFR(L858R,T790M), which is clinically resistant to the EGFR-specific kinase inhibitors erlotinib and gefitinib. In an enzyme assay, MP-412 inhibited the EGFR variants and ErbB2 in the nanomolar range with over 100-fold selectivity compared with other kinases, apart from abl and flt-1, which were both moderately sensitive to the compound. In cells, MP-412 inhibited autophosphorylation of EGFR and ErbB2 with IC(50) of 43 and 282 nM, respectively. It also inhibited epidermal growth factor (EGF)-dependent cell proliferation with an IC(50) of 100 nM. Moreover, MP-412 abrogated EGFR signaling in the gefitinib-resistant H1975 cell line, which harbors a double mutation of L858R and T790M in EGFR. In animal studies using cancer xenograft models, MP-412 (30 mg/kg) demonstrated complete inhibition of tumor growth of the A431 and BT-474 cell lines, which overexpress EGFR and ErbB2, respectively. MP-412 suppressed autophosphorylation of EGFR and ErbB2 at the dose corresponding to its antitumor efficacy. When various dosing schedules were applied, MP-412 showed significant effects with daily and every-other-day schedules, but not with a once-weekly schedule, suggesting that frequent dosing is preferable for this compound. Furthermore, MP-412 showed a significant antitumor effect on the ErbB2-overexpressing breast cancer KPL-4 cell line, which is resistant to gefitinib. These studies indicate that MP-412 has potential as a therapeutic agent for the treatment of cancers expressing EGFR and ErbB2, especially those resistant to the first generation of small-molecule inhibitors.	esophagus
[Expression of DNA damage checkpoint mediator 1 and p53-binding protein 1 in human esophageal cancer cell lines TE-1, TE-13, and Eca109].	OBJECTIVE: To observe the expression of DNA damage checkpoint mediator 1 (MDC1) and p53-binding protein 1 (53BP1) at both mRNA and protein levels and their significance in different human esophageal cancer cell lines. METHODS: In 3 human esophageal carcinoma cell lines, TE-1, TE-13 and Eca109 cells, the expressions of MDC1 and 53BP1 mRNA were detected with RT-PCR, and MDC1 and 53BP1 protein expressions were measured with immunohistochemistry, indirect immunofluorescence and Western blotting, respectively. RESULTS AND CONCLUSIONS: MDC1 and 53BP1 expressions were observed for the first time in human esophageal carcinoma cell lines TE-1,TE-13 and Eca109 cells, at both the mRNA and protein levels. The expressions of MDC1 and 53BP1 proteins may be implicated in the radiosensitivity of human esophageal carcinoma.	esophagus
[Esophago-bronchial fistula confirmed with bronchoscopy utilized an indocyanine green].	The patient was a 54-year-old female with both headache and vomit presented to the emergency room. Endoscopic examination revealed an advanced esophageal cancer located on the middle thoracic esophagus. Histological analysis revealed squamous cell carcinoma. The clinical stage was diagnosed as T4N2M0 and this case was treated by the chemoradiation. She presented progressive moist cough after chemoradiotherapy. Esophagography demonstrated esophago-bronchial fistula (EBF). EBF was not detected by routine broncoscopy. To confirm fistula, we were performed the bronchoscopy which utilized an indocyanine green. Contrast media colored green were over from the superior segmental bronchus in a bronchoscope. The bronchoscope which utilized an indocyanine green is effective for EBF.	esophagus
Clinical significance of perioperative immunonutrition for patients with esophageal cancer.	BACKGROUND: We hypothesized that preoperative and/or postoperative enteral immune-enhanced formulas that are supplemented with arginine, omega-3 fatty acids, and RNA may reduce postoperative complications in patients undergoing esophagectomy for thoracic esophageal squamous cell carcinoma (ESCC). METHODS: Forty patients who underwent esophagectomy were divided into three groups: group A (n = 20) received a control enteral diet (Erental) through the jejunostomy after surgery. group B (n = 6) received an enteral diet supplemented with immune-enhancing substrates (Impact) containing arginine, omega-3 fatty acids, and RNA after surgery. group C (n = 14) received the impact before and after surgery. RESULTS: Lymphocyte counts in group C on postoperative day (POD) 7 were somewhat higher than that in group A (p = 0.07) and significantly higher than in group B (p = 0.03). Furthermore the incidence of incisional wound infection in group C was significantly lower than that in group A (p = 0.03). Moreover, the duration of postoperative systemic inflammatory response syndrome (SIRS) was significantly shorter in group C than in group A (p < 0.05). CONCLUSIONS: This study reveals that the perioperative immune-enhanced formula may be superior to postoperative control enteral formulas in terms of reducing surgical wound infection and postoperative SIRS, which may result in serious postoperative complications for patients who have undergone esophagectomy.	esophagus
