|Cancer of the Oesophagus|
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Cancer of the Oesophagus
The oesophagus (US spelling: esophagus) or gullet is a long hollow muscular tube which connects the throat to the stomach. Oesophageal cancer is a disease where malignant (cancerous) cells arise in the tissues of the oesophagus. The most common symptom is difficulty in swallowing. It can also be associated with weight loss and sometimes pain or discomfort behind the breast bone or in the back - these symptoms should be checked by a doctor but not are sure signs of cancer. There are two main types of oesophageal cancer (depending on how the cells appear under the microscope); approximately half are classed as "squamous cell carcinomas" and half as "adenocarcinomas". People with frequent gastric reflux leading to Barrett's Oesophagus have an increased risk of developing oesophageal cancer.
In 2010, 8,477 people in the UK were diagnosed with oesophageal cancer (Source: Cancer Research UK)
This page shows only UK resources. For a more extensive list of resources from around the world see CancerIndex: Cancer of the Oesophagus Information for Patients and the Public
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MeSH term: Esophageal Neoplasms
US National Library of Medicine
PubMed has over 22 million citations for biomedical literature from MEDLINE, life science journals, and online books. Constantly updated.
Showing publications with corresponding authors from the UK (Source: PubMed).
Minimally invasive and robotic esophagectomy: Evolution and evidence.
J Surg Oncol. 2016; 114(6):731-735 [PubMed] Related Publications
Worldwide Esophageal Cancer Collaboration: pathologic staging data.
Dis Esophagus. 2016; 29(7):724-733 [PubMed] Related Publications
An Analysis of Plan Robustness for Esophageal Tumors: Comparing Volumetric Modulated Arc Therapy Plans and Spot Scanning Proton Planning.
Int J Radiat Oncol Biol Phys. 2016; 95(1):199-207 [PubMed] Free Access to Full Article Related Publications
METHODS AND MATERIALS: For 21 patients, SIB plans with a physical dose prescription of 2 Gy or 2.5 Gy/fraction in 25 fractions to planning target volume (PTV)50Gy or PTV62.5Gy (primary tumor with 0.5 cm margins) were created and evaluated for robustness to random setup errors and proton range errors. Dose-volume metrics were compared for the optimal and uncertainty plans, with P<.05 (Wilcoxon) considered significant.
RESULTS: SFO reduced the mean lung dose by 51.4% (range 35.1%-76.1%) and the mean heart dose by 40.9% (range 15.0%-57.4%) compared with VMAT. Proton plan robustness to a 3.5% range error was acceptable. For all patients, the clinical target volume D98 was 95.0% to 100.4% of the prescribed dose and gross tumor volume (GTV) D98 was 98.8% to 101%. Setup error robustness was patient anatomy dependent, and the potential minimum dose per fraction was always lower with SFO than with VMAT. The clinical target volume D98 was lower by 0.6% to 7.8% of the prescribed dose, and the GTV D98 was lower by 0.3% to 2.2% of the prescribed GTV dose.
CONCLUSIONS: The SFO plans achieved significant sparing of normal tissue compared with the VMAT plans for midesophageal cancer. The target dose coverage in the SIB proton plans was less robust to random setup errors and might be unacceptable for certain patients. Robust optimization to ensure adequate target coverage of SIB proton plans might be beneficial.
Characterising timing and pattern of relapse following surgery for localised oesophagogastric adenocarcinoma: a retrospective study.
BMC Cancer. 2016; 16:112 [PubMed] Free Access to Full Article Related Publications
METHODS: We performed a retrospective review of all patients with OGA who had undergone surgery with radical intent at the Royal Marsden between January 2001 and December 2010.
RESULTS: Of the 360 patients with OGA who underwent potentially curative surgery, 100/214 patients (47%) with oesophageal/gastro-oesophageal junction (GOJ) adenocarcinoma and 47/146 patients (32%) with gastric adenocarcinoma developed recurrent disease. 51, 79 and 92% of relapses occurred within 1, 2 and 3 years respectively and the majority of patients relapsed at distant sites. Of the patients who relapsed, 67% (67/100) with oesophageal/GOJ adenocarcinoma and 72% of patients with gastric cancer (34/47) were symptomatic at the time of relapse. The majority of asymptomatic relapses were first detected by a rise in tumour markers. There was no difference in disease-free survival between asymptomatic and symptomatic patients, but asymptomatic patients were more likely to receive further treatment and had a longer survival beyond relapse.
