Abstract
Although colorectal cancer (CRC) is the second leading cause of death in developed countries, current diagnostic tests for early disease stages are suboptimal. We have performed a combination of UHPLC-MS metabolomics and 16S microbiome analyses on 224 feces samples in order to identify early biomarkers for both advanced adenomas (AD) and CRC. We report differences in fecal levels of cholesteryl esters and sphingolipids in CRC. We identified Fusobacterium, Parvimonas and Staphylococcus to be increased in CRC patients and Lachnospiraceae family to be reduced. We finally described Adlercreutzia to be more abundant in AD patients’ feces. Integration of metabolomics and microbiome data revealed tight interactions between bacteria and host and performed better than FOB test for CRC diagnosis. This study identifies potential early biomarkers that outperform current diagnostic tools and frame them into the stablished gut microbiota role in CRC pathogenesis.
Highlights
Colorectal cancer (CRC) represents almost 10% of global cancer incidence [1], being the second leading cause of death in developed countries [2]
Male individuals presented with major prevalence of both AD and colorectal cancer (CRC) when compared to healthy group (62.23%, 59.60% vs. 44.74%) and they were older that control group (67.99, 70.16 vs. 64.62 years old respectively)
Both group of patients presented with higher presence of fecal occult blood (FOB) compared to controls, as well as CEA
Summary
Colorectal cancer (CRC) represents almost 10% of global cancer incidence [1], being the second leading cause of death in developed countries [2]. There is a need for new molecular parameters that are able to distinguish between CRC types for a better treatment outcome [1] In this context, metabolomics of feces samples have provided new non-invasive, accurate and predictive biomarkers for CRC, as our group and other authors have suggested [7,8,9]. Among the factors that influence these metabolisms, and may be related to CRC development and progression, the microbiota has been recurrently pointed to be one of them and suggested the bacterial driver-passenger hypothesis for CRC initiation and progression [15,16] This hypothesis is highly supported by the fact that germ-free mice models susceptible to CRC have fewer tumors that non-germ-free mice [17,18,19]
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