Table 2.
Potential diagnostic biomarkers of pancreatic cancer
| Biomarker | Site | Proposed Mechanisms | Effects | Ref. |
|---|---|---|---|---|
| phylum and genus Verrucomicrobia, Deferribacteres, and Bacteroidetes | Blood microbial extracellular vesicles | Akkermansia (in Verrucomicrobia phylum) is an immune modulator related to the programmed cell death protein 1 blockade pathway | Higher in PC patients compared to HC | [82] |
| Genus Lachnospiraceae, Ruminococcaceae, Turicibacter, Akkermansia, Ruminiclostridium | Blood microbial extracellular vesicles | Akkermansia is an immune modulator related to the programmed cell death protein 1 blockade pathway | Higher in PC patients compared to HC | [82] |
| phyllum and genus Acintobacter | Blood microbial extracellular vesicles | Actinobacteria are known to produce butyrate and modulate immune function | Less abundant in PC patients compared to HC | [82] |
| Genus Stenotrophomonas, Propionibacterium, Sphingomonas and Corynebacterium | Blood microbial extracellular vesicles | May lead to an increased amount of acute phase inflammatory cytokines which might pave the way for cancer | Less abundant in PC patients compared to HC | [82] |
| Proteobacteria, Actinobacteria, and Fusobacteria | Oral cavity and gut | NA | Significant increase in Proteobacteria, Actinobacteria, and Fusobacteria in the gut of PC patients, while a significant decrease in oral Proteobacteria was observed. | [83] |
| Gammaproteobacteria | Oral cavity and gut | NA | Decreased oral/gut ratio in PC patients compared to healthy controls, which is indicative of early tumorigenesis | [83] |
| Proteobacteria | Pancreas tissue | NA | Significant increase in PC tissues compared to duodenum and stomach tissues | [85] |
| Firmicutes, Bacteroidetes, and Fusobacteria | Pancreas tissue | NA | Significant decrease in PC tissues compared to duodenum and stomach tissues | [85] |
| N. elongata and S. mitis | Oral cavity | S. mitis plays a protective role against the adhesion of cariogenic bacteria | Significant reductions in PC patients | [87] |
| G. adiacens | Oral cavity | associated with systemic inflammations | Significantly higher in PC patients | [87] |
| S. mitis | Oral cavity | The proliferation of periodontal pathogens leads to systemic inflammation and cancer progression | No difference in levels between saliva samples of PC patients and healthy individuals | [88] |
| Streptococcus | Gut | NA | More abundant in PC patients, especially in liver metastasis | [89] |
| Porphyromonas gingivalis | Oral cavity/Plasma (antibodies) | elevated levels of antibodies to oral bacteria serve as a marker for a genetically stronger immune response, providing protection against carcinogenesis | Elevated anti-Porphyromonas gingivalis antibody beneficial for cancer prevention | [90] |
| Hepatitis B virus | Liver | Chronic inflammation leading to malignant transformation, HBV DNA integration disrupting tumor suppressing gens | Impact on PC development in Asia and Oceania, but inconsequential in Europe | [97] |
| Streptococcus and Veillonella | Gut | Induce interleukin (IL)-6, IL-8, IL-10, and tumor necrosis factor-a reactions in dendritic cells | Abundance in PDAC patients | [36] |
| Faecalibacterium prausnitzii | Gut | Short-chain fatty acids regulate intestinal immune functions through cell surface G-protein coupled receptors, and their decrease leads to inflammation | Reduced numbers in PDAC patients | [36] |
| Faecalibacterium, Parvimonas, Alistipes, and Anaerostipes | Gut | Less suppression of proinflammatory and promotion of anti-inflammatory cytokines | Decrease in PDAC patients | [109] |
| Anaerotruncus, Pseudonocardia, Mucispirillum, and Cloacibacterium | Gut | NA | Increased PDAC patients | [109] |