CONCLUSION: The majority of relapses occur within the first 3 years and at distant sites. Monitoring of tumour markers should be considered as part of a surveillance program.
Association Between Statin Use After Diagnosis of Esophageal Cancer and Survival: A Population-Based Cohort Study.
Gastroenterology. 2016; 150(4):854-65.e1; quiz e16-7 [PubMed] Related Publications
METHODS: We identified a cohort of 4445 men and women in the United Kingdom diagnosed with esophageal cancer from January 2000 through November 2009 using the General Practice Research Database. The National Cancer Registry and Office of National Statistics datasets established the histologic subtype and cancer-specific mortality, respectively. Cox proportional hazard regression analysis with time-dependent exposures estimated the association between statin use after diagnosis and esophageal cancer-specific and all-cause mortality.
RESULTS: The median survival time of the entire cohort was 9.2 months (interquartile range [IQR], 3.7-23.2 mo). Among subjects who used statins after a diagnosis of esophageal cancer, the median survival time was 14.9 months (IQR, 7.1-52.3 mo) compared with 8.1 months for nonusers (IQR, 3.3-20 mo). In the entire cohort, statin use after diagnosis was associated with a decreased risk of esophageal cancer-specific mortality (adjusted hazard ratio [HR], 0.62; 95% confidence interval [CI], 0.44-0.86) and all-cause mortality (HR, 0.67; 95% CI, 0.58-0.77). In patients with esophageal adenocarcinoma, statin use after diagnosis was associated with a decreased risk of esophageal cancer-specific mortality (HR, 0.61; 95% CI 0.38-0.96) and all-cause mortality (HR, 0.63; 95% 0.43-0.92). This effect was not observed in patients with esophageal squamous cell carcinoma. There was no evidence for effect modification of these associations with statin use before the cancer diagnosis.
CONCLUSIONS: In a large population-based cohort, statin use after a diagnosis of esophageal adenocarcinoma, but not esophageal squamous cell carcinoma, was associated with reduced esophageal cancer-specific and all-cause mortality.
A model for predicting individuals' absolute risk of esophageal adenocarcinoma: Moving toward tailored screening and prevention.
Int J Cancer. 2016; 138(12):2813-9 [PubMed] Related Publications
Lapatinib in Combination With Capecitabine Plus Oxaliplatin in Human Epidermal Growth Factor Receptor 2-Positive Advanced or Metastatic Gastric, Esophageal, or Gastroesophageal Adenocarcinoma: TRIO-013/LOGiC--A Randomized Phase III Trial.
J Clin Oncol. 2016; 34(5):443-51 [PubMed] Related Publications
PATIENTS AND METHODS: Patients with HER2-positive advanced gastroesophageal adenocarcinoma were randomly assigned at a one-to-one ratio to CapeOx plus lapatinib 1,250 mg or placebo daily. Primary end point was overall survival (OS) in patients with centrally confirmed HER2 amplification in the primary efficacy population.
RESULTS: A total of 545 patients were randomly assigned, and 487 patients comprised the primary efficacy population. Median OS in the lapatinib and placebo arms was 12.2 (95% CI, 10.6 to 14.2) and 10.5 months (95% CI, 9.0 to 11.3), respectively, which was not significantly different (hazard ratio, 0.91; 95% CI, 0.73 to 1.12). Median progression-free survival in the lapatinib and placebo arms was 6.0 (95% CI, 5.6 to 7.0) and 5.4 months (95% CI, 4.4 to 5.7), respectively (hazard ratio, 0.82; 95% CI, 0.68 to 1.00; P = .0381). Response rate was significantly higher in the lapatinib arm: 53% (95% CI, 46.4 to 58.8) compared with 39% (95% CI, 32.9 to 45.3) in the placebo arm (P = .0031). Preplanned exploratory subgroup analyses showed OS in the lapatinib arm was prolonged in Asian and younger patients. No correlation was observed between HER2 immunohistochemistry status and survival. There were increased toxicities in the lapatinib arm, particularly diarrhea.
