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

Large prospective studies show a significant association with obesity for several cancers, and the International Agency for Research on Cancer has classified the evidence of a causal link as 'sufficient' for cancers of the colon, female breast (postmenopausal), endometrium, kidney (renal cell), and esophagus (adenocarcinoma). These data, and the rising worldwide trend in obesity, suggest that overeating may be the largest avoidable cause of cancer in nonsmokers. Few obese people are successful in long-term weight reduction, and thus there is little direct evidence regarding the impact of weight reduction on cancer risk. If the correlation between obesity and cancer mortality is entirely causal, we estimate that overweight and obesity now account for one in seven of cancer deaths in men and one in five in women in the US.
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PMID:Obesity and cancer. 1532 11

Symptoms of gastro-oesophageal reflux disease are highly prevalent in Western countries; however, it is less certain how many individuals with heartburn have clinically relevant disease. Although the prevalence of gastro-oesophageal reflux disease in Asia is substantially lower, the incidence may be increasing. How much of this increase is explained by the increasing recognition of heartburn in clinical practice, dietary changes and increasing obesity, or the eradication of Helicobacter pylori, remains unclear. There has been speculation that endoscopy-negative reflux disease represents a separate entity from reflux oesophagitis (as defined by the Los Angeles classification), but the evidence that might support this proposal is unconvincing. Patients with chronic reflux symptoms have a higher risk of Barrett's oesophagus, and the increased risk of developing oesophageal adenocarcinoma in individuals with a long history of heartburn is also well documented, but whether this always occurs via Barrett's oesophagus is debatable. Moreover, treatment with standard-dose antisecretory therapies and anti-reflux surgery seems unlikely, based on current evidence, to reduce the cancer risk in patients with Barrett's oesophagus. Gastro-oesophageal reflux disease has also been implicated in an increasing array of other conditions, but arguably in these settings it is often over-diagnosed.
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PMID:Review article: gastro-oesophageal reflux disease -- how wide is its span? 1545 61

The major oesophageal complications associated with persistent gastro-oesophageal reflux disease (GERD) include erosive oesophagitis, ulceration, strictures and gastrointestinal (GI) bleeding. Although the causes of these complications are uncertain, studies indicate that erosive oesophagitis may progress to the development of ulcers, strictures and GI bleeding. Pharmacological treatment with proton pump inhibitors is favoured over that with H(2)-receptor antagonists for the treatment of strictures. The treatment of strictures is accomplished with dilation and many favour the concomitant use of proton pump inhibitors. Most gastroenterologists are seeing far fewer oesophageal strictures these days since the introduction of proton pump inhibitors. In addition, research has shown that oesophageal complications have a greater impact on patients suffering from night-time GERD than on those suffering from daytime GERD. Barrett's oesophagus is a significant complication associated with persistent GERD and those at risk generally experience a longer duration of symptoms, especially those with a high degree of severity. In addition, there is a strong relationship between Barrett's oesophagus and oesophageal adenocarcinoma. This is in part due to the association of obesity and the development of hiatal hernias. Furthermore, endoscopic screening is being used to detect Barrett's oesophagus and oesophageal adenocarcinoma in persons suffering from chronic GERD, even though screening may not have an impact on outcomes (Sharma P, McQuaid K, Dent J, et al. A critical review of the diagnosis and management of Barrett's esophagus: The AGA Chicago Workshop. Gastroenterology 2004; 127: 310-30.).
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PMID:Review article: oesophageal complications and consequences of persistent gastro-oesophageal reflux disease. 1552 64

The incidence of esophageal adenocarcinoma (AC) has increased dramatically in the Western world over the past 20 years and the majority of these cancers arise on the background of the preinvasive lesion Barrett's esophagus. The epidemiologic factors that contribute to an individual's susceptibility for Barrett's esophagus and associated cancer are likely to be multifactorial. However, the short time frame over which the incidence of adenocarcinoma has increased, and the increase across populations, provides a strong argument for environmental factors as etiologic agents, perhaps interacting with genetically determined characteristics that define personal susceptibility. In this review we discuss the epidemiologic evidence for the proposed demographic and environmental risk factors for the development of both Barrett's esophagus and AC. The current evidence suggests that significant risk factors include male sex, Caucasian race, and the presence of duodenogastroesophageal reflux disease. The susceptibility for reflux disease may in turn be influenced by factors such as obesity, the use of drugs that lower the lower-esophageal sphincter tone, and a protective effect of Helicobacter pylori colonization. There appears to be a weak association between smoking and AC. The role of dietary factors has not been studied adequately and deserves further attention. An understanding of the factors that predispose to the development and progression of Barrett's esophagus is crucial to the implementation of effective screening and prevention programs.
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PMID:Epidemiologic risk factors for Barrett's esophagus and associated adenocarcinoma. 1564 98

