Are carcinomas of the cardia oesophageal or gastric adenocarcinomas?
Introduction
Epidemiological studies reveal that gastric cancer is the second most common cause of cancer mortality worldwide [1]. However, during the past few decades the overall incidence rates of gastric adenocarcinomas have gradually decreased in the United States of America (USA) and Western Europe, but this decline does not apply to all forms of gastric cancer 2, 3. In contrast to the decline in the incidence of gastric cancer, the incidence rates of cardiac cancer have dramatically increased, up to 4–5% annually in the USA [4]. Simultaneously, there has been a dramatic shift in the incidence of oesophageal squamous carcinomas towards adenocarcinomas, as a result of which the latter account for 50% of the oesophageal cancers in Western Europe and USA [5]. In keeping with the parallel increase in incidence, oesophageal adenocarcinomas and cardiac adenocarcinomas share some epidemiological features, which distinguish them from adenocarcinomas of the distal part of the stomach. There is an equal gender distribution in gastric carcinomas, but the male/female ratio in oesophageal and cardiac carcinomas is 9.2 and 5.5, respectively. The disease, both in the distal oesophagus and the cardia, is most common in middle-aged patients [6]. A survival analysis has shown that patients with an adenocarcinoma of the cardia have a similar survival to those having an adenocarcinoma of the distal oesophagus [7].
The dramatic increase in incidence of oesophageal carcinomas is related to the well-established association of gastro-oesophageal reflux and Barrett's oesophagus [8]. Additional risk factors, involved in the development of oesophageal adenocarcinomas, are smoking and a poor socio-economic status. According to some authors, these risk factors are also found in association with cardiac adenocarcinomas 9, 10. Other studies could not confirm these results and showed either no relationship or an opposite relationship in which a high socio-economic status was related to cardiac cancer 11, 12. Some authors found that smoking was associated with a higher risk for the development of gastric cancer 13, 14. Thus, neither smoking nor socio-economic status could allow differentiation of risk by anatomical sub-site.
In contrast to the plethora of studies concerning the aetiopathogenesis of oesophageal adenocarcinoma, the histogenesis of cardiac adenocarcinomas is less clear. Although both adenocarcinomas share similar epidemiological characteristics, the relationship between gastro-oesophageal reflux and adenocarcinomas of the cardia is less obvious. According to some authors, ‘carditis’ is a more sensitive marker of gastro-oesophageal reflux that could even precede the clinical signs of refluxoesophagitis. Others, however, could not confirm this 15, 16, 17. They believe that inflammation of the cardia is part of a Helicobacter pylori-related pangastritis. However, the role of H. pylori in the development of cardiac adenocarcinomas is uncertain. For example, the rising incidence of cardiac cancers is in contrast to the decline of H. pylori infection in the same populations. The relationship between H. pylori chronic pangastritis and gastric cancer is more firmly established, as the infection is associated with a 9-fold increased risk for this type of cancer [18]. As would be expected, the decrease in H. pylori infection is paralleled by a decline in the prevalence of gastric cancer [19].
Hence, the purpose of this study was to analyse the inflammatory changes present in the gastric mucosa in cases of oesophageal and cardiac adenocarcinomas, according to the updated Sydney system [20]. The same assessment has been performed on gastric biopsies of a control population with gastric carcinomas. Special attention has been given to the presence of H. pylori in the inflamed mucosa.
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Patients and methods
Our retrospective study comprised 342 patients, who underwent surgery for an adenocarcinoma of the oesophagus or stomach between 1993 and 2000 at the University Hospitals in Leuven, Belgium. The tumours were classified as oesophageal, cardiac or gastric cancer on the basis of two parameters: (1) the localisation of the major bulk of the tumour, and/or (2) the presence or absence of Barrett's oesophagus, determined on preoperative endoscopic biopsies or using tissue from the resection specimen,
Classification of the proximal tumours (Table 1)
The 342 tumours in our study population were classified according to the different criteria.
When we categorised our 242 proximal tumours according to the localisation of the bulk of the tumoral mass, 98 (40%) and 94 (39%) tumours were lower oesophageal and cardiac adenocarcinomas, respectively. 50 patients had a tumour centred on the gastro-oesophageal junction, and these tumours were classified as gastro-oesophageal junction-adenocarcinomas (21%).
A Barrett's oesophagus, as defined above, was
Discussion
It is commonly accepted that H. pylori is a risk factor for the development of gastric cancer. The histogenesis of this type of cancer is a multifactorial process involving a progressive evolution from superficial gastritis, atrophy, intestinal metaplasia, dysplasia to cancer [25]. Although other aetiopathogenetic factors are likely to be involved in this process, infection with H. pylori is associated with a 9-fold increased risk for gastric cancer 18, 25. Similar to gastric cancer, the
Acknowledgments
We gratefully acknowledge Prof. Dr. M. Dixon for his help in the preparation of this manuscript.
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2011, Human PathologyCitation Excerpt :In fact, 8p23.1 deletions have recently been shown to have a role in the genesis of diaphragmatic hernia [27], a known cause of gastroesophageal reflux disease, which in turn is known to be related with esophageal and cardial adenocarcinoma [28]. Indeed, adenocarcinoma of the cardia and gastroesophageal junction differs in several aspects from more common distal gastric cancer, for instance, concerning the role of Helicobacter pylori or EBV infection and epidemiology [29]. Thus, a distinctive role of pertinent genetic lesions would not be surprising.
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Current address: Department of Hepatogastroenterology, University Hospital Ghent, De Pintelaan 185, 9000 Ghent, Belgium.