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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a Swedish nationwide case-control study, gastroesophageal reflux and obesity were identified as strong and independent risk factors for esophageal adenocarcinoma. A moderately strong association was found with adenocarcinoma of the gastric cardia. No significant association was found with squamous cell carcinoma of the esophagus. With increasing duration and severity of reflux symptoms and with increasing body mass index (BMI) the risk increased in a dose-dependent manner. When combined, reflux symptoms and obesity entailed greatly increased risk estimates, with relative risks exceeding 100 compared with persons with neither reflux symptoms nor obesity. However, because adenocarcinoma of the esophagus and gastric cardia are rarities, the absolute risk of developing these tumors was still not high. Our calculations revealed that even in the group with the highest risk, endoscopic surveillance is not readily recommended. Possible reasons for the increasing incidence of adenocarcinoma of the esophagus include 1) a suspected increase in the prevalence of reflux disease; 2) the increasing prevalence of obesity reported in western populations; and 3) the widespread use of medications that relax the lower esophageal sphincter and might cause reflux. All of these hypotheses suffer from inconsistencies that need to be solved before any firm conclusions can be drawn concerning the reasons for the increasing incidence of esophageal adenocarcinoma.
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PMID:[Increased incidence of adenocarcinoma of the esophagus and cardia. Reflux and obesity are strong and independent risk factors according to the SECC study]. 1082 53

The demographics of esophageal and gastric cancer have been changing dramatically in the United States over the past several decades. While incidence rates for esophageal squamous cell carcinoma and distal gastric carcinoma have been declining, the trends for adenocarcinoma of the esophagus and proximal stomach have been rising rapidly, particularly among white males. The incidence of these upper gastrointestinal (GI) malignancies varies widely based on geographic location, race, and socioeconomic status. The primary causes of squamous cell carcinoma of the esophagus are tobacco use and alcohol consumption, whereas the main risk factors for adenocarcinoma of the esophagus are gastroesophageal reflux disease and obesity. Dietary factors and Helicobacter pylori infection play an important role in the development of gastric cancer. Understanding the epidemiology and etiologies of esophageal and gastric carcinomas will lead to the development of interventions for screening and prevention in high-risk populations.
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PMID:Epidemiology of upper gastrointestinal malignancies. 1529 38

Esophageal adenocarcinoma rates may be increasing, whereas, squamous cell carcinoma rates appear to be decreasing in the United States. Previous population-based research on esophageal cancer has only covered up to 68% of the country. Additional, updated research on a larger percentage of the country is needed to describe racial, ethnic and regional trends in histologic subtypes of esophageal cancer. Invasive esophageal cancer cases diagnosed between 1998 and 2003 (n = 65,926), collected by the National Program of Cancer Registries or the Surveillance, Epidemiology, and End Results program, were included. These data cover 83% of the US population. Esophageal squamous cell carcinoma incidence fell by 3.6%/year, whereas esophageal adenocarcinoma increased by 2.1%/year. Squamous cell carcinoma rates decreased among both sexes in most racial or ethnic groups, whereas adenocarcinoma rates increased primarily among white or non-Hispanic men. Except for white or non-Hispanic men, squamous cell carcinoma rates were similar to, or greater than, adenocarcinoma rates for men and women of all other races and ethnicities. The largest decrease in squamous cell carcinoma rates occurred in the West census region, which also exhibited no increase in adenocarcinoma rates. The rate of regional and distant-staged adenocarcinomas increased, while rates for local-staged adenocarcinoma remained stable. This is the first article to characterize esophageal cancer trends using data covering the majority of the US. Substantial racial, ethnic and regional variation in esophageal cancer is present in the US. Our work may inform interventions related to tobacco and alcohol use, and overweight/obesity prevention, and provide avenues for further research.
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PMID:Trends in esophageal cancer incidence by histology, United States, 1998-2003. 1854 59

Esophageal adenocarcinoma (EAC) has been rapidly increasing in Western countries during the past half century, especially in white men. Esophageal squamous cell carcinoma (ESCC) used to be the dominant type of esophageal malignancy both in Western and Asian countries. The rapid increase of EAC in Western countries has occurred in parallel with an increased prevalence of gastroesophageal reflux disease (GERD) and its major determinant, obesity. Such an increase in EAC has not yet been observed in Asia, despite a recent increase in prevalence of GERD. In this mini-review, we analyze possible factors influencing such east-west ('Orient to Occident') differences, particularly possible roles of ethnicity and environmental factors, such as Helicobacter pylori infection and nutritional factors, and how these might interact with socioeconomic differences. Development of Barrett's esophagus and esophageal adenocarcinoma appears to be strongly affected by ethnic factors, with populations resident at the west end of the Eurasian continent, such as Anglo-Celtics, being more prone to both conditions. On the other hand, ethnic groups from the eastern and southern ends of Eurasia, such as Chinese, Koreans and Japanese, and Africans might be more prone to developing esophageal squamous cell carcinoma. Future trends will also be discussed.
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PMID:Epidemiology of esophageal cancer: Orient to Occident. Effects of chronology, geography and ethnicity. 1964 15