Reactive oxygen species mediated apoptosis of esophageal cancer cells induced by marine triprenyl toluquinones and toluhydroquinones.	Marine invertebrates, algae, and microorganisms are prolific producers of novel secondary metabolites. Some of these secondary metabolites have the potential to be developed as chemotherapeutic agents for the treatment of a wide variety of diseases, including cancer. We describe here the mechanism leading to apoptosis of esophageal cancer cell lines in the presence of triprenylated toluquinones and toluhydroquinones originally isolated from the Arminacean nudibranch Leminda millecra. Triprenylated toluquinone-induced and toluhydroquinone-induced cell death is mediated via apoptosis after a cell cycle block. Molecular events include production of reactive oxygen species (ROS), followed by induction and activation of c-Jun (AP1) via c-Jun-NH2-kinase-mediated and extracellular signal-regulated kinase-mediated pathways. Partial resistance to these compounds could be conferred by the ROS scavengers Trolox and butylated hydroxyanisol, a c-Jun-NH2-kinase inhibitor, and inhibition of c-Jun with a dominant negative mutant (TAM67). Interestingly, the levels of ROS produced varied between compounds, but was proportional to the ability of each compound to kill cells. Because cancer cells are often more susceptible to ROS, these compounds present a plausible lead for new antiesophageal cancer treatments and show the potential of the South African marine environment to provide new chemical entities with potential clinical significance.	esophagus
Barrett's oesophagus: intestinal metaplasia is not essential for cancer risk.	OBJECTIVE: Barrett's oesophagus is the main identifiable risk factor for oesophageal adenocarcinoma. It has been suggested that only patients with intestinal metaplasia are at risk of cancer, but the British Society of Gastroenterology (BSG) guidelines suggest that glandular mucosa is all that is needed. The aim of this study was to quantify the risk of adenocarcinoma in columnar-lined lower oesophagus, with or without specialized intestinal metaplasia. MATERIAL AND METHODS: All patients who had endoscopic biopsies of the lower oesophagus between 1980 and 1994 in a single-centre teaching hospital were included in the study. All histological specimens were re-examined and reported according to whether they contained columnar epithelial-lined lower oesophagus, glandular mucosa, with or without intestinal metaplasia. The primary outcome measure was the development of adenocarcinoma. RESULTS: In total, 712 patients were identified. Of these, 379 (55.1%) were found to have specialized intestinal metaplasia (SIM), and the remaining 309 (44.9%, p = NS) were reported as having glandular mucosa (GM). The median follow-up for patients was 12 years (range 8-20 years). Twenty-eight patients went on to develop adenocarcinoma (4.1%) during the follow-up period - 17 in the SIM group (4.5%) and 11 in the GM group (3.6%, p =NS). The oesophageal malignancy rate was 0.34% per year (SIM 0.37%, GM 0.30%; p =NS). CONCLUSIONS: Patients who have glandular mucosa on biopsy without intestinal metaplasia have a similar cancer risk to those with specialized intestinal metaplasia.	esophagus
Bile acids induce overexpression of homeobox gene CDX-2 and vascular endothelial growth factor (VEGF) in human Barrett's esophageal mucosa and adenocarcinoma cell line.	