Caroline J. Bull

TL;DR: An overview of the key principles and assumptions of Mendelian randomization are provided, focusing on applications of this method to the study of cancer etiology and prognosis, and strengths of this approach compared with conventional epidemiological studies are highlighted.

TL;DR: Fructose reprograms cellular metabolic pathways to favour glutaminolysis and oxidative metabolism, which are required to support increased inflammatory cytokine production in both LPS-treated human monocytes and mouse macrophages, underpins a pro-inflammatory role for dietary fructose in L PS-stimulated mononuclear phagocytes which occurs at the expense of metabolic flexibility.

TL;DR: To evaluate the association of genetically proxied inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase with epithelial ovarian cancer among the general population and in BRCA1/2 mutation carriers, single-nucleotide polymorphisms associated with low-density lipoprotein cholesterol in a genome-wide association study (GWAS) meta-analysis were used.

TL;DR: In this article, Mendelian randomization was used as unconfounded instruments for specific lipid traits (Mendelian Randomization) to assess whether circulating lipids causally influence prostate cancer risk.

TL;DR: Adiposity was associated with numerous metabolic alterations, but none of these explained associations between adiposity and CRC, and it is suggested that higher BMI more greatly raises CRC risk among men, whereas higher WHR more greatly rises CRCrisk among women.