Esophageal squamous cell carcinoma is linked to alcohol drinking, whereas esophageal adenocarcinoma risk is increased by overweight and obesity. Both histologies are directly related to tobacco smoking. We wanted to define the risk of esophageal cancer by histology and length of stay among immigrants in Sweden. The nationwide Swedish Family Cancer database (2010 version: data on cancers originate from the nationwide Swedish Cancer Registry) was used to calculate standardized incidence ratios (SIRs) for esophageal cancer among immigrants compared with the native Swedes. SIRs for lung cancer were also calculated as a proxy for smoking prevalence. The patient series covered 5930 male and 1998 female Swedes, and 410 and 198 immigrants. The risk of esophageal cancer was increased in female Finns (SIR=1.66), Britons (3.73), and Southeast Africans (5.26), whereas male Baltic (0.44), former Yugoslavian (0.47), other Europeans (0.58), and other Asians (0.52) showed a decreased risk. The risk of squamous cell carcinoma was increased among Finns (men=1.32, women=1.90) and Iranian women (3.80), whereas Danish men (1.66) had an increased risk of adenocarcinoma. No trend was observed for the risks in immigrants according to the length of stay. We found no covariation between the birth region-specific SIRs for squamous cell carcinoma and lung cancer. Early childhood exposures or preservation of original habits might be the main environmental exposures influencing squamous cell carcinoma risks in some immigrants. The increased risk of adenocarcinoma among Danish men may confirm the role of obesity in adenocarcinoma risk.
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PMID:Esophageal cancer risk among immigrants in Sweden. 2115 Jul 82

There is growing evidence that many aspects of our lifestyle and the environment we now live in contribute to the development of disease. The luminal digestive tract is a clear target of the influence of dietary components, alcohol, microbial organisms, and other ingested materials. External factors including obesity, lack of physical exercise, and tobacco consumption also impact diseases of the luminal gastrointestinal (GI) tract. A growing understanding of the microbiome which forms an integral part of the human organism indicates that this is another important external force that impacts human health and disease. The luminal GI tract conditions that arise, at least in part, from these external factors range from malignancies (squamous cell esophageal cancer, Barrett's esophagus and associated esophageal adenocarcinoma, gastric cancer, and colorectal cancer), idiopathic inflammatory disorders such as inflammatory bowel diseases, and post-infectious syndromes including post-infectious irritable bowel syndrome, post-infectious dyspepsia and other functional GI disorders. Of particular interest, given their increase in prevalence in much of the world, are immune-mediated conditions in which food antigens are the driving force behind disease development. These entities include celiac disease, eosinophilic esophagitis, and food allergies. Celiac disease is a prime example of a condition mediated by dietary factors whose pathogenesis has only recently been determined, providing opportunities for developing treatment options beyond the gluten-free diet. While a genetic basis for this disease clearly exists, it is believed that environmental factors such as an increase in gluten in the human diet account for its rising prevalence, now roughly 1% of genetically susceptible populations in all continents. Proposed therapeutic strategies span from preventing disease by modulating the time of gluten introduction in infants, to reducing exposure to gluten by developing strains of wheat with lower levels of gluten, degrading ingested gluten peptides within the intestinal lumen via endopeptidases or modulating uptake of these peptides across intestinal tight junctions. Other novel treatments in development focus on interfering with the immune events that lead to disease once gluten accesses the lamina propria including altering the immune milieu from a Th1-predominant response via hookworm infection, inhibiting tissue transglutaminase, and blocking antigen presentation and/or T-cell responses to gluten peptides. While new treatment options for celiac disease reflect the complex interaction of diet, genetic factors and the host immune response, the implications for treatment of many conditions of the large and small intestine that arise from environmental and lifestyle are as basic as ensuring adequate nutrition, regular exercise and cessation of tobacco use. Much more needs to be learned about the microbiome, dietary and other factors and their interaction with the human host in order to develop potential new treatment strategies for diseases that result from the environment and lifestyle.
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PMID:Environmental and lifestyle influences on disorders of the large and small intestine: implications for treatment. 2173 92

