Colorectal cancer |
Oral microbes |
Members of oral microbes, including Gemella, Peptostreptococcus, Parvimonas, and Leptotrichia, were enriched in colorectal adenocarcinoma tissue (Nakatsu et al. 2015).
Members of oral microbes, including Parvimonas micra, Peptostreptococcus stomatis, and Peptostreptococcus anaerobius, were enriched in fecal specimens from patients with metastatic colorectal adenocarcinoma (Thomas et al. 2019; Wirbel et al. 2019; Yachida et al. 2019).
Peptostreptococcus anaerobius can activate the NFKB signaling pathway in colorectal cancer cell lines and inhibit T-cell-mediated immune responses against colorectal tumors through the recruitment of myeloid-derived suppressor cells and tumor-associated macrophages into the tumor microenvironment in the ApcMin/+ mouse model (Long et al. 2019).
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Viral microbiome |
Some specific viral taxa, such as Orthobunyavirus, Inovirus, or Tunalikevirus, were enriched in fecal specimens from patients with colorectal cancer, and dysbiosis of intestinal viral microbiome was associated with worse clinical outcomes in colorectal cancer (Nakatsu et al. 2018).
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Fungal microbiome |
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Fusobacterium nucleatum |
The amount of Fusobacterium nucleatum was increased in tumor tissue and fecal specimens from patients with colorectal cancer (Mima et al. 2017).
Fusobacterium nucleatum was detected not only in primary colorectal tumors, but also in metastatic lymph nodes and liver metastases (Bullman et al. 2017; Yu et al. 2016).
Fusobacterium nucleatum can inhibit T-cell-mediated immune responses against colorectal tumors through the recruitment of myeloid-derived suppressor cells into the tumor microenvironment in the ApcMin/+ mouse model (Kostic et al. 2013). The Fap2 protein of Fusobacterium nucleatum has been shown to interact with T cell immunoglobulin and ITIM domain receptor and inhibit activities of NK cells and T cells (Gur et al. 2015).
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Campylobacter species |
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Escherichia coli |
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Bacteroides fragilis |
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Enterococcus faecalis |
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Streptococcus gallolyticcus |
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