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Lung cancer associated with combustion particles and fine particulate matter (PM2.5) The roles of polycyclic aromatic hydrocarbons (PAHs) and the aryl hydrocarbon receptor (AhR)

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F23%3A00576971" target="_blank" >RIV/68081707:_____/23:00576971 - isvavai.cz</a>

  • Alternative codes found

    RIV/00027162:_____/23:N0000130

  • Result on the web

    <a href="https://www.sciencedirect.com/science/article/pii/S0006295223003921?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0006295223003921?via%3Dihub</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.bcp.2023.115801" target="_blank" >10.1016/j.bcp.2023.115801</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Lung cancer associated with combustion particles and fine particulate matter (PM2.5) The roles of polycyclic aromatic hydrocarbons (PAHs) and the aryl hydrocarbon receptor (AhR)

  • Original language description

    Air pollution is the leading cause of lung cancer after tobacco smoking, contributing to 20% of all lung cancer deaths. Increased risk associated with living near trafficked roads, occupational exposure to diesel exhaust, indoor coal combustion and cigarette smoking, suggest that combustion components in ambient fine particulate matter (PM2.5), such as polycyclic aromatic hydrocarbons (PAHs), may be central drivers of lung cancer. Activation of the aryl hydrocarbon receptor (AhR) induces expression of xenobiotic-metabolizing enzymes (XMEs) and increase PAH metabolism, formation of reactive metabolites, oxidative stress, DNA damage and mutagenesis. Lung cancer tissues from smokers and workers exposed to high combustion PM levels contain mutagenic signatures derived from PAHs. However, recent findings suggest that ambient air PM2.5 exposure primarily induces lung cancer development through tumor promotion of cells harboring naturally acquired oncogenic mutations, thus lacking typical PAH-induced mutations. On this background, we discuss the role of AhR and PAHs in lung cancer development caused by air pollution focusing on the tumor promoting properties including metabolism, immune system, cell proliferation and survival, tumor microenvironment, cell-to-cell communication, tumor growth and metastasis. We suggest that the dichotomy in lung cancer patterns observed between smoking and outdoor air PM2.5 represent the two ends of a dose-response continuum of combustion PM exposure, where tumor promotion in the peripheral lung appears to be the driving factor at the relatively low-dose exposures from ambient air PM2.5, whereas genotoxicity in the central airways becomes increasingly more important at the higher combustion PM levels encountered through smoking and occupational exposure.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30104 - Pharmacology and pharmacy

Result continuities

  • Project

    <a href="/en/project/GA21-00533S" target="_blank" >GA21-00533S: Non-conventional environmental Ah receptor ligands and their complex effects in vitro</a><br>

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2023

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Biochemical Pharmacology

  • ISSN

    0006-2952

  • e-ISSN

    1873-2968

  • Volume of the periodical

    216

  • Issue of the periodical within the volume

    OCT 2023

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    24

  • Pages from-to

    115801

  • UT code for WoS article

    001080818900001

  • EID of the result in the Scopus database

    2-s2.0-85170653835