Barrett's esophagus, with gastroesophageal reflux disease and obesity as risk factors, predisposes to esophageal adenocarcinoma (EAC). Recently a British genome wide association study identified two Barrett's esophagus susceptibility loci mapping within the major histocompatibility complex (MHC; rs9257809) and closely to the Forkhead-F1 (FOXF1; rs9936833) coding gene. An interesting issue is whether polymorphisms associated with Barrett's esophagus, are also implicated in esophageal carcinoma (EC), and more specifically EAC genesis. Assessing the individual genetic susceptibility can help identify high risk patients more prone to benefit from surveillance programs. Our hypothesis: Barrett associated MHC and FOXF1 variants modify EC risk in Caucasians. In a Dutch case-control study, 431 patients with EC and 605 healthy controls were included. Polymorphisms at chromosomes 6p21 (MHC) and 16q24 (FOXF1) were determined by means of real-time polymerase chain reaction (RT-PCR). Logistic regression analysis was used to calculate odds ratios with 95% confidence intervals. The FOXF1 rs9936833 variant C allele was associated with an increased EAC susceptibility; OR, [95% CI]; 1.21, [0.99-1.47]. A sex-stratified analysis revealed a similar association in males; 1.24 [1.00-1.55]. The variant MHC rs9257809 G allele as well as the MHC heterozygous AG genotype significantly increased ESCC risk; 1.76 [1.16-2.66] and 1.74 [1.08-2.80], respectively. Sex-stratification showed that the variant G allele was especially present in female patients; 2.32 [1.04-5.20]. In conclusion, this study provides evidence that MHC rs9257809 and FOXF1 rs9936833 variants, associated with Barrett's esophagus, also increase ESCC and EAC susceptibility in Caucasians. FOX proteins are transcription factors involved in organogenesis of the GI tract, while MHC haplotypes are strongly associated with smoking behavior, a crucial risk factor for ESCC. Assessing the individual genetic susceptibility can help identify high risk patients more prone to benefit from (Barrett) surveillance programs.
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PMID:Barrett associated MHC and FOXF1 variants also increase esophageal carcinoma risk. 2350 27

Mortality from esophageal cancer remains high despite advances in medical therapy. Although the incidence of squamous cell carcinoma of the esophagus remains unchanged, the incidence of the esophageal adenocarcinoma has increased over time. Gastroesophageal reflux disease (GERD and obesity are contributing factors to the development of Barrett's esophagus and subsequent development of adenocarcinoma. Early recognition of the disease can lead to resection of esophageal cancer prior to the development of lymphovascular invasion. Various modalities have been implemented to aid identification of precancerous lesions and early esophageal cancer. Chromoendoscopy, narrowband imaging and endoscopic ultrasound examination are typically used for evaluating early esophageal lesions. Recently, confocal laser endomicroscopy (CLE) and volumetric laser scanning were implemented with promising results. Endoscopic management of early esophageal cancer may be done using endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD). Both techniques allow resection of the mucosa (and possibly a portion of the submucosa) containing the early tumor without interruption of deeper layers. A submucosal injection creating a cushion coupled with snare resection or cap assisted mucosal suction followed by ligation and snare resection are the most common techniques of EMR. EMR can remove lesions less than 2 cm in size en bloc. Larger lesions may require resection in piecemeal fashion. This may limit assessment of the margins of the lesion and orienting the lesion's border. ESD offers en bloc dissection of the lesion regardless of its size. ESD is performed with specialized needle knives, which allow incision followed by careful dissection of the lesion within the submucosal layer. Tumor recurrence after ESD is rare but the technique is labor intensive and has an increased risk of perforation. Esophageal stenosis remains a concern after extensive EMR or ESD. Dilation with balloon or stent placement is usually sufficient to treat post-resection stenosis.
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PMID:Endoscopic submucosal dissection and endoscopic mucosal resection for early stage esophageal cancer. 2844 97

Esophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related death worldwide. Xanthohumol is a prenylated flavonoid isolated from hops. Although xanthohumol has been reported to exert anti-obesity, hypoglycemic, anti-hyperlipidemia and anti-cancer activities, the mechanisms underlying its chemotherapeutic activity are yet to be elucidated. In the present study, we found that xanthohumol inhibited ESCC cell proliferation in vitro and in vivo by targeting keratin (KRT)-18. Xanthohumol suppressed the proliferation, foci formation, and anchorage-independent colony growth of KYSE30 cells. Using xanthohumol-sepharose conjugated bead pull-down and mass/mass analysis, we found that KRT18 is a novel target of xanthohumol in KYSE30 cells. KRT18 protein was highly expressed in patient ESCC tissues compared to adjunct tissues. Anti-proliferative activity of xanthohumol was abrogated or enhanced according to the knockdown or overexpression of KRT18 protein, respectively. Xanthohumol also induced apoptosis and cell cycle arrest at G1 phase which was associated with the modulation of expression of related makers including cyclin D1, cyclin D3, and cleaved-PARP, Bcl-2, cytochrome c and Bax. While xanthohumol attenuated KRT18 protein expression, it failed to cause any change in the KRT18 mRNA level. Furthermore, oral administration of xanthohumol decreased tumor volume and weight in patient-derived xenografts (PDXs) tumors having overexpressed KRT18. Overall these results suggest that xanthohumol acts as a KRT18 regulator to suppress the growth of ESCC.
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PMID:Xanthohumol Inhibits the Growth of Keratin 18-Overexpressed Esophageal Squamous Cell Carcinoma in vitro and in vivo. 3250 87