Association of visceral adiposity with oesophageal and junctional adenocarcinomas

Beddy, Peter; Howard, Julia; McMahon, Colm J.; Knox, Mark; Blacam, Catherine de; Ravi, Narayanasamy; Reynolds, John V.; Keogan, Mary T.

doi:10.1002/bjs.7100

Cited by 66 publications

(51 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is, to the best of our knowledge, only one study that has addressed the association between the metabolic syndrome and risk of esophageal cancer, and one of gastric cancer [12,13]. Abdominal obesity has been suggested to contribute to the increased risk of esophageal and gastric adenocarcinoma [14,15], while the role of other variables that constitute the metabolic syndrome is uncertain. The aim of the present study was to investigate the relation between the metabolic syndrome and the risk of esophageal adenocarcinoma, esophageal squamous-cell carcinoma and gastric adenocarcinoma using a large population-based cohort study with long-term follow-up in Norway.…”

Section: Introductionmentioning

confidence: 99%

Metabolic syndrome and esophageal and gastric cancer

Lin

Ness-Jensen

Hveem

et al. 2015

Cancer Causes Control

View full text Add to dashboard Cite

Background The role of the metabolic syndrome in the etiology of esophageal and gastric cancer is unclear. Methods This was a large nationwide cohort study based on data from 11 prospective population-based cohorts in Norway with long-term follow-up, the Cohort of Norway (CONOR) and the third Nord-Trøndelag Health Study (HUNT3). The metabolic syndrome was assessed by objective anthropometric and metabolic biochemical measures and was defined by the presence of at least three of the following five factors: increased waist circumference, elevated triglycerides, low highdensity lipoprotein cholesterol, hypertension and high glucose. Newly diagnosed cases of esophageal adenocarcinoma, esophageal squamous-cell carcinoma and gastric adenocarcinoma were identified from the Norwegian Cancer Registry. Hazard ratios (HRs) and 95 % confidence intervals (CIs) were estimated using Cox proportional hazard models with adjustment for potential confounders. Result Among 192,903 participants followed up for an average of 10.6 years, 62 developed esophageal adenocarcinoma, 64 had esophageal squamous-cell carcinoma and 373 had gastric adenocarcinoma. The metabolic syndrome was significantly associated with an increased risk of gastric adenocarcinoma (HR 1.44, 95 % CI 1.14-1.82), but not associated with esophageal adenocarcinoma (HR 1.32, 95 % CI 0.77-2.26) or esophageal squamous-cell carcinoma (HR 1.08, 95 % CI 0.64-1.83). Increased waist circumference was associated with an increased HR of esophageal adenocarcinoma (HR 2.48,. No significant association was found between any single component of the metabolic syndrome and risk of esophageal squamous-cell carcinoma. High waist circumference (HR 1.71, 95 % CI 1.05-2.80), hypertension (HR 2.41, 95 % CI 1.44-4.03) and non-fasting glucose (HR 1.74, 95 % CI 1.18-2.56) were also related to an increased risk of gastric adenocarcinoma in women, but not in men. Conclusion Metabolic syndrome was associated with an increased risk of gastric adenocarcinoma in women. Of the individual components of the metabolic syndrome, high waist circumference was positively associated with risk of esophageal adenocarcinoma. Positive associations were also observed for women between high waist circumference, hypertension, high non-fasting glucose and risk of gastric adenocarcinoma. However, further evidence is warranted due to the limited number of cases and the inability to effectively identify gastric cardia adenocarcinoma.

show abstract

Section: Introductionmentioning

confidence: 99%

Metabolic syndrome and esophageal and gastric cancer

Lin

Ness-Jensen

Hveem

et al. 2015

Cancer Causes Control

View full text Add to dashboard Cite

show abstract

“…In conclusion, GCA and EAC are associated with obesity as measured by BMI and additional parameters like WC and visceral fat [7,28]. The rising incidence of these cancers has been associated with the epidemic of obesity, especially in the Western world; however, race and age cannot completely explain the trend.…”

Section: What Does the Current Study Add?mentioning

confidence: 95%

“…The underlying mechanism is unclear. It has been shown that various adipokines and hormones like TNF-a, adiponectin, leptin, insulin, and interleukin-6 may play a role in development of EAC, Barrett's esophagus and GCA [28][29][30].…”

Section: What Does the Current Study Add?mentioning

confidence: 99%

Gastric Cardia Cancer: How Much Is It from Fat?

Sinh

2012

Dig Dis Sci

View full text Add to dashboard Cite

“…Obese patients often have a relative abundance of fat in one or other compartment (22) . Those with excess visceral fat have an increased risk (independent of BMI) of breast cancer, oesophageal adenocarcinoma, colorectal adenocarcinoma and colorectal adenoma (9,(23)(24)(25)(26) . Adipose tissue in obese subjects has altered endocrine function and a secretory profile with predominantly pro-inflammatory cytokines, which are secreted by both adipocytes (and called adipokines) and immune cells.…”

Section: Epidemiologymentioning

confidence: 99%

“…Obesity contributes to between 3 and 20 % of cancer deaths in western populations (8,9) . Since obesity is a pro-inflammatory state, an altered immune system may fuel this process, with visceral adipose tissue and liver being primary sources of cells and cytokines.…”

mentioning

confidence: 99%

Obesity-associated cancer: an immunological perspective

et al. 2015

View full text Add to dashboard Cite

Epidemiological studies have established an association between obesity, insulin resistance, type 2 diabetes and a number of cancer types. Research has focused predominantly on altered endocrine factors, growth factors and signalling pathways, with little known in man about the immune involvement in the relevant pathophysiological processes. Moreover, in an era of exciting new breakthroughs in cancer immunotherapy, there is also a need to study the safety and efficacy of immunotherapeutics in the complex setting of inflammatory-driven obesityassociated cancer. This review addresses key immune cell subsets underpinning obesityassociated inflammation and describes how such immune compartments might be targeted to prevent and treat obesity-associated cancer. We propose that the modulation, metabolism, migration and abundance of pro-and anti-inflammatory cells and tumour-specific T cells might be therapeutically altered to both restore immune balance, alleviating pathological inflammation, and to improve anti-tumour immune responses in obesity-associated cancer. Obesity: Cancer: Lymphocytes: Immunotherapeutics: InflammationThe burgeoning global health burden of obesity is of grave concern, affecting over half a billion adults worldwide, with approximately 3·5 million attributable deaths each year (1) . Despite national and international interventions to promote a healthy diet and lifestyle, recent reports predict that global obesity rates show no signs of abating, with predictions that half of all adults will be overweight or obese by 2030 (WHO). The worldwide prevalence of obesity almost doubled in the period 1980-2008. In 1980, 5 % of men and 8 % of women were obese and by 2008, these rates were 10 and 14 %, respectively. In many areas of the western world, the overweight phenotype is now the most prevalent body type. For example, in the USA in 2010 the prevalence of a BMI ≥ 25 was 69·2 %, with 35·9 % of people being obese (BMI ≥ 30) (2)

show abstract

Association of visceral adiposity with oesophageal and junctional adenocarcinomas

Abstract: Patients with oesophageal/junctional adenocarcinoma, in particular oesophageal and Siewert type I junctional tumours, have greater CT-defined visceral adiposity than patients with gastric adenocarcinoma or oesophageal squamous cell carcinoma, or controls.

Cited by 66 publications

References 30 publications

Metabolic syndrome and esophageal and gastric cancer

Metabolic syndrome and esophageal and gastric cancer

Gastric Cardia Cancer: How Much Is It from Fat?

Obesity-associated cancer: an immunological perspective

Contact Info

Product

Resources

About