CONCLUSION: Addition of lapatinib to CapeOx did not increase OS in patients with HER2-amplified gastroesophageal adenocarcinoma. There were clear differences in the effect of lapatinib depending on region and age. Future studies could examine this correlation.
Aspirin and other non-steroidal anti-inflammatory drug prescriptions and survival after the diagnosis of head and neck and oesophageal cancer.
Cancer Epidemiol. 2015; 39(6):1015-22 [PubMed] Related Publications
METHODS: An observational cohort study of patients with UADT cancer was undertaken using Primary Care Clinical Informatics Unit (PCCIU) database of electronic medical records in Scotland. Information was available on all prescriptions of aspirin and other NSAIDs before and after diagnosis. The main outcome measure was all-cause mortality. Cox regression was used for statistical data analysis.
RESULTS: There were 2392 patients diagnosed with UADT cancer between 1996 and 2010. Mean age of patients was 66 years (SD 12) and most were male (63%). Median survival in head and neck (HNC) patients was 94 months, while median survival in oesophageal cancer patients was 10 months. For HNC improved survival was observed with aspirin prescription (ever vs never hazard ratio (HR) 0.56 95% Confidence Interval (CI) 0.44, 0.71), there was no association with Cyclooxygenase 2 Inhibitors (COX-2) prescriptions. Improved survival was observed with other NSAIDs prescription (ever vs never HR 0.74 95% CI 0.60, 0.90). For oesophageal cancer patients, improved survival was observed with aspirin prescriptions (ever vs never HR 0.54 95% CI 0.45, 0.64), COX-2 prescriptions (HR 0.78 95% CI 0.62, 0.98) and other NSAIDs (HR 0.67 95% CI 0.56, 0.80).
CONCLUSIONS: Aspirin and other NSAIDs prescriptions after diagnosis are associated with a reduced all-cause mortality in UADT cancer patients.
Regulation of cellular sphingosine-1-phosphate by sphingosine kinase 1 and sphingosine-1-phopshate lyase determines chemotherapy resistance in gastroesophageal cancer.
BMC Cancer. 2015; 15:762 [PubMed] Free Access to Full Article Related Publications
METHODS: Cell lines were selected for resistance to oxaliplatin, cisplatin and docetaxel and gene expression examined using Affymetrix Exon 1.0 ST arrays. Leads were validated by qRT-PCR and HPLC of tumour metabolites. Protein expression and pharmacological inhibition of lead target SPHK1 was evaluated in independent cell lines, and by immunohistochemistry in gastroesophageal cancer patients.
RESULTS: Genes with differential expression in drug resistant cell lines compared to the parental cell line they were derived from, were identified for each drug resistant cell line. Biological pathway analysis of these gene lists, identified over-represented pathways, and only 3 pathways - lysosome, sphingolipid metabolism and p53 signalling- were identified as over-represented in these lists for all three cytotoxic drugs investigated. The majority of genes differentially expressed in chemoresistant cell lines from these pathways, were involved in metabolism of glycosphingolipids and sphingolipids in lysosomal compartments suggesting that sphingolipids might be important mediators of cytotoxic drug resistance in gastroeosphageal cancers . On further investigation, we found that drug resistance (IC50) was correlated with increased sphingosine kinase 1(SPHK1) mRNA and also with decreased sphingosine-1-phosphate lysase 1(SGPL1) mRNA. SPHK1 and SGPL1 gene expression were inversely correlated. SPHK1:SGPL1 ratio correlated with increased cellular sphingosine-1-phosphate (S1P), and S1P correlated with drug resistance (IC50). High SPHK1 protein correlated with resistance to cisplatin (IC50) in an independent gastric cancer cell line panel and with survival of patients treated with chemotherapy prior to surgery but not in patients treated with surgery alone. Safingol a SPHK1 inhibitor, was cytotoxic as a single agent and acted synergistically with cisplatin in gastric cancer cell lines.
CONCLUSION: Agents that inhibit SPHK1 or S1P could overcome cytotoxic drug resistance in gastroesophageal cancer. There are several agents in early phase human trials including Safingol that could be combined with chemotherapy or used in patients progressing after chemotherapy.
The Male Predominance in Esophageal Adenocarcinoma.
Clin Gastroenterol Hepatol. 2016; 14(3):338-347.e1 [PubMed] Related Publications
Variations among 5 European countries for curative treatment of resectable oesophageal and gastric cancer: A survey from the EURECCA Upper GI Group (EUropean REgistration of Cancer CAre).
