The rising trend in oesophageal adenocarcinoma and gastric cardia

Powell, Jean; McConkey, CC

doi:10.1097/00008469-199204000-00008

Cited by 225 publications

(113 citation statements)

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“…It is considered to be a consequence of longlasting and severe gastroesophageal reflux disease (GERD). A metaplasia-dysplasia-carcinoma sequence links Barrett's esophagus with adenocarcinoma of the distal esophagus (EAC), which is one of the fastestincreasing cancers in the Western world (Powell and McConkey, 1992;Blot and McLaughlin, 1999;Burdiles et al, 2003;Cossentino and Wong, 2003;von Rahden et al, 2003). BE progresses toward EAC without causing obvious symptoms.…”

Section: Introductionmentioning

confidence: 99%

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis

Wang

Zhan

Yin³

et al. 2006

Oncogene

112

106

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To investigate the relationship between Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), we determined gene expression profiles of discrete pathological stages of esophageal neoplasia using a sequence-verified human cDNA microarray. Fifty one RNAs, comprising 24 normal esophagi (NE), 18 BEs, and nine EACs were hybridized to cDNA microarrays. Five statistical analyses were used for the data analysis. Genes showing significantly different expression levels among the three sample groups were identified. Genes were grouped into functional categories based on the Gene Ontology Consortium. Surprisingly, the expression pattern of BE was significantly more similar to EAC than to NE, notwithstanding the known histopathologic differences between BE and EAC. The pattern of NE was clearly distinct from that of EAC. Thirty-six genes were the most differentially modulated, according to these microarray data, in BE-associated neoplastic progression. Twelve genes were significantly differentially expressed in cancer-associated BE's plus EAC (as a single combined tissue group) vs noncancer-associated BE's. These genes represent potential biomarkers to diagnose EAC at its early stages. Our results demonstrate that molecular events at the transcriptional level in BE are remarkably similar to BE's-associated adenocarcinoma of the esophagus. This finding alarmingly implies that BE is biologically closer to cancer than to normal esophagus, and that the cancer risk of BE is perhaps higher than we had imagined. These findings suggest that changes modulated at the molecular biologic level supervene earlier than histologic changes, and that BE is an early intermediate stage in the process of EAC.

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Section: Introductionmentioning

confidence: 99%

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis

Wang

Zhan

Yin³

et al. 2006

Oncogene

112

106

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“…In contrast, the diffuse subtype is usually postulated to be more genetically predetermined (Correa and Shiao, 1994). Reports of a disparate incidence trend for cardia tumours (Blot et al, 1991;Powell and McConkey, 1992) strongly suggest that this subsite has a distinct aetiology.The concurrently falling prevalence of infection with Helicobacter pylori (H. pylori) (Haruma et al, 1997;Parsonnet et al, 1992;Roosendaal et al, 1997;Xia and Talley, 1997), suggests that its association with non-cardia gastric carcinoma is confined to the intestinal subtype. This hypothesis is in line with Correa's model of H. pylori-induced carcinogenesis (Correa, 1995).…”

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confidence: 99%

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confidence: 99%

Decreasing incidence of both major histologic subtypes of gastric adenocarcinoma – a population-based study in Sweden

Hansson

et al. 2000

Br J Cancer

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Gastric carcinoma continues to claim an increasing number of victims (approximately 900 000 per year) partly due to the ageing of the population (Munoz and Franceschi, 1997), but as we enter the 21st century, the aetiology of the world's second most common cancer (Parkin et al, 1993) remains relatively poorly understood. Risk factors for the different subtypes, both according to tumour histology (intestinal/diffuse) (Lauren, 1965) and site (cardia/noncardia), need to be identified.The remarkable global decline in gastric carcinoma incidence has mainly been attributed to intestinal type (Correa and Shiao, 1994;Lauren and Nevalainen, 1993;Munoz and Asvall, 1971) although firm consensus is lacking. Its variation over time and across populations (Coleman et al, 1993) is presumed to have a predominantly environmental aetiology. In contrast, the diffuse subtype is usually postulated to be more genetically predetermined (Correa and Shiao, 1994). Reports of a disparate incidence trend for cardia tumours (Blot et al, 1991;Powell and McConkey, 1992) strongly suggest that this subsite has a distinct aetiology.The concurrently falling prevalence of infection with Helicobacter pylori (H. pylori) (Haruma et al, 1997;Parsonnet et al, 1992;Roosendaal et al, 1997;Xia and Talley, 1997), suggests that its association with non-cardia gastric carcinoma is confined to the intestinal subtype. This hypothesis is in line with Correa's model of H. pylori-induced carcinogenesis (Correa, 1995). A stable incidence of the diffuse subtype would contradict an important role of H. pylori.We conducted a prospective population-based study over 6 years, with an extensive search for all incident gastric cancer cases in well-defined populations and a strictly uniform classification of tumour site and histologic type. Our aim was to analyse the incidence of the intestinal and diffuse types separately, while taking subsite into account. Sweden, with a two-fold variation in gastric cancer risk within the country and declining gastric cancer rates, is a particularly suitable environment for studying these questions. MATERIALS AND METHODS SubjectsAll new cases of gastric adenocarcinoma diagnosed before death, from 1989 through 1994, occurring in two northern high-risk counties (Norrbotten, Västerbotten) and three southern lowaverage-risk counties (Södermanland, Uppsala, Västmanland), with a total population 1.3 million, were identified through: contacting clinicians at all hospitals; surveillance of all suspected gastric cancer specimens at the departments of pathology; monthly double-checks with all regional cancer registers; and record linkages with the nation-wide Swedish cancer and death registries. All Decreasing incidence of both major histologic subtypes of gastric adenocarcinoma Ð a population-based study in Sweden Summary While the overall incidence of gastric cancer has fallen, presumably to a large extent in parallel with Helicobacter pylori infection, the occurrence of the diffuse histologic type is thought to have remained more stable, quest...

