ArticleWorld journal of gastroenterology2010
Modifier-concept of colorectal carcinogenesis: lipidomics as a technical tool in pathway analysis.
Article in World journal of gastroenterology, 2010. 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, 8 citations in OpenAlex.
- Untargeted lipidomic features associated with colorectal cancer in a prospective cohort.BMC cancer · 2018Article
- Human intestinal acyl-CoA synthetase 5 is sensitive to the inhibitor triacsin C.World journal of gastroenterology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the modifier concept of intestinal carcinogenesis, lipids have been established as important variables and one focus is given to long-chain fatty acids. Increased consumption of long-chain fatty acids is in discussion to modify the development of colorectal carcinoma in humans. Saturated long-chain fatty acids, in particular, are assumed to promote carcinogenesis, whereas polyunsaturated forms are likely to act in the opposite way. At present, the molecular mechanisms behind these effects are not well understood. Recently, it has been demonstrated by lipidomics and associated molecular techniques, that activation and metabolic channeling of long-chain fatty acids are important mechanisms to modify colorectal carcinogenesis. In this Editorial, an overview about the present concept of long-chain fatty acids and its derivatives in colorectal carcinogenesis as well as technical algorithms in lipid analysis is given.
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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.