The incidence of oesophageal adenocarcinoma is increasing and the prognosis is poor. There is a strong predominance of white males, and heredity plays a minor role. The established risk factors are Barrett's oesophagus, gastro-oesophageal reflux, and obesity. Infection with Helicobacter pylori and use of non-steroidal anti-inflammatory drugs might reduce the risk. Medications that relax the lower oesophageal sphincter might contribute to increasing the risk. Among dietary factors, low intake of fruit, vegetables, and cereal fibres seem to increase the risk of oesophageal adenocarcinoma. The role of tobacco smoking is probably limited and alcohol consumption is not a risk factor. It is uncertain which factors cause the increasing incidence. Increasing prevalences of reflux and obesity, and decreasing prevalence of H pylori infection may contribute to this development; however, the sex distributions of these factors do not match the incidence trends well. Endoscopic surveillance for oesophageal adenocarcinoma among persons with reflux and obesity is discussed, but presently there is no evidence that strongly supports such a strategy.
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PMID:Adenocarcinoma of oesophagus: what exactly is the size of the problem and who is at risk? 1571 Oct 2

Among men there is epidemiological evidence for an association between obesity and increased risk of renal cell carcinoma, colon cancer and adenocarcinoma of the oesophagus. The evidence for other cancer sites remains inconsistent. We conducted a large population-based, multi-site, case-control study of environmental causes of cancer among males in Montreal, Canada. Among the many questionnaire items collected by interview were height and usual weight. We compared height, weight and body mass index (BMI) among individuals with 11 different cancer types (combined N=3016) and population-based controls (N=509). Linear regression was used to model the relationship of the disease status with each of three dependent continuous variables (height, weight and BMI), while adjusting for covariates. For most cancer groups, weight and BMI were lower than among population controls. Because of potential information bias and reverse causality bias, we focused on the comparisons among cancer types. The lowest BMI values were observed among men with squamous cell carcinoma of the oesophagus, lung and stomach cancers. The highest BMIs were reported by men with prostate and kidney cancers, and oesophageal adenocarcinoma. Inconsistencies in the epidemiological literature on obesity and cancer risk could be related to the difficulties in obtaining unbiased reports of pre-disease weight and to publication bias.
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PMID:Comparison of self-reported height and weight by cancer type among men from Montreal, Canada. 1617 48

Esophageal cancer is a highly aggressive neoplasm. In 2005, 14,520 Americans will be diagnosed with esophageal cancer, and more than 90% will die of their disease. On a global basis, cancer of the esophagus is the sixth leading cause of cancer death worldwide. In fact, gastric and esophageal cancers together accounted for nearly 1.3 million new cases and 980,000 deaths worldwide in 2000-more than lung, breast, or colorectal cancer. Although esophageal squamous cell carcinoma cases have steadily declined, the incidence of gastroesophageal junction adenocarcinoma has increased 4%-10% per year among U.S. men since 1976, more rapidly than for any other cancer type, and parallels rises in population trends in obesity and reflux disease. With advances in surgical techniques and treatment, the prognosis of esophageal cancer has slowly improved over the past three decades. However, the 5-year overall survival rate (14%) remains poor, even in comparison with the dismal survival rates (4%) from the 1970s. The underlying reasons for this disappointingly low survival rate are multifold: (a) ineffective screening tools and guidelines; (b) cancer detection at an advanced stage, with over 50% of patients with unresectable disease or distant metastasis at presentation; (c) high risk for recurrent disease after esophagectomy or definitive chemoradiotherapy; (d) unreliable noninvasive tools to measure complete response to chemoradiotherapy; and (e) limited survival achieved with palliative chemotherapy alone for patients with metastatic or unresectable disease. Clearly, additional strategies are needed to detect esophageal cancer earlier and to improve our systemic treatment options. Over the past decade, the field of drug development has been transformed with the identification of and ability to direct treatment at specific molecular targets. This review focuses on novel targeted treatments in development for esophageal squamous cell carcinoma and distal esophageal and gastroesophageal junction adenocarcinoma.
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PMID:Targeted therapies for esophageal cancer. 1617 83

