The Rapid Rise in Gastroesophageal Junction Tumors: Is Inflammation of the Gastric Cardia the Underwater Iceberg?

Quante, Michael; Abrams, Julian A.; Wang, Yichen

doi:10.1053/j.gastro.2013.08.023

Cited by 16 publications

(14 citation statements)

References 18 publications

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“…The authors also observed a more proximal extension of gastric acid which was attributed to the higher intra‐abdominal pressure and may have favored the expansion of adjacent cardia glands . Further studies are needed to elucidate the importance of cardia inflammation and expansion as a precursor to EAC and GCC …”

Section: Discussionmentioning

confidence: 93%

“…38 The authors also observed a more proximal extension of gastric acid which was attributed to the higher intraabdominal pressure and may have favored the expansion of adjacent cardia glands. 38,39 Further studies are needed to elucidate the importance of cardia inflammation and expansion as a precursor to EAC and GCC. 39 Apart from mechanical mechanisms, accumulating evidence suggests humoral mechanisms to link abdominal obesity with EAC, and maybe also GCC, involving alterations in estrogen signaling, the insulin/insulin-like growth factor I (IGF-I) axis and the secretion of adipokines.…”

Section: Epidemiologymentioning

confidence: 99%

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General and abdominal obesity and risk of esophageal and gastric adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition

et al. 2015

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General obesity, as reflected by BMI, is an established risk factor for esophageal adenocarcinoma (EAC), a suspected risk factor for gastric cardia adenocarcinoma (GCC) and appears unrelated to gastric non-cardia adenocarcinoma (GNCC). How abdominal obesity, as commonly measured by waist circumference (WC), relates to these cancers remains largely unexplored. Using measured anthropometric data from 391,456 individuals from the European Prospective Investigation into Cancer and Nutrition (EPIC) study and 11 years of follow-up, we comprehensively assessed the association of anthropometric measures with risk of EAC, GCC and GNCC using multivariable proportional hazards regression. One hundred twenty-four incident EAC, 193 GCC and 224 GNCC were accrued. After mutual adjustment, BMI was unrelated to EAC, while WC showed a strong positive association (highest vs. lowest quintile HR = 1.19; 95% CI, 0.63–2.22 and HR = 3.76; 1.72–8.22, respectively). Hip circumference (HC) was inversely related to EAC after controlling for WC, while WC remained positively associated (HR = 0.35; 0.18–0.68, and HR=4.10; 1.94-8.63, respectively). BMI was not associated with GCC or GNCC. WC was related to higher risks of GCC after adjustment for BMI and more strongly after adjustment for HC (highest vs. lowest quintile HR = 1.91; 1.09–3.37, and HR = 2.23; 1.28–3.90, respectively). Our study demonstrates that abdominal, rather than general, obesity is an indisputable risk factor for EAC and also provides evidence for a protective effect of gluteofemoral (subcutaneous) adipose tissue in EAC. Our study further shows that general obesity is not a risk factor for GCC and GNCC, while the role of abdominal obesity in GCC needs further investigation

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Section: Discussionmentioning

confidence: 93%

Section: Epidemiologymentioning

confidence: 99%

General and abdominal obesity and risk of esophageal and gastric adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition

et al. 2015

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“…In that study, inflammatory cells were found to be present in the cardia in all cases, irrespective of BMI, but the obese subjects had more proximal acid reflux and a longer cardia length (2.5 mm vs 1.75 mm in the normal BMI cases, p = 0.008). Conceivably, this lengthening may encourage the expansion and outward migration of cardia progenitor cells into the gastroesophageal junction, thereby promoting gastroesophageal junction neoplasia [67].…”

Section: Possible Mechanisms Linking Obesity With Gcamentioning

confidence: 99%

Obesity and related risk factors in gastric cardia adenocarcinoma

Olefson

Moss

2014

Gastric Cancer

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Over recent decades, the incidence of cancers of the gastroesophageal junction, including gastric cardia tumors, has increased markedly. This is a trend that has been well documented, especially in studies from the USA and northern Europe that have also demonstrated a concomitant rise in the ratio of cardia to distal gastric cancers. The rise in the prevalence of gastric cardia adenocarcinoma has been paralleled by the worldwide obesity epidemic, with almost all epidemiological studies reporting increased body mass index and obesity increase the risk of cardia cancer development. However, the strength of this association is less marked than the link between obesity and esophageal adenocarcinoma, and the mechanisms remain poorly understood. Other possible confounders of the relationship between obesity and cardia cancer include the decline in Helicobacter pylori infection and the widespread use of proton pump inhibitors, although these have rarely been controlled for in case-control and cohort studies investigating associations between obesity and cardia cancer. We review these epidemiological trends and discuss proposed mechanisms for the association, drawing attention to controversies over the difficulty of defining cardia cancer. The relative paucity of high-quality epidemiological studies from other regions of the world should prompt further investigation of this issue, especially in populations undergoing rapid socioeconomic change.

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“…Moreover, the lengthening of the cardiac mucosa may arise from the metaplasia of the most distal esophageal squamous epithelium; therefore, a large waist circumference/obesity may be used to predispose the expansion of cardiac glands associated with EAC (Robertson et al, ). However, another group supports the viewpoint that the expansion of the gastric cardia originates from the proximal extension of original cardiac mucosa but not from the metaplasia of the most distal esophageal squamous epithelium (Quante, Abrams, & Wang, ).…”

Section: Roles Of Basal Cells In the Eac Formationmentioning

confidence: 99%

Basal progenitor cells bridge the development, malignant cancers, and multiple diseases of esophagus

Lin

Xie

Xiao³

et al. 2017

Journal Cellular Physiology

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The esophagus is a pivotal organ originating from anterior foregut that links the mouth and stomach. Moreover, its development involves precise regulation of multiple signal molecules and signal transduction pathways. After abnormal regulation of these molecules in the basal cells of the esophagus occurs, multiple diseases, including esophageal atresia with or without tracheoesophageal fistula, Barrett esophagus, gastroesophageal reflux, and eosinophilic esophagitis, will take place as a result. Furthermore, expression changes of signal molecules or signal pathways in basal cells and the microenvironment around basal cells both can initiate the switch of malignant transformation. In this review, we highlight the molecular events underlying the transition of normal development to multiple esophageal diseases. Additionally, the animal models of esophageal development and related diseases, challenges, and strategies are extensively discussed.

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The Rapid Rise in Gastroesophageal Junction Tumors: Is Inflammation of the Gastric Cardia the Underwater Iceberg?

Cited by 16 publications

References 18 publications

General and abdominal obesity and risk of esophageal and gastric adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition

General and abdominal obesity and risk of esophageal and gastric adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition

Obesity and related risk factors in gastric cardia adenocarcinoma

Basal progenitor cells bridge the development, malignant cancers, and multiple diseases of esophagus

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