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Review
. 2022 Apr 4:12:836004.
doi: 10.3389/fonc.2022.836004. eCollection 2022.

Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far

Affiliations
Review

Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far

Shashanka K Prasad et al. Front Oncol. .

Abstract

Cancers are known to have multifactorial etiology. Certain bacteria and viruses are proven carcinogens. Lately, there has been in-depth research investigating carcinogenic capabilities of some bacteria. Reports indicate that chronic inflammation and harmful bacterial metabolites to be strong promoters of neoplasticity. Helicobacter pylori-induced gastric adenocarcinoma is the best illustration of the chronic inflammation paradigm of oncogenesis. Chronic inflammation, which produces excessive reactive oxygen species (ROS) is hypothesized to cause cancerous cell proliferation. Other possible bacteria-dependent mechanisms and virulence factors have also been suspected of playing a vital role in the bacteria-induced-cancer(s). Numerous attempts have been made to explore and establish the possible relationship between the two. With the growing concerns on anti-microbial resistance and over-dependence of mankind on antibiotics to treat bacterial infections, it must be deemed critical to understand and identify carcinogenic bacteria, to establish their role in causing cancer.

Keywords: Helicobacter pylori; bacteria; carcinogen; chronic inflammation; oncogenesis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Roles of phosphorylated and non-phosphorylated cagA in neoplastic transformation.
Figure 2
Figure 2
Etiopathogenesis of gastric adenocarcinoma with H. pylori infection.
Figure 3
Figure 3
C. trachomatis affecting host cervical cells.
Figure 4
Figure 4
Fusobacterium nucleatum and cancer associations.

References

    1. Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M, et al. . Cancer Incidence and Mortality Worldwide: Sources, Methods and Major Patterns in GLOBOCAN 2012. Int J Cancer (2015) 136(5):E359–86. doi: 10.1002/ijc.29210 - DOI - PubMed
    1. International Agency for Research on Cancer . (2021). Available at: https://gco.iarc.fr/today/data/factsheets/cancers/39-All-cancers-fact-sh....
    1. Blot WJ, McLaughlin JK, Winn DM, Austin DF, Greenberg RS, Preston-Martin S, et al. . Smoking and Drinking in Relation to Oral and Pharyngeal Cancer. Cancer Res (1988) 48(11):3282–7. - PubMed
    1. Mons U, Gredner T, Behrens G, Stock C, Brenner H. Cancers Due to Smoking and High Alcohol Consumption. Dtsch Arztebl Int (2018) 115(35–36):571–7. doi: 10.3238/arztebl.2018.0571 - DOI - PMC - PubMed
    1. van Elsland D, Neefjes J. Bacterial Infections and Cancer. EMBO Rep (2018) 19(11):e46632. doi: 10.15252/embr.201846632 - DOI - PMC - PubMed

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