ArticleBMC cancer2025
Basal metabolic rate shapes the development and progression of hepatocellular carcinoma.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
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.
Funding
Abstract
backgroundAmong several cancer risk factors, the variation in basal metabolism rate (BMR), which constitutes up to 70% of total energy expenditures in humans, may be causally linked with neoplasm development. As BMR reflects the mass of metabolically active organs, being the function of cell size and/or cell number, it may serve as a critical metabolic proxy of cancer susceptibility in the context of cell growth and cell size.
methodsWe examined the progression and rate of development of chemically induced hepatocellular carcinoma, using lines of mice divergently selected for high or low BMR and differing with respect to both the size of metabolically active organs and their cellular architecture.
resultsThe high BMR mouse line developed hepatocellular carcinoma much faster and with a higher progression rate, accompanied by a considerable increase in liver size and hepatocyte enlargement, as compared to the low BMR mouse line. The HBMR mice also manifested an increased expression of metabolism- and cell size-related genes (mTOR, PI3K, c-myc, but not IGF-1), with a simultaneous decrease in the activity of tumor suppressors (p-53, APC) at the beginning of cancerogenic processes, promoting further neoplasm expansion.
conclusionPresented results suggest that genetically determined high BMR may additionally burden liver cells via changes in the action of specific genes, leading to higher tumorigenesis.
Indexed as
Identifiers
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.