OBJECTIVE: Barrett's esophagus (BE) is an acquired precancerous condition that develops from mucosal injury incurred after chronic gastroesophageal acid and bile reflux. The mechanism of progression of carcinogenesis in BE is still not fully understood. Recently, the role of bile acids and the homeobox gene transcription factor CDX-2 has been suggested in the pathogenesis of BE. The aims of the present study were 1) to compare the mRNA and protein expression of CDX-2 in biopsies obtained from patients with BE and normal squamous epithelium and 2) to study the effect of two different bile salts, ursodeoxycholic acid (UDCA) and deoxycholic acid (DCA), on the mRNA expression of CDX-2 and vascular endothelial growth factor (VEGF) in Barrett's the adenocarcinoma cell line (OE-33). MATERIAL AND METHODS: CDX-2 expression was measured in Barrett's mucosa and normal esophageal mucosa obtained from 15 patients with BE histologically diagnosed by immunohistochemistry, Western blot, and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). In in vitro experiments, OE-33 cells were incubated with DCA (100 microM) and UDCA (100 microM) in neutral and shortly acidified media (pulse acidification). The expression of CDX-2 and VEGF was assessed by quantitative RT-PCR. RESULTS: Both mRNA and protein expression of CDX-2 were significantly up-regulated in Barrett's mucosa as compared to normal esophageal mucosa. In neutral medium, OE-33 cells showed an increase in CDX-2 expression after incubation with DCA or UDCA. After short acidification of the medium, expression of CDX-2 in OE-33 cells was significantly higher than that in cells incubated in neutral pH. The addition of DCA and UDCA did not cause any further alteration in CDX-2 expression. In neutral and acidified medium, VEGF mRNA expression was only significantly up-regulated by DCA, but not by UDCA. CONCLUSIONS: Bile acids, especially in acidic medium, increase expression of CDX-2. DCA appears to be a stronger stimulant of the expression of VEGF than UDCA in the Barrett's carcinoma cell line, indicating a stronger carcinogenic potential of this bile salt.	esophagus
[Study on the association between STK15 Phe31Ile polymorphisms and esophageal squamous cell carcinoma].	OBJECTIVE: To study the relation between single nucleotide polymorphism(SNP) at the 91T-->A(Phe31Ile) position of the STK15 gene and the susceptibility of esophageal squamous cell carcinoma (ESCC) in She county--a ESCC high incidence region in North China. METHODS: Polymerase-chain reaction(PCR)-restriction fragment length polymorphism (RFLP) analysis was used to detect the genotypes of STKl5 Phe31Ile(91T-->A) SNP, and the samples came from 296 ESCC patients and 302 healthy controls. RESULTS: The risk of ESCC significantly increased in the group which had been smoking or having a family history of upper gastrointestinal cancer (UGIC) (the OR = 1.68 and 1.77, 95% CI: 1.34-2.10 and 1.44-2.19, respectively). Rates of the three genotypes (Phe/Phe, Phe/Ile, Ile/Ile) of the STK15 Phe31Ile (91T-->A) SNPs in ESCC patients were 11.5%, 34.8% and 53.7%, respectively, and were not significantly different from that in the healthy group (11.9%, 36.8% and 51.3%) (chi2 = 0.35, P = 0.84). When compared to Phe/Phe genotype, Phe/Ile and Ile/Ile of STK15 91T-->A(Phe31Ile)did not show effect on the risk of ESCC according to the odds ratio results which were 0.98 (95% CI: 0.57-1.69) and 1.09 (0.65-1.82) respectively. STK15 91T-->A (Phe31Ile) SNP also did not significantly influence on the development of ESCC even the samples were stratified by sex, smoking status and family history of upper gastrointestinal cancer. CONCLUSION: The STK15 Phe31Ile(91T-->A) polymorphisms seemed irrelevant with the risk of ESCC in She county.	esophagus
Health-related quality of life among patients with adenocarcinoma of the gastro-oesophageal junction treated by gastrectomy or oesophagectomy.	BACKGROUND: Tumours of the gastro-oesophageal junction may be resected by total gastrectomy (TG) or transthoracic oesophagectomy (TTO). This study compared health-related quality of life (HRQL) following these procedures. METHODS: Prospective clinical and HRQL data (European Organization for Research and Treatment of Cancer QLQ-C30) were collected from 63 consecutive patients (20 TG and 43 TTO) before and 6 months after surgery for Siewert type I-III gastro-oesophageal tumours. RESULTS: Questionnaire response rates exceeded 90 per cent. Patients were similar with respect to disease stage, treatment-related mortality and survival, but those selected for TTO were younger with less co-morbidity than those undergoing TG. These differences were reflected in baseline HRQL scores, which were better in patients selected for TTO. Six months after surgery, however, HRQL showed a greater deterioration after TTO than after TG in terms of role and social function, global quality of life and fatigue. Symptom scores for pain and diarrhoea increased in both groups. CONCLUSION: TTO had a greater negative impact on HRQL than TG for tumours of the gastro-oesophageal junction.	esophagus