Eur J Surg Oncol. 2016; 42(1):116-22 [PubMed] Related Publications
METHODS: Participating countries presented data using common data items describing patients', disease, strategies, and outcome characteristics. Patients treated with curative surgery for squamous cell carcinoma (SCC) or adenocarcinoma (ACA) were included.
RESULTS: United Kingdom, the Netherlands, France, Spain and Ireland participated. There were differences in data source ranging from national registries to large collaborative groups. 4668 oesophagogastric cancer cases over a 12 months period were included. The predominant histological type was ACA. Disease stage tended to be earlier in France and Ireland. In oesophageal and junctional cancers neoadjuvant chemoradiotherapy was preferred in the Netherlands and Ireland contrasting with chemotherapy in the UK and France. All countries used perioperative chemotherapy in gastric cancer but 1/3 of patients received this treatment. The mean R0 resection rate was 86% for oesophageal and junctional resections and 88% for gastric resections. Postoperative mortality varied from 1% to 7%.
CONCLUSION: This European survey shown that implementing a uniform treatment and outcome data format of oesophagogastric cancer is feasible. It identified differences in disease presentation, treatment approaches and outcome, which need to be investigated, especially by increasing the number of participating countries. Future comparisons will facilitate developments in treatment for the benefit of patient outcomes.
Africa's Oesophageal Cancer Corridor: Geographic Variations in Incidence Correlate with Certain Micronutrient Deficiencies.
PLoS One. 2015; 10(10):e0140107 [PubMed] Free Access to Full Article Related Publications
METHODS: Across Africa we assessed associations between a country's oesophageal cancer incidence rate and food balance sheet-derived estimates of mean national dietary supplies of 7 nutrients: calcium (Ca), copper (Cu), iron (Fe), iodine (I), magnesium (Mg), selenium (Se) and zinc (Zn). We included 32 countries which had estimates of dietary nutrient supplies and of better-quality GLOBCAN 2012 cancer incidence rates. Bayesian hierarchical Poisson lognormal models were used to estimate incidence rate ratios for oesophageal cancer associated with each nutrient, adjusted for age, gender, energy intake, phytate, smoking and alcohol consumption, as well as their 95% posterior credible intervals (CI). Adult dietary deficiencies were quantified using an estimated average requirements (EAR) cut-point approach.
RESULTS: Adjusted incidence rate ratios for oesophageal cancer associated with a doubling of mean nutrient supply were: for Fe 0.49 (95% CI: 0.29-0.82); Mg 0.58 (0.31-1.08); Se 0.40 (0.18-0.90); and Zn 0.29 (0.11-0.74). There were no associations with Ca, Cu and I. Mean national nutrient supplies exceeded adult EARs for Mg and Fe in most countries. For Se, mean supplies were less than EARs (both sexes) in 7 of the 10 highest oesophageal cancer ranking countries, compared to 23% of remaining countries. For Zn, mean supplies were less than the male EARs in 8 of these 10 highest ranking countries compared to in 36% of other countries.
CONCLUSIONS: Ecological associations are consistent with the potential role of Se and/or Zn deficiencies in squamous cell oesophageal cancer in Africa. Individual-level analytical studies are needed to elucidate their causal role in this setting.
Marital status, education, and income in relation to the risk of esophageal and gastric cancer by histological type and site.
Cancer. 2016; 122(2):207-12 [PubMed] Related Publications
METHODS: A nationwide, Swedish population-based cohort study from 1991 to 2010 included individuals who were 50 years old or older. Data on exposures, covariates, and outcomes were obtained from well-maintained registers. Four esophagogastric tumor subtypes were analyzed in combination and separately: esophageal adenocarcinoma, esophageal squamous cell carcinoma, cardia adenocarcinoma, and noncardia gastric adenocarcinoma. Poisson regression was used to estimate incidence rate ratios (IRRs) and 95% confidence intervals (CIs). Analyses were stratified by sex and adjusted for confounders.
