title: Microbial influences on hormesis, oncogenesis, and therapy: A review of the literature.
abstract: Utilization of environmental stimuli for growth is the main factor contributing to the evolution of prokaryotes and eukaryotes, independently and mutualistically. Epigenetics describes an organism's ability to vary expression of certain genes based on their environmental stimuli. The diverse degree of dose-dependent responses based on their variances in expressed genetic profiles makes it difficult to ascertain whether hormesis or oncogenesis has or is occurring. In the medical field this is shown where survival curves used in determining radiotherapeutic doses have substantial uncertainties, some as large as 50% (Barendsen, 1990). Many in-vitro radiobiological studies have been limited by not taking into consideration the innate presence of microbes in biological systems, which have either grown symbiotically or pathogenically. Present in-vitro studies neglect to take into consideration the varied responses that commensal and opportunistic pathogens will have when exposed to the same stimuli and how such responses could act as stimuli for their macro/microenvironment. As a result many theories such as radiation carcinogenesis explain microscopic events but fail to describe macroscopic events (Cohen, 1995). As such, this review shows how microorganisms have the ability to perturb risks of cancer and enhance hormesis after irradiation. It will also look at bacterial significance in the microenvironment of the tumor before and during treatment. In addition, bacterial systemic communication after irradiation and the host's immune responses to infection could explain many of the phenomena associated with bystander effects. Therefore, the present literature review considers the paradigms of hormesis and oncogenesis in order to find a rationale that ties them all together. This relationship was thus characterized to be the microbiome.
authors.affiliation: Department of Nuclear Engineering, Texas A&M University, College Station, TX 77843, USA; Texas A&M Institute for Preclinical Studies, Texas A&M University, College Station, TX 77843, USA.
authors.forename: Ryan
authors.initials: R
authors.lastname: Clanton
authors.affiliation: Department of Nuclear Engineering, Texas A&M University, College Station, TX 77843, USA.
authors.forename: David
authors.initials: D
authors.lastname: Saucier
authors.affiliation: Department of Nuclear Engineering, Texas A&M University, College Station, TX 77843, USA.
authors.forename: John
authors.initials: J
authors.lastname: Ford
authors.affiliation: Department of Nuclear Engineering, Texas A&M University, College Station, TX 77843, USA; Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX 77843, USA; Texas A&M Institute for Preclinical Studies, Texas A&M University, College Station, TX 77843, USA.
authors.forename: Gamal
authors.initials: G
authors.lastname: Akabani
mesh_terms: D000818:Animals; D001419:Bacteria; D063646:Carcinogenesis; D059165:Hormesis; D006801:Humans; D064307:Microbiota; D009369:Neoplasms / Q000188:drug therapy / Q000382:microbiology; D017382:Reactive Oxygen Species; D059016:Tumor Microenvironment
chemical_list: D017382:Reactive Oxygen Species
keywords: Hormesis; Lipid peroxidation; Microbiome; Oncogenesis; Tumor microenvironment