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Infection and Cancer: Bi-Directorial Interactions pp 49–74Cite as

Bacterial Infections and Cancer Development

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Abstract

Multiple epidemiological and clinical studies have identified an association between specific bacterial infection and cancers. Several bacterial infections have been proven to serve as risk factors for the initial development and survival of cancerous cells in different tissues and organs. It is estimated that about 20–25 % of all human cancers are caused by chronic infection-derived inflammation. A sustained production of various reactive aldehydes, oxygen and nitrogen species, as well as cytokines, chemokines and growth factors, at the inflammatory microenvironment can perturb normal biological and physiological processes leading to genomic instability and an increased risk of cancer development. Furthermore, toxins produced by bacteria, different bacteria-derived metabolites and some bacterial virulence factors may be also involved in the associated tumorigenic processes via DNA damage response, cell cycle regulation and other mechanisms. Unfortunately, it is still not fully clear which combinations of specific bacteria-associated factors and microenvironmental stimuli contribute to high incidence of cancer during certain infectious diseases. Understanding the mechanisms of how bacterial infections affect cancer development and progression will promote new or more efficient approaches to cancer prevention and therapy.

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Abbreviations

AP-1:

activator protein-1

BALF:

bronchoalveolar lavage fluid

CDT:

cytolithal distending toxin

CKD:

chronic kidney disease

COX2:

cyclooxygenase-2

CRC:

colorectal cancer

DC:

dendritic cell(s)

EMT:

epithelial-to-mesenchymal transition

LPS:

lipopolysaccharide

MALT:

mucosa-associated lymphoid tissue

MAPK:

mitogen-activated protein kinase

NO:

nitric oxide

NLR:

NOD-like receptors

PI3K:

phosphatidylinositol 3-kinase

ROS:

reactive oxygen species

PRR:

pattern recognition receptor(s)

STAT3:

signal transducer and activator of transcription 3

TLR:

Toll-like receptor

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  1. Departments of Pathology and Immunology, University of Pittsburgh Medical Center, Scaife Hall S733 3550 Terrace Street, Pittsburgh, PA, 15261, USA

    Marianna Agassandian & Galina V. Shurin

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  1. Marianna Agassandian
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  2. Galina V. Shurin
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Correspondence to Marianna Agassandian .

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  1. Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

    Michael R. Shurin

  2. Department of Immunology, Roswell Park Cancer Institute, Buffalo, New York, USA

    Yasmin Thanavala

  3. Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

    Nahed Ismail

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Agassandian, M., Shurin, G.V. (2015). Bacterial Infections and Cancer Development. In: Shurin, M., Thanavala, Y., Ismail, N. (eds) Infection and Cancer: Bi-Directorial Interactions. Springer, Cham. https://doi.org/10.1007/978-3-319-20669-1_4

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