RESULTS: Among 4,734,227 participants (60,634,007 person-years), 24,095 developed esophageal or gastric cancer. In comparison with individuals in a long marriage, increased IRRs were found among participants who were in a shorter marriage or were never married, remarried, divorced, or widowed. These associations were indicated for each tumor subtype but were generally stronger for esophageal squamous cell carcinoma. Higher education and income were associated with decreased IRRs in a seemingly dose-response manner and similarly for each subtype. In comparison with the completion of only primary school, higher tertiary education rendered an IRR of 0.64 (95% CI, 0.60-0.69) for men and an IRR of 0.68 (95% CI, 0.61-0.75) for women. Comparing participants in the highest and lowest income brackets (highest 20% vs lowest 20%) revealed an IRR of 0.74 (95% CI, 0.70-0.79) for men and an IRR of 0.83 (95% CI, 0.76-0.91) for women.
CONCLUSIONS: Divorce, widowhood, living alone, low educational attainment, and low income increase the risk of each subtype of esophageal and gastric cancer. These associations require attention when high-risk individuals are being identified. Cancer 2016;122:207-212. © 2015 American Cancer Society.
Oral Bisphosphonate Exposure and the Risk of Upper Gastrointestinal Cancers.
PLoS One. 2015; 10(10):e0140180 [PubMed] Free Access to Full Article Related Publications
Cancers prevented in Australia in 2010 through the consumption of aspirin.
Aust N Z J Public Health. 2015; 39(5):414-7 [PubMed] Free Access to Full Article Related Publications
METHODS: We calculated the Prevented Fraction (PF) of colorectal and oesophageal cancers using standard formulae. The PF is the proportion of the hypothetical total load of cancer in the population that was prevented by exposure to aspirin. The formula incorporates estimates of the prevalence of aspirin use in Australian adult populations, the relative risks associated with aspirin use and cancer incidence.
RESULTS: An estimated 335 colorectal cancers, 22 oesophageal adenocarcinomas and 29 oesophageal squamous cell carcinomas (SCC) were potentially prevented due to daily aspirin use. These figures equate to 2.2%, 3.1% and 5.4% of all colorectal cancers, oesophageal adenocarcinomas and oesophageal SCCs, respectively, that would otherwise have occurred but were potentially avoided due to the daily use of aspirin pertaining in the Australian population.
CONCLUSIONS: At current levels of consumption, a small but measurable reduction in cancer incidence can be attributed to daily aspirin use.
IMPLICATIONS: Assuming the benefits outweigh the harms of known gastrointestinal toxicity and other hazards, aspirin use may be considered for some people to prevent the development of particular gastrointestinal cancers.
Corneal Confocal Microscopy Detects Small Fibre Neuropathy in Patients with Upper Gastrointestinal Cancer and Nerve Regeneration in Chemotherapy Induced Peripheral Neuropathy.
PLoS One. 2015; 10(10):e0139394 [PubMed] Free Access to Full Article Related Publications
Polymorphisms in genes in the androgen pathway and risk of Barrett's esophagus and esophageal adenocarcinoma.
Int J Cancer. 2016; 138(5):1146-52 [PubMed] Free Access to Full Article Related Publications
Polymorphisms in Genes of Relevance for Oestrogen and Oxytocin Pathways and Risk of Barrett's Oesophagus and Oesophageal Adenocarcinoma: A Pooled Analysis from the BEACON Consortium.
PLoS One. 2015; 10(9):e0138738 [PubMed] Free Access to Full Article Related Publications
METHODS: This genetic-epidemiological study pooled 14 studies from three continents, Australia, Europe, and North America. Polymorphisms in 3 key genes coding for the oestrogen pathway (receptor alpha (ESR1), receptor beta (ESR2), and aromatase (CYP19A1)), and 3 key genes of the oxytocin pathway (the oxytocin receptor (OXTR), oxytocin protein (OXT), and cyclic ADP ribose hydrolase glycoprotein (CD38)), were analysed using a gene-based approach, versatile gene-based test association study (VEGAS).
RESULTS: Among 1508 OAC patients, 2383 BO patients, and 2170 controls, genetic variants within ESR1 were associated with BO in males (p = 0.0058) and an increased risk of OAC and BO combined in males (p = 0.0023). Genetic variants within OXTR were associated with an increased risk of BO in both sexes combined (p = 0.0035) and in males (p = 0.0012). We followed up these suggestive findings in a further smaller data set, but found no replication. There were no significant associations between the other 4 genes studied and risk of OAC, BO, separately on in combination, in males and females combined or in males only.