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“…It shows a varied geographical distribution and very poor survival rates. 1 Esophageal cancer accounts for 5% of all gastrointestinal cancers, and the overall number of new cases each year is steadily increasing. 2 Esophageal cancer can be divided into squamous cell carcinomas and adenocarcinomas.…”

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confidence: 99%

Frequent accumulation of nuclear E-cadherin and alterations in the Wnt signaling pathway in esophageal squamous cell carcinomas

et al. 2008

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Esophageal squamous cell carcinoma is frequently associated with poor prognosis, as a result of high levels of lymph node metastasis. So far, very few genetic abnormalities have been associated with this disease, and its molecular etiology remains largely unknown. To assess whether the Wnt pathway contributes to esophageal squamous cell carcinoma, we characterized the expression and subcellular localization of the key Wnt signaling components in all 30 cases of esophageal squamous cell carcinomas analyzed. We found abnormal expression and/or localization in glycogen synthase kinase-3 a/b (34%), Axin2 (48%), a-catenin (31%), MYC (73%) and cyclin D1 in 46% of cases. Only 13% of tumors showed nuclear accumulation of b-catenin. By contrast, 60% showed nuclear expression of E-cadherin using an antibody that recognizes the cytoplasmic domain of E-cadherin. When the same tumors were stained with antibody raised against the extracellular domain of E-cadherin, the expression was lost. A direct correlation was found between nuclear E-cadherin and the increased nuclear cyclin D1, one of the AP-1 target genes in these tumors. By transfection experiments, the cytoplasmic portion of E-cadherin was found to activate the AP-1 transcription factor pathway and induced cyclin D1 promoter activity, but b-catenin/Tcf transcription activity was unaffected. Nuclear expression of E-cadherin was also detected in tumors other than squamous cell carcinoma, including pancreatic and colon cancers, albeit at lower frequency. Nuclear accumulation of a portion of E-cadherin in esophageal squamous cell carcinoma and the other types of tumors indicates that, in addition to the previously implicated tumor suppressor activity of E-cadherin, modified forms of this glycoprotein might also play a role in growth promotion. Keywords: Wnt signaling; esophageal squamous cell carcinomas; pancreatic cancer; colon cancer; E-cadherin Esophageal cancer is one of the deadliest but least studied forms of cancer and the sixth ranking cause of death from cancer in North America. It shows a varied geographical distribution and very poor survival rates. 1 Esophageal cancer accounts for 5% of all gastrointestinal cancers, and the overall number of new cases each year is steadily increasing. 2 Esophageal cancer can be divided into squamous cell carcinomas and adenocarcinomas. So far, very few genetic abnormalities have directly been linked to esophageal carcinogenesis. In this study, we sought to examine the expression and localization of the key components of the Wnt signaling pathway that have previously been shown to play important roles in colorectal, breast, stomach and prostate cancer. Wnt signaling regulates cell growth, motility and differentiation. Upon binding to their receptor, specific Wnt ligands trigger phosphorylation of LRP5/6 (low density lipoprotein) by glycogen synthase kinase-3 (GSK3a/b) and casein kinase-1 (CK1g), which distances Axin (Axin1 and Axin2) from the b-catenin destruction-complex. [3][4][5][6] As a result, the b-catenin is stabilized a...

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The rising trend in oesophageal adenocarcinoma and gastric cardia

Cited by 225 publications

References 0 publications

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis

Decreasing incidence of both major histologic subtypes of gastric adenocarcinoma – a population-based study in Sweden

Frequent accumulation of nuclear E-cadherin and alterations in the Wnt signaling pathway in esophageal squamous cell carcinomas

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