Obesity alters immunopathology in cancers and inflammatory diseases

Zhang, Xiaofen; Gao, Li; Meng, Haiyang; Zhang, Ailing; Liang, Yan; Lu, Jingli

doi:10.1111/obr.13638

Cited by 5 publications

(2 citation statements)

References 158 publications

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“…Pesticide exposure also augmented IL-17A in eutrophic breast cancer patients. Despite obesity dysregulates IL17-A production ( 47 ), and no data was found concerning its meaning in eutrophic patients, these findings support that pesticide exposure induce significant immunological changes in breast cancer patients, which vary according to the clinicopathological status of patients.…”

Section: Discussionmentioning

confidence: 97%

Occupational exposure to pesticides dysregulates systemic Th1/Th2/Th17 cytokines and correlates with poor clinical outcomes in breast cancer patients

Santos,

da Silva,

Jaques

et al. 2023

Front. Immunol.

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Pesticides are compounds known to cause immunetoxicity in exposed individuals, which have a potential to substantially modify the prognosis of pathologies dependent on an efficient immune response, such as breast cancer. In this context, we examined the circulating cytokine profile of Th1/Th2/Th17 patterns in women occupationally exposed to pesticides and their correlation with worse prognostic outcomes. Peripheral blood samples were collected from 187 rural working women with breast cancer, occupationally exposed or not to pesticides, to quantify the levels of cytokines IL-1β, IL-12, IL-4, IL-17-A, and TNF -α. Data on the disease profile and clinical outcomes were collected through medical follow-up. IL-12 was reduced in exposed women with tumors larger than 2 cm and in those with lymph node metastases. Significantly reduced levels of IL-17A were observed in exposed patients with Luminal B subtype tumors, with high ki67 proliferation rates, high histological grade, and positive for the progesterone receptor. Reduced IL-4 was also seen in exposed women with lymph node invasion. Our data show that occupational exposure to pesticides induces significant changes in the levels of cytokines necessary for tumor control and correlates with poor prognosis clinical outcomes in breast cancer.

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Section: Discussionmentioning

confidence: 97%

Occupational exposure to pesticides dysregulates systemic Th1/Th2/Th17 cytokines and correlates with poor clinical outcomes in breast cancer patients

Santos,

da Silva,

Jaques

et al. 2023

Front. Immunol.

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“…Likewise, population-based analyses have revealed a nearly 3-fold higher prevalence of asthma among esophageal cancer cases versus matched controls. Proposed common contributors to pathogenesis of both malignancy and lung disease include tobacco use, which damages the esophageal mucosa while promoting airway inflammation and remodeling 40 - 43 . Additionally, systemic inflammatory states may facilitate esophageal carcinogenesis while also exacerbating pulmonary disease severity 44 , 45 .…”

Section: Discussionmentioning

confidence: 99%

Exploring the Common Genetic Underpinnings of Chronic Pulmonary Disease and Esophageal Carcinoma Susceptibility

Zhang,

Zhou,

et al. 2024

J. Cancer

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Background: Pulmonary diseases and esophageal cancer are highly prevalent conditions with rising incidence worldwide. Prior evidence supports shared environmental and behavioral factors, but less is known regarding potential genetic links underlying this comorbidity. This study aimed to elucidate the complex genetic relationship between chronic lung diseases and esophageal cancer risk. Methods: Linkage disequilibrium score regression assessed the genetic correlation between esophageal cancer and asthma, COPD, and idiopathic pulmonary fibrosis leveraging extensive GWAS datasets. Pleiotropic analysis, gene-set enrichment, eQTL mapping, and mendelian randomization causality analyses were then conducted to identify specific shared genetic variants, enriched pathways, causal relationships and gene regulatory mechanisms connecting lung disease and cancer susceptibility. Results: Significant genetic correlations were observed between esophageal cancer and both COPD and asthma, but not idiopathic pulmonary fibrosis. Further analyses identified 13 pleiotropic loci and 6 shared genes including CHRNA4, ERBB3, and SMAD3, as well as pathways related to immune function. eQTL integration highlighted 53 genes like SOCS1, FGF2, and CHRNA5 with tissue-specific regulatory effects on disease risk. Bidirectional relationships were noted, whereby genetic predisposition to asthma and COPD increased esophageal cancer risk, while cancer liability reciprocally raised pulmonary fibrosis risk. Conclusions: These genomic analyses provide initial evidence that shared genetic factors may underpin the comorbidity between lung conditions and esophageal malignancy. The genes and pathways identified offer insights into biological mechanisms linking both diseases, aiding future screening, prevention and therapeutic efforts to mitigate this growing comorbidity burden.

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