CONCLUSION: Genetic variants in the oestrogen receptor alpha and the oxytocin receptor may be associated with an increased risk of BO or OAC, but replication in other large samples are needed.
Acetic acid chromoendoscopy for the diagnosis of early neoplasia and specialized intestinal metaplasia in Barrett's esophagus: a meta-analysis.
Gastrointest Endosc. 2016; 83(1):57-67.e1 [PubMed] Related Publications
METHODS: We performed a meta-analysis of all primary studies that compared AAC-based diagnoses (index test) with histopathology as the reference standard. The data were extracted on a per-patient, per-area, and per-procedure basis whenever available.
RESULTS: Thirteen prospective studies met the inclusion criteria. For the diagnosis of HGD/EC, the pooled sensitivity, specificity, positive likelihood ratio (LR+), and negative likelihood ratio (LR-) for all included studies (9 studies, 1379 patients) were 0.92 (95% confidence interval [CI], 0.83-0.97), 0.96 (95% CI, 0.85-0.99), 25.0 (95% CI, 5.9-105.3), and 0.08 (95% CI, 0.04-0.18), respectively. Results were not significantly different when considering only studies with a per-patient analysis. For the characterization of SIM, the pooled sensitivity, specificity, LR+, and LR- for all the included studies (8 studies, 516 patients) were 0.96 (95% CI, 0.83-0.99), 0.69 (95% CI, 0.54-0.81), 3.0 (95% CI, 2.0-4.7), and 0.06 (95% CI, 0.01-0.26), respectively. No significant sources of heterogeneity were identified on subgroup analysis.
CONCLUSION: AAC has an overall high diagnostic accuracy for detecting HGD/EC in patients with BE. For SIM characterization, AAC sensitivity is very high but has poor specificity, suggesting that histological confirmation is necessary when AAC is positive.
Pleiotropic analysis of cancer risk loci on esophageal adenocarcinoma risk.
Cancer Epidemiol Biomarkers Prev. 2015; 24(11):1801-3 [PubMed] Free Access to Full Article Related Publications
METHODS: We examined the associations between risks of EA and Barrett's esophagus and 387 SNPs that have been associated with risks of other cancers, by using genotype imputation data on 2,163 control participants and 3,885 (1,501 EA and 2,384 Barrett's esophagus) case patients from the Barrett's and Esophageal Adenocarcinoma Genetic Susceptibility Study, and investigated effect modification by smoking history, body mass index (BMI), and reflux/heartburn.
RESULTS: After correcting for multiple testing, none of the tested 387 SNPs were statistically significantly associated with risk of EA or Barrett's esophagus. No evidence of effect modification by smoking, BMI, or reflux/heartburn was observed.
CONCLUSIONS: Genetic risk variants for common cancers identified from GWAS appear not to be associated with risks of EA or Barrett's esophagus.
IMPACT: To our knowledge, this is the first investigation of pleiotropic genetic associations with risks of EA and Barrett's esophagus.
Predicting Response to Neoadjuvant Chemotherapy with PET Imaging Using Convolutional Neural Networks.
PLoS One. 2015; 10(9):e0137036 [PubMed] Free Access to Full Article Related Publications
In Vitro Radiosensitization of Esophageal Cancer Cells with the Aminopeptidase Inhibitor CHR-2797.
Radiat Res. 2015; 184(3):259-65 [PubMed] Related Publications
Analysis of dysplasia in patients with Barrett's esophagus based on expression pattern of 90 genes.
Gastroenterology. 2015; 149(6):1511-1518.e5 [PubMed] Related Publications
METHODS: We performed a stringent histologic assessment of 150 frozen esophageal tissues samples collected from 4 centers in the United Kingdom (from 2000 through 2006). The following samples with homogeneous diagnoses were selected for gene expression profiling: 28 from patients with nondysplastic BE, 10 with low-grade dysplasia, 13 with high-grade dysplasia (HGD), and 8 from patients with esophageal adenocarcinoma. A leave-one-out cross-validation analysis was used identify a gene expression signature associated with HGD vs nondysplastic BE. Functional pathways associated with gene signature sets were identified using the MetaCore analysis. Gene expression signature sets were validated using gene expression data on BE and esophageal adenocarcinoma accessed through National Center for Biotechnology Information Gene Expression Omnibus, as well as a separate set of samples (n = 169) collected from patients who underwent endoscopy in the United Kingdom or the Netherlands and analyzed histologically.