Risk factors for esophageal adenocarcinoma include obesity, high fat intake, and low consumption of fruits and vegetables. This trial tested whether an intervention to reduce these risk factors in patients with Barrett esophagus, a preneoplastic condition for esophageal adenocarcinoma, could reduce biomarkers of cellular proliferation and, by inference, the risk of neoplastic progression. Eighty-seven men and women with Barrett esophagus were randomized to an intensive dietary intervention or control group. At baseline, 18 and 36 months after intervention, biopsies were obtained at 2-cm intervals throughout the length of the Barrett segment. Ki67/DNA content flow cytometry was used to assess (a) % Ki67-positive proliferating diploid G(1) cells, (b) % total Ki67-positive proliferating cells, (c) presence of aneuploidy, and (d) presence of >6% of cells in the 4N (G(2)/tetraploid) fraction of the cell cycle. We also assessed re-epithelialization and length of the Barrett segment, reflux symptoms, and medication use. The intervention effects for energy, fat, fruits and vegetables, and weight were, respectively, -314 kcal, -12.2% energy, 1.8 servings/d, and -4.0 kg at 18 months (all P < 0.005) and were smaller but remained significant at 36 months. There were no significant effects of the intervention on any biomarker of cellular proliferation. The intervention effects +/- SE for mean %G(1) Ki67+ cells were 0.98 +/- 1.58 at 18 months and 1.79 +/- 1.31 at 36 months; the relative risks (95% confidence interval) for developing >6% of cells in 4N were 0.5 (0.1-2.6) at 18 months and 0.75 (0.2-3.1) at 36 months. A single control participant developed aneuploidy. There were no significant effects on re-epithelialization, segment length, or reflux medication use. We conclude that substantial dietary change has no short-term effects on biomarkers of cellular proliferation in Barrett esophagus or on clinical observations of the Barrrett segment.
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PMID:Low-fat, high fruit and vegetable diets and weight loss do not affect biomarkers of cellular proliferation in Barrett esophagus. 1621 20

The aim of our study was to evaluate the association between the expression of cathepsin D and clinical prognostic data in endometrioid adenocarcinoma of different histological grade. We studied 104 postmenopausal women with diagnosis of endometrioid adenocarcinoma. We evaluated the presence of obesity and vaginal bleeding. Surgical specimens were fixed in 10% neutral buffered formalin solution and embedded in paraffin. 4 mm sections were stained by hematoxylin and eosin, von Gieson, and histological type of cancer, metastatic lesion of lymph nodes and depth of myometrial invasion were evaluated. Histological grade of cancer was assessed by FIGO grading system. All samples were analysed by immunohistochemistry for cathepsin D (Dakocytomation). We assessed the number of cathepsin D-positive stromal and tumor cells and degree of positivity (low, moderate, high). Histological study by hematoxylin and eosin showed grade 1 endometrioid carcinoma in 35 cases (33,7%, group 1), grade 2 in 44 cases (42,3%, group 2), grade 3 in 25 cases (24%, grade 3). Our results suggest that the expression of cathepsin D is associated with the higher histological grade of endometrioid adenocarcinoma, depth of myometrial invasion, lymph node positivity, coexistence of obesity and vaginal bleeding. It seems that local invasion and metastatic spread of tumor should be preceeded by the expression of cathepsin D in stromal cells which can be assessed in grade 1 and 2 endometrioid adenocarcinomas. The expression of cathepsin D can be used as a prognostic factor and more aggressive chemothepery regimen should be used.
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PMID:Clinical prognostic factors and expression of cathepsin D in endometrioid adenocarcinoma. 1623 88

The incidence of esophageal adenocarcinoma has risen rapidly over the past 25 years in the United States as well as in several Western European countries. This increase had been most dramatic among white males. The majority of these cancers arise from a background of premalignant Barrett esophagus. However, less than 10% of the patients with esophageal adenocarcinoma were known to have Barrett esophagus previously. It is uncertain which risk factors contribute to the increasing incidence of esophageal adenocarcinoma, although gastroesophageal reflux disease, cigarette smoking, and obesity have been implicated. Whereas infection with Helicobacter pylori and use of non-steroidal anti-inflammatory drugs are associated with reduced risk, low intakes of fruit, vegetables, and cereal fibers seem to increase the risk of esophageal adenocarcinoma. Presently there is no evidence that strongly supports any specific strategy to screen a subgroup of the population at risk for Barrett esophagus and adenocarcinoma of the esophagus.
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PMID:Epidemiology of esophageal adenocarcinoma. 1629 86


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