| Literature DB >> 26002081 |
Julia Kravchenko1, Emanuela Corsini2, Marc A Williams3, William Decker4, Masoud H Manjili5, Takemi Otsuki6, Neetu Singh7, Faha Al-Mulla8, Rabeah Al-Temaimi8, Amedeo Amedei9, Anna Maria Colacci10, Monica Vaccari10, Chiara Mondello11, A Ivana Scovassi11, Jayadev Raju12, Roslida A Hamid13, Lorenzo Memeo14, Stefano Forte14, Rabindra Roy15, Jordan Woodrick15, Hosni K Salem16, Elizabeth P Ryan17, Dustin G Brown17, William H Bisson18, Leroy Lowe19, H Kim Lyerly20.
Abstract
An increasing number of studies suggest an important role of host immunity as a barrier to tumor formation and progression. Complex mechanisms and multiple pathways are involved in evading innate and adaptive immune responses, with a broad spectrum of chemicals displaying the potential to adversely influence immunosurveillance. The evaluation of the cumulative effects of low-dose exposures from the occupational and natural environment, especially if multiple chemicals target the same gene(s) or pathway(s), is a challenge. We reviewed common environmental chemicals and discussed their potential effects on immunosurveillance. Our overarching objective was to review related signaling pathways influencing immune surveillance such as the pathways involving PI3K/Akt, chemokines, TGF-β, FAK, IGF-1, HIF-1α, IL-6, IL-1α, CTLA-4 and PD-1/PDL-1 could individually or collectively impact immunosurveillance. A number of chemicals that are common in the anthropogenic environment such as fungicides (maneb, fluoxastrobin and pyroclostrobin), herbicides (atrazine), insecticides (pyridaben and azamethiphos), the components of personal care products (triclosan and bisphenol A) and diethylhexylphthalate with pathways critical to tumor immunosurveillance. At this time, these chemicals are not recognized as human carcinogens; however, it is known that they these chemicalscan simultaneously persist in the environment and appear to have some potential interfere with the host immune response, therefore potentially contributing to promotion interacting with of immune evasion mechanisms, and promoting subsequent tumor growth and progression.Entities:
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Year: 2015 PMID: 26002081 PMCID: PMC4565606 DOI: 10.1093/carcin/bgv033
Source DB: PubMed Journal: Carcinogenesis ISSN: 0143-3334 Impact factor: 4.944