RESULTS: We identified an expression pattern of 90 genes that could separate nondysplastic BE tissues from those with HGD (P < .0001). Genes in a pathway regulated by retinoic acid-regulated nuclear protein made the largest contribution to this gene set (P < .0001); the transcription factor MYC regulated at least 30% of genes within the signature (P < .0001). In the National Center for Biotechnology Information Gene Expression Omnibus validation set, the signature separated nondysplastic BE samples from esophageal adenocarcinoma samples (P = .0012). In the UK and Netherlands validation cohort, the signature identified dysplastic tissues with an area under the curve value of 0.87 (95% confidence interval: 0.82-0.93). Of samples with low-grade dysplasia (LGD), 64% were considered high risk according to the 90-gene signature; these patients had a higher rate of disease progression than those with a signature categorized as low risk (P = .047).
CONCLUSIONS: We identified an expression pattern of 90 genes in esophageal tissues of patients with BE that was associated with low- or high-risk for disease progression. This pattern might be used in combination with histologic analysis of biopsy samples to stratify patients for treatment. It would be most beneficial for analysis of patients without definitive evidence of HGD but for whom early endoscopic intervention is warranted.
MicroRNA-330-5p as a Putative Modulator of Neoadjuvant Chemoradiotherapy Sensitivity in Oesophageal Adenocarcinoma.
PLoS One. 2015; 10(7):e0134180 [PubMed] Free Access to Full Article Related Publications
Salvage Surgery After Chemoradiotherapy in the Management of Esophageal Cancer: Is It a Viable Therapeutic Option?
J Clin Oncol. 2015; 33(33):3866-73 [PubMed] Related Publications
PATIENTS AND METHODS: Data from consecutive adult patients undergoing resection for esophageal cancer in 30 European centers from 2000 to 2010 were collected. First, groups undergoing SALV (n = 308) and neoadjuvant chemoradiotherapy followed by planned esophagectomy (NCRS; n = 540) were compared. Second, patients who benefited from SALV for persistent (n = 234) versus recurrent disease (n = 74) were compared. Propensity score matching and multivariable analyses were used to compensate for differences in some baseline characteristics.
RESULTS: SALV versus NCRS groups: In-hospital mortality was similar in both groups (8.4% v 9.3%). The only significant differences in complications were seen for anastomotic leak (17.2% v 10.7%; P = .007) and surgical site infection, which were both more frequent in the SALV group. At 3 years, groups had similar overall (43.3% v 40.1%; P = .542) and disease-free survival (39.2% v 32.8%; P = .232) after matching, along with a similar recurrence pattern. Persistent versus recurrent disease groups: There were no significant differences between groups in incidence of in-hospital mortality or major complications. At 3 years, overall (40.9% v 56.2%; P = .046) and disease-free survival (36.6% v 51.6%; P = .095) were lower in the persistent disease group.
CONCLUSION: The results of this large multicenter study from the modern era suggest that SALV can offer acceptable short- and long-term outcomes in selected patients at experienced centers. Persistent cancer after definitive chemoradiotherapy seems to be more biologically aggressive, with poorer survival compared with recurrent cancer.
Significance of Microscopically Incomplete Resection Margin After Esophagectomy for Esophageal Cancer.
Ann Surg. 2016; 263(4):712-8 [PubMed] Related Publications
METHODS: Data were collected from 30 European centers from 2000 to 2010. Patients with an R1 resection margin (n = 242) were compared with those with an R0 margin (n = 2573) in terms of short- and long-term outcomes. Propensity score matching and multivariable analyses were used to compensate for differences in baseline characteristics.
RESULTS: Independent factors significantly associated with an R1 resection margin included an upper third esophageal tumor location, preoperative malnutrition, and pathological stage III. There were significant differences between the groups in postoperative histology, with an increase in pathological stage III and TRG 4-5 in the R1 group. Total average lymph node harvests were similar between the groups; however, there was an increase in the number of positive lymph nodes seen in the R1 group. Propensity matched analysis confirmed that R1 resection margin was significantly associated with reduced overall survival and increased overall, locoregional, and mixed tumor recurrence. Similar observations were seen in the subgroup that received neoadjuvant chemoradiation. In R1 patients adjuvant therapy improved survival and reduced distant recurrence however failed to affect locoregional recurrence.