Detection of distant metastases in patients with oesophageal or gastric cardia cancer: a diagnostic decision analysis.	Computed tomography (CT) is presently a standard procedure for the detection of distant metastases in patients with oesophageal or gastric cardia cancer. We aimed to determine the additional diagnostic value of alternative staging investigations. We included 569 oesophageal or gastric cardia cancer patients who had undergone CT neck/thorax/abdomen, ultrasound (US) abdomen, US neck, endoscopic ultrasonography (EUS), and/or chest X-ray for staging. Sensitivity and specificity were first determined at an organ level (results of investigations, i.e., CT, US abdomen, US neck, EUS, and chest X-ray, per organ), and then at a patient level (results for combinations of investigations), considering that the detection of distant metastases is a contraindication to surgery. For this, we compared three strategies for each organ: CT alone, CT plus another investigation if CT was negative for metastases (one-positive scenario), and CT plus another investigation if CT was positive, but requiring that both were positive for a final positive result (two-positive scenario). In addition, costs, life expectancy and quality adjusted life years (QALYs) were compared between different diagnostic strategies. CT showed sensitivities for detecting metastases in celiac lymph nodes, liver and lung of 69, 73, and 90%, respectively, which was higher than the sensitivities of US abdomen (44% for celiac lymph nodes and 65% for liver metastases), EUS (38% for celiac lymph nodes), and chest X-ray (68% for lung metastases). In contrast, US neck showed a higher sensitivity for the detection of malignant supraclavicular lymph nodes than CT (85 vs 28%). At a patient level, sensitivity for detecting distant metastases was 66% and specificity was 95% if only CT was performed. A higher sensitivity (86%) was achieved when US neck was added to CT (one-positive scenario), at the same specificity (95%). This strategy resulted in lower costs compared to CT only, at an almost similar (quality adjusted) life expectancy. Slightly higher specificities (97-99%) were achieved if liver and/or lung metastases found on CT, were confirmed by US abdomen or chest X-ray, respectively (two-positive scenario). These strategies had only slightly higher QALYs, but substantially higher costs. The combination of CT neck/thorax/abdomen and US neck was most cost-effective for the detection of metastases in patients with oesophageal or gastric cardia cancer, whereas the performance of CT only had a lower sensitivity for metastases detection and higher costs. The role of EUS seems limited, which may be due to the low number of M1b celiac lymph nodes detected in this series. It remains to be determined whether the application of positron emission tomography will further increase sensitivities and specificities of metastases detection without jeopardising costs and QALYs.	esophagus
"Management of intractable nausea and vomiting in patients at the end of life: ""I was feeling nauseous all of the time . . . nothing was working""."	Nausea and vomiting, symptoms that occur commonly near the end of life, represent a substantial source of physical and psychological distress for patients and families. In the context of the case of Mr Q, a 50-year-old man with metastatic esophageal cancer admitted to the hospital with intractable nausea and vomiting, we review the evaluation and treatment of this symptom complex. A thorough history and physical examination are essential first steps in the management of these patients because they define the severity of the symptoms and clues to their underlying etiology. Once the most likely cause is determined, the clinician discerns the mechanism, specific transmitters, and receptors by which this etiology is triggering nausea and vomiting. Subsequent pharmacological management focuses on prescribing the appropriate antagonist to the implicated receptors. If symptoms are refractory despite adequate dosage and around-the-clock prophylactic administration, an empirical trial combining several therapies to block multiple emetic pathways should be attempted. Less traditional agents are also discussed, although evidence for their use is limited. Often, oral administration of medication is not feasible and alternate routes such as rectal suppositories, subcutaneous infusions, and orally dissolvable tablets should be considered. Using this step-wise approach, nausea and vomiting can be successfully managed in most patients at the end of life.	esophagus