ArticleMedical oncology (Northwood, London, England)2014
Association between gastric cardia adenocarcinoma risk and alcohol flushing response, but not alcohol consumption.
Article in Medical oncology (Northwood, London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.
- Pooled it
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The relationship between the development of gastric cardia cancer (GCA) and alcohol consumption remains unclear. Alcohol flushing response reflects an accumulation of the carcinogenic acetaldehyde and has been proved to be a risk factor for many cancers. The main objective of the present study was to assess the impact of alcohol flushing response on GCA risk in a Chinese population in conjunction with lifetime alcohol consumption. The study subjects consist of 281 male patients [130 with GCA and 151 with esophageal squamous cell carcinoma (ESCC)] and 160 non-cancer male controls, matched with respect to age. Conditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (95% CI). There is no significant association between GCA risk and alcohol consumption. However, the adjusted ORs for flushing response of GCA and ESCC was 2.03 (95% CI 1.15-3.56, p=0.014) and 2.32 (95% CI 1.34-4.03, p=0.003), respectively, compared with those reporting no flushing response. Furthermore, compared with non-drinkers, the heavy drinkers and moderate drinkers with current/former flushing response experienced significant GCA risk (heavy drinkers: OR 2.59, 95% CI 1.06-6.31, p=0.037; moderate drinkers: OR 3.11, 95% CI 1.17-8.26, p=0.023), while drinkers without flushing response did not have increased risk. The drinkers with flushing response also had a higher ESCC risk than those without flushing response. In conclusion, alcohol flushing response is a clinically useful biomarker of susceptibility to GCA and ESCC risk from alcohol.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.