CONCLUSIONS: This large multicenter European study provides evidence to support the notion that R1 resection margin is a prognostic indication of aggressive tumor biology with a poor long-term prognosis.
Comparing outcome of radiofrequency ablation in Barrett's with high grade dysplasia and intramucosal carcinoma: a prospective multicenter UK registry.
Endoscopy. 2015; 47(11):980-7 [PubMed] Related Publications
PATIENTS AND METHODS: Prior to RFA, visible lesions and nodularity were removed entirely by EMR. Thereafter, patients underwent RFA every 3 months until all visible Barrett's mucosa was ablated or cancer developed (end points). Biopsies were taken at 12 months or when end points were reached.
RESULTS: A total of 515 patients, 384 with HGD and 131 with IMC, completed treatment. Prior to RFA, EMR was performed for visible lesions more frequently in the IMC cohort than in HGD patients (77 % vs. 47 %; P < 0.0001). The 12-month complete response for dysplasia and intestinal metaplasia were almost identical in the two cohorts (HGD 88 % and 76 %, respectively; IMC 87 % and 75 %, respectively; P = 0.7). Progression to invasive cancer was not significantly different at 12 months (HGD 1.8 %, IMC 3.8 %; P = 0.19). A trend towards slightly worse medium-term durability may be emerging in IMC patients (P = 0.08). In IMC, EMR followed by RFA was definitely associated with superior durability compared with RFA alone (P = 0.01).
CONCLUSION: The Registry reports on endoscopic therapy for Barrett's neoplasia, representing real-life outcomes. Patients with IMC were more likely to have visible lesions requiring initial EMR than those with HGD, and may carry a higher risk of cancer progression in the medium term. The data consolidate the approach to ensuring that these patients undergo thorough endoscopic work-up, including EMR prior to RFA when necessary.
Anastomotic reinforcement with omentoplasty following gastrointestinal anastomosis: A systematic review and meta-analysis.
Surg Oncol. 2015; 24(3):181-6 [PubMed] Related Publications
MiRNA-Related SNPs and Risk of Esophageal Adenocarcinoma and Barrett's Esophagus: Post Genome-Wide Association Analysis in the BEACON Consortium.
PLoS One. 2015; 10(6):e0128617 [PubMed] Free Access to Full Article Related Publications
Dietary intake of minerals and risk of esophageal squamous cell carcinoma: results from the Golestan Cohort Study.
Am J Clin Nutr. 2015; 102(1):102-8 [PubMed] Free Access to Full Article Related Publications
OBJECTIVE: The objective was to evaluate the associations of dietary intake of minerals with risk of esophageal squamous cell carcinoma (ESCC).
DESIGN: We used data from the Golestan Cohort Study, which was launched in a high-risk region for esophageal cancer in Iran. Participants were enrolled in 2004-2008 and were followed to 2014. Intakes of minerals were assessed with a validated food-frequency questionnaire. A Cox proportional hazards model was used to estimate HRs and 95% CIs of ESCC for dietary intakes of selected minerals.
RESULTS: We identified 201 ESCC cases among 47,405 subjects. Calcium intake was significantly inversely associated with the risk of ESCC (HR per 100-mg/d increase: 0.88; 95% CI: 0.81, 0.96; P = 0.005; quartile 4 vs. quartile 1 HR: 0.49; 95% CI: 0.29, 0.82; P-trend = 0.013). Zinc intake was also inversely associated with ESCC, but the quartile association did not reach significance (HR per 1-mg/d increase: 0.87; 95% CI: 0.77, 0.98; P = 0.027; quartile 4 vs. quartile 1 HR: 0.56; 95% CI: 0.28, 1.12; P-trend = 0.097). The relations between dietary intakes of selenium, magnesium, and copper and risk of ESCC were nonlinear (P-nonlinear trend = 0.001, 0.016, and 0.029, respectively). There was no relation between dietary intake of manganese and the risk of ESCC.
CONCLUSION: The results suggest that higher intakes of calcium and zinc are associated with a lower risk of ESCC in a high-risk region of Iran.
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