ReviewHepatic oncology2015
Genetic risk markers for hepatocellular carcinoma in patients with alcoholic liver disease.
Review in Hepatic oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed, 2 citations in OpenAlex.
- Characterizing the mechanism behind the progression of NAFLD to hepatocellular carcinoma.Hepatic oncology · 2020Review
- Effects of interactions between environmental factors and KIF1B genetic variants on the risk of hepatocellular carcinoma in a Chinese cohort.World journal of gastroenterology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various single nucleotide polymorphisms have been reported to be associated with a higher risk of hepatocellular carcinoma in alcoholic cirrhotic patients. Until now, only common variants conferring a small increase in liver cancer risk have been identified. These inherited factors are able to modulate several biological pathways involved in alcohol-induced hepatocarcinogenesis, such as ethanol metabolism, inflammation, oxidative stress, or iron and lipid homeostasis. How the combination of these variants might collectively define an individual genomic risk prediction is currently being investigated. The other challenge in clinical practice lies in defining how to integrate this genetic information with other clinical parameters so as to refine selection of alcoholic cirrhotic patients according to various classes of hepatocellular carcinoma risk.
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What OpenQuestion holds
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.