an independent prognostic factor for survival in non-small cell lung cancer patients

Higher levels of IL-17A were detected in serum of patients with lung adenocarcinoma than healthy controls.IL-17A might affect lung adenocarcinoma by promoting angiogenesis

The role of the CCL20/CCR6/IL-17 axis in non-small-cell-lung-cancer tumor growth, was investigated.

Higher levels of IL-17 is associated with the formation of an M2-macrophage-dominant tumor microenvironment in lung cancer.

Quantitative analysis showed high concentrations of IL-10 and IL-17 in pleural fluid and blood of lung cancer patients. Statistical correlation between blood and pleural concentations was proven.

High IL-17 expression is associated with non-small cell lung cancer.

CD4, IL-17and Foxp3 may be involved in the tumor suppression caused by host immune response, and are related with non-small cell lung cancer invasion and metastasis.

The association of three single-nucleotide polymorphisms (SNPs: -152 G/A, 7488 A/G and 7383 A/G) in the IL-17A and IL-17F genes with lung cancer risk, was investigated.

Il-6, IL-17, TNF-alpha and VEGF levels were measured in exhaled breath condensate and serum of 15 patients with stage I-IIA non-small cell lung cancer.

Measurement of IL-17 levels might be a useful diagnostic and prognostic test for lung cancer patients with malignant pleural effusion

results indicate that IL-17 stimulates lung tumor growth and regulates MMP-9 mRNA levels in a p53- and SRSF1-dependent manner.

IL-17A polymorphism is associated with increased risk of nonsmall cell lung cancer probably by elevating gene expression.

IL-17A polymorphism was associated with increased susceptibility to non-small cell lung cancer and could affect gene expression.

Study provides evidence that polymorphisms of both IL-17A and IL-17F may increase lung cancer risk in Chinese population.

IL-17 may play an important role in tumor dissemination in small cell lung cancer patients.

Data show that serum interleukin 17 (IL-17) was elevated and the levels positively correlated with vascular endothelial growth factor (VEGF) concentration in non-small-cell lung cancer (NSCLC) patients.

IL-17 plays a role in lung cancer progression via different mechanisms. [review]

IL-17 contributes to the metastasis and progression of lung cancer [review]

high IL-17 expression was an indicator of poor prognosis for Chinese patients with lung cancer

expression of IL-17A, E, and F and their receptors in non-small-cell lung cancer; data suggest that IL-17A, E, F and their receptors IL-17RA, RB, RC may be involved in the pathogenesis of non-small cell lung cancer

IL-17A promoted lung tumor growth and angiogenesis.

The aim of the study was to assess the levels of expression of interleukin 17A (IL-17A) and microRNA 93 (miRNA-9) in patients with non-small cell lung cancer (NSCLC) in relation to the tumor characteristic (histopathological subtype, cancer stage (TNM and AJCC classification)), and to determine whether correlation between gene IL-17A and miR-9 expression exists.

Long-term PM2.5 exposure increases the risk of non-small cell lung cancer (NSCLC) progression by enhancing interleukin-17a (IL-17a)-regulated proliferation and metastasis.

IL-17 inhibits tumor necrosis factor(TNF)-induced chemokine Rantes expression in human synovial fibroblasts and mouse lung fibroblasts.

tumor growth and lung metastasis were enhanced in IL-17-deficient mice

Intratracheal coadministration of IL-17A and tumor necrosis alpha-alpha in mice induces production of CXCL1, CXCL2, and CXCL5 chemokines, which is associated with increased neutrophil influx in the lung.

During lung metastasis, manipulation of IL-1/IL-17 may affect local inflammatory responses at tumor sites, which may result in an improved antitumor immune response and a more favorable prognosis.

IL-17 could directly promote the invasion of Non-small cell lung cancer cells both in vitro and in vivo.

Lack of IL-17, but not IL-17F, resulted in a significant reduction in lung tumor numbers in CCSP-cre/K-ras-G12D mice and also those treated with a lysate of nontypeable Haemophilus influenza.

IL17A promotes the formation of lung metastases through tumor-endothelial transmigration.

Report provides evidence that IL-17 can promote Lewis lung carcinoma growth through inhibition of myeloid-derived suppressor cells apoptosis, which maybe dependent on ERK1/2 signaling pathway.