01 February 2024 | Aref Yarahmadi and Hamed Afkhami
Gastrointestinal (GI) cancers, which account for over 33% of new cancer cases globally, pose a significant public health challenge. Recent studies have highlighted the role of the gut microbiome in the development and progression of various GI cancers, including colorectal, gastric, hepatic, and esophageal cancers. The gut microbiome, composed of a diverse array of bacteria, viruses, fungi, and other microorganisms, plays a crucial role in maintaining homeostasis and influencing immune responses. Dysbiosis, or an imbalance in the gut microbiome, has been linked to the onset and progression of GI cancers through mechanisms such as chronic inflammation, immune system disruption, and altered metabolic pathways.
In colorectal cancer (CRC), specific bacterial species like *Fusobacterium nucleatum*, *Bacteroides fragilis*, *Escherichia coli*, and *Peptostreptococcus anaerobius* have been identified as potential risk factors. These bacteria can promote tumor growth, enhance treatment resistance, and influence immune responses. For instance, *F. nucleatum* has been associated with advanced stages of CRC, increased recurrence rates, and reduced survival. *B. fragilis* produces toxins that trigger inflammatory responses and immune suppression, while *E. coli* can produce virulence factors that control CRC progression. Dietary interventions and fecal microbial transplantation (FMT) are potential strategies to modulate the gut microbiome and prevent or treat CRC.
In gastric cancer (GC), *Helicobacter pylori* infection is a significant risk factor, causing chronic inflammation and leading to cancer development. The eradication of *H. pylori* can reduce the risk of GC, but it also disrupts the gut microbiome, potentially leading to dysbiosis. Probiotics and antibiotics are being explored as therapeutic options to restore a balanced gut microbiome and prevent or treat GC.
In liver cancer, both viral infections and alcohol consumption can lead to gut dysbiosis, contributing to the development of hepatocellular carcinoma (HCC). Viral infections like hepatitis B and C can cause chronic hepatitis, while alcohol consumption can lead to alcoholic liver disease (ALD). Both conditions can alter the gut microbiome, promoting carcinogenesis. Non-alcoholic fatty liver disease (NAFLD) and its progression to NASH and HCC are also influenced by gut microbiome changes.
In esophageal cancer, the gut microbiome plays a role in the development of Barrett's esophagus and gastroesophageal reflux disease (GERD), which can lead to esophageal squamous cell carcinoma (ESCC) and adenocarcinoma (AC). Specific bacterial species, such as *Campylobacter*, *Lactobacillus*, *E. coli*, and *P. gingivalis*, have been linked to the risk and progression of esophageal cancer. The gut microbiome's role in esGastrointestinal (GI) cancers, which account for over 33% of new cancer cases globally, pose a significant public health challenge. Recent studies have highlighted the role of the gut microbiome in the development and progression of various GI cancers, including colorectal, gastric, hepatic, and esophageal cancers. The gut microbiome, composed of a diverse array of bacteria, viruses, fungi, and other microorganisms, plays a crucial role in maintaining homeostasis and influencing immune responses. Dysbiosis, or an imbalance in the gut microbiome, has been linked to the onset and progression of GI cancers through mechanisms such as chronic inflammation, immune system disruption, and altered metabolic pathways.
In colorectal cancer (CRC), specific bacterial species like *Fusobacterium nucleatum*, *Bacteroides fragilis*, *Escherichia coli*, and *Peptostreptococcus anaerobius* have been identified as potential risk factors. These bacteria can promote tumor growth, enhance treatment resistance, and influence immune responses. For instance, *F. nucleatum* has been associated with advanced stages of CRC, increased recurrence rates, and reduced survival. *B. fragilis* produces toxins that trigger inflammatory responses and immune suppression, while *E. coli* can produce virulence factors that control CRC progression. Dietary interventions and fecal microbial transplantation (FMT) are potential strategies to modulate the gut microbiome and prevent or treat CRC.
In gastric cancer (GC), *Helicobacter pylori* infection is a significant risk factor, causing chronic inflammation and leading to cancer development. The eradication of *H. pylori* can reduce the risk of GC, but it also disrupts the gut microbiome, potentially leading to dysbiosis. Probiotics and antibiotics are being explored as therapeutic options to restore a balanced gut microbiome and prevent or treat GC.
In liver cancer, both viral infections and alcohol consumption can lead to gut dysbiosis, contributing to the development of hepatocellular carcinoma (HCC). Viral infections like hepatitis B and C can cause chronic hepatitis, while alcohol consumption can lead to alcoholic liver disease (ALD). Both conditions can alter the gut microbiome, promoting carcinogenesis. Non-alcoholic fatty liver disease (NAFLD) and its progression to NASH and HCC are also influenced by gut microbiome changes.
In esophageal cancer, the gut microbiome plays a role in the development of Barrett's esophagus and gastroesophageal reflux disease (GERD), which can lead to esophageal squamous cell carcinoma (ESCC) and adenocarcinoma (AC). Specific bacterial species, such as *Campylobacter*, *Lactobacillus*, *E. coli*, and *P. gingivalis*, have been linked to the risk and progression of esophageal cancer. The gut microbiome's role in es