Dietary fat intake is associated with increased risk of colorectal cancer (CRC). In this study, the team led by Jun Yu examined the role of high-fat diet (HFD) in driving CRC through modulating gut microbiota and metabolites. They found that HFD promotes colorectal carcinogenesis in CRC mice models, an effect that was attenuated by antibiotics treatment, suggesting that the microbiota underlies HFD-induced CRC. Next, metagenome sequencing revealed that HFD triggered a significant shift in the microbiome composition in HFD-fed mice. Pathogenic bacteria Alistipes sp. Marseille-P5997 and Alistipes sp. 5CPEGH6 were increased while the levels of probiotic Parabacteroides distasonis was depleted. Moreover, microbial dysbiosis was associated with compromised gut barrier function in HFD fed mice. Faecal microbiota transplantation of HFD-fed mice stool to germfree mice was found to accelerated chemicallyinduced CRC, confirming the functional role of dysbiosis in HFD-induced CRC development. Finally, metabolomic analysis demonstrated that the gut metabolite lysophosphatidic acid was elevated with HFD fed mice. Lysophosphatidic acid was found to promote CRC growth and impair gut barrier function. In summary, their work showed that gut dysbiosis as a crucial link to diet-induced CRC. (Gastroenterology, 2021)

Gut microbial dysbiosis has pivotal involvement in CRC. The team is the first to report a comprehensive mapping of the intratumoural gut microbiome heterogeneity in CRC patients. To this end, they collected multiple biopsies (N=436) from patients with CRC (N=36) or adenomas (N=32), with 2-6 samples from each tumour plus 2-5 biopsies from adjacent normal tissues for each patient. They then performed microbial genome sequencing on these samples, and discovered that there are substantial differences in intratumoural microbial communities even within the same tumour. In particular, abundances of some CRC-associated pathobionts (eg, Fusobacterium, Bacteroides, Parvimonas, and Prevotella) were found to be highly varied within a single neoplasia. Moreover, they found that the intra-neoplasia variation in abundance of individual microbes changed along the adenoma-carcinoma sequence. They also observed that tumour intrinsic factors KRAS mutation and microsatellite instability were correlated with of intratumoural microbial heterogeneity. Their work thus shed light on the impact of microbial heterogeneity on CRC development. (Gastroenterology, 2021)

Dietary fat intake is associated with increased risk of colorectal cancer (CRC). In this study, the team led by Jun Yu examined the role of high-fat diet (HFD) in driving CRC through modulating gut microbiota and metabolites. They found that HFD promotes colorectal carcinogenesis in CRC mice models, an effect that was attenuated by antibiotics treatment, suggesting that the microbiota underlies HFD-induced CRC. Next, metagenome sequencing revealed that HFD triggered a significant shift in the microbiome composition in HFD-fed mice. Pathogenic bacteria Alistipes sp. Marseille-P5997 and Alistipes sp. 5CPEGH6 were increased while the levels of probiotic Parabacteroides distasonis was depleted. Moreover, microbial dysbiosis was associated with compromised gut barrier function in HFD fed mice. Faecal microbiota transplantation of HFD-fed mice stool to germfree mice was found to accelerated chemicallyinduced CRC, confirming the functional role of dysbiosis in HFD-induced CRC development. Finally, metabolomic analysis demonstrated that the gut metabolite lysophosphatidic acid was elevated with HFD fed mice. Lysophosphatidic acid was found to promote CRC growth and impair gut barrier function. In summary, their work showed that gut dysbiosis as a crucial link to diet-induced CRC. (Gastroenterology, 2021)

Gut microbial dysbiosis has pivotal involvement in CRC. The team is the first to report a comprehensive mapping of the intratumoural gut microbiome heterogeneity in CRC patients. To this end, they collected multiple biopsies (N=436) from patients with CRC (N=36) or adenomas (N=32), with 2-6 samples from each tumour plus 2-5 biopsies from adjacent normal tissues for each patient. They then performed microbial genome sequencing on these samples, and discovered that there are substantial differences in intratumoural microbial communities even within the same tumour. In particular, abundances of some CRC-associated pathobionts (eg, Fusobacterium, Bacteroides, Parvimonas, and Prevotella) were found to be highly varied within a single neoplasia. Moreover, they found that the intra-neoplasia variation in abundance of individual microbes changed along the adenoma-carcinoma sequence. They also observed that tumour intrinsic factors KRAS mutation and microsatellite instability were correlated with of intratumoural microbial heterogeneity. Their work thus shed light on the impact of microbial heterogeneity on CRC development. (Gastroenterology, 2021)

Dietary fat intake is associated with increased risk of colorectal cancer (CRC). In this study, the team led by Jun Yu examined the role of high-fat diet (HFD) in driving CRC through modulating gut microbiota and metabolites. They found that HFD promotes colorectal carcinogenesis in CRC mice models, an effect that was attenuated by antibiotics treatment, suggesting that the microbiota underlies HFD-induced CRC. Next, metagenome sequencing revealed that HFD triggered a significant shift in the microbiome composition in HFD-fed mice. Pathogenic bacteria Alistipes sp. Marseille-P5997 and Alistipes sp. 5CPEGH6 were increased while the levels of probiotic Parabacteroides distasonis was depleted. Moreover, microbial dysbiosis was associated with compromised gut barrier function in HFD fed mice. Faecal microbiota transplantation of HFD-fed mice stool to germfree mice was found to accelerated chemicallyinduced CRC, confirming the functional role of dysbiosis in HFD-induced CRC development. Finally, metabolomic analysis demonstrated that the gut metabolite lysophosphatidic acid was elevated with HFD fed mice. Lysophosphatidic acid was found to promote CRC growth and impair gut barrier function. In summary, their work showed that gut dysbiosis as a crucial link to diet-induced CRC. (Gastroenterology, 2021)

Gut microbial dysbiosis has pivotal involvement in CRC. The team is the first to report a comprehensive mapping of the intratumoural gut microbiome heterogeneity in CRC patients. To this end, they collected multiple biopsies (N=436) from patients with CRC (N=36) or adenomas (N=32), with 2-6 samples from each tumour plus 2-5 biopsies from adjacent normal tissues for each patient. They then performed microbial genome sequencing on these samples, and discovered that there are substantial differences in intratumoural microbial communities even within the same tumour. In particular, abundances of some CRC-associated pathobionts (eg, Fusobacterium, Bacteroides, Parvimonas, and Prevotella) were found to be highly varied within a single neoplasia. Moreover, they found that the intra-neoplasia variation in abundance of individual microbes changed along the adenoma-carcinoma sequence. They also observed that tumour intrinsic factors KRAS mutation and microsatellite instability were correlated with of intratumoural microbial heterogeneity. Their work thus shed light on the impact of microbial heterogeneity on CRC development. (Gastroenterology, 2021)