ArticleRespiratory research2010
Allergic inflammation does not impact chemical-induced carcinogenesis in the lungs of mice.
Article in Respiratory research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Long-term exposure to house dust mites accelerates lung cancer development in mice.Journal of experimental & clinical cancer research : CR · 2023Article
- IgE-Based Therapeutic Combination Enhances Antitumor Response in Preclinical Models of Pancreatic Cancer.Molecular cancer therapeutics · 2021Article
- Safety of Eosinophil-Depleting Therapy for Severe, Eosinophilic Asthma: Focus on Benralizumab.Drug safety · 2020Review
- Mutant KRAS promotes malignant pleural effusion formation.Nature communications · 2017Article
- Inhibition of tumor progression during allergic airway inflammation in a murine model: significant role of TGF-β.Cancer immunology, immunotherapy : CII · 2015Article
- Interleukin-5 facilitates lung metastasis by modulating the immune microenvironment.Cancer research · 2015Article
- Article
- Enhancement of lung tumorigenesis in a Gprc5a Knockout mouse by chronic extrinsic airway inflammation.Molecular cancer · 2012Article
- Neutralization of tumor necrosis factor bioactivity ameliorates urethane-induced pulmonary oncogenesis in mice.Neoplasia (New York, N.Y.) · 2011Article
- The BATTLE to personalize lung cancer prevention through reverse migration.Cancer prevention research (Philadelphia, Pa.) · 2011Article
- Tumor-derived osteopontin isoforms cooperate with TRP53 and CCL2 to promote lung metastasis.OncoimmunologyArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough the relationship between allergic inflammation and lung carcinogenesis is not clearly defined, several reports suggest an increased incidence of lung cancer in patients with asthma. We aimed at determining the functional impact of allergic inflammation on chemical carcinogenesis in the lungs of mice.
methodsBalb/c mice received single-dose urethane (1 g/kg at day 0) and two-stage ovalbumin during tumor initiation (sensitization: days -14 and 0; challenge: daily at days 6-12), tumor progression (sensitization: days 70 and 84; challenge: daily at days 90-96), or chronically (sensitization: days -14 and 0; challenge: daily at days 6-12 and thrice weekly thereafter). In addition, interleukin (IL)-5 deficient and wild-type C57BL/6 mice received ten weekly urethane injections. All mice were sacrificed after four months. Primary end-points were number, size, and histology of lung tumors. Secondary end-points were inflammatory cells and mediators in the airspace compartment.
resultsOvalbumin provoked acute allergic inflammation and chronic remodeling of murine airways, evident by airspace eosinophilia, IL-5 up-regulation, and airspace enlargement. Urethane resulted in formation of atypical alveolar hyperplasias, adenomas, and adenocarcinomas in mouse lungs. Ovalbumin-induced allergic inflammation during tumor initiation, progression, or continuously did not impact the number, size, or histologic distribution of urethane-induced pulmonary neoplastic lesions. In addition, genetic deficiency in IL-5 had no effect on urethane-induced lung tumorigenesis.
conclusionsAllergic inflammation does not impact chemical-induced carcinogenesis of the airways. These findings suggest that not all types of airway inflammation influence lung carcinogenesis and cast doubt on the idea of a mechanistic link between asthma and lung cancer.
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