Saturated fatty acid intake, genetic risk and colorectal cancer incidence: A large‐scale prospective cohort study

Abstract

Previous investigations mainly focused on the associations of dietary fatty acids with colorectal cancer (CRC) risk, which ignored gene-environment interaction and mechanisms interpretation. We conducted a case-control study (751 cases and 3058 controls) and a prospective cohort study (125 021 participants) to explore the associations between dietary fatty acids, genetic risks, and CRC. Resultsshowed that high intake of saturated fatty acid (SFA) was associated with a higher risk of CRC than low SFA intake (HR =1.22, 95% CI:1.02-1.46). Participants at high genetic risk had a greater risk of CRC with the HR of 2.48 (2.11-2.91) than those at low genetic risk. A multiplicative interaction of genetic risk and SFA intake with incident CRC risk was found (P Interaction = 7.59 Â 10 À20 ), demonstrating that participants with high genetic risk and high SFA intake had a 3.75-fold greater risk of CRC than those with low genetic risk and low SFA intake. Furthermore, incorporating PRS and SFA into traditional clinical risk factors improved the discriminatory accuracy for CRC risk stratification (AUC from 0.706 to 0.731). Multi-omics data showed that exposure to SFA-rich high-fat dietary (HFD) can responsively induce epigenome reprogramming of some oncogenes and pathological activation of fatty

Identification of tumor stemness and immunity related prognostic factors and sensitive drugs in head and neck squamous cell carcinoma

“…Fatty acid metabolic pathways are frequently reprogrammed in cancer cells to fulfill their energy demands for rapid growth and proliferation 51 . Alterations in fatty acid metabolism can facilitate the survival and proliferation of tumor cells by providing energy, modulating signal molecules, and influencing membrane synthesis 52 , 53 . Moreover, IL2, STAT5, and KRAS have been shown to play very critical roles in cancer progression 54 – 56 .…”