Interleukin-17 (IL-17) is a proinflammatory cytokines produced by T helper 17 (Th17) cells, which plays an important role in both innate and adaptive immune systems. Genetic variants in the IL-17 genes may influence the immunopathogenesis of many cancers. In our study, we investigated 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, in the Tunisian population. The genotypic and allelic distributions of IL-17A and IL-17F genes polymorphisms were analyzed by Polymerase Chain-Reaction (PCR) and Restriction Fragment Length Polymorphism (RFLP) for 239 patients and 258 healthy controls. Our results revealed a statistically significant association between IL-17F 7488G allele and increased lung cancer risk (P=0.028). Stratification analysis indicated that IL-17F 7488G allele enhances the risk of lung cancer development among men and oldest age subject groups (P<0.05). Patients with IL-17F 7488G allele were also more likely to be diagnosed at advanced stage (P=0.04), or with metastatic lung cancer (P=0.035). Furthermore, no significant association between IL-17F 7383 A/G, IL-17 -152G/A polymorphisms and lung cancer risk was observed (P>0.05). However, we reported contradictory findings on the association of IL-17 -152 G/A polymorphisms with lung cancer risk. In addition, we suggested the existence of a biological interaction between IL-17A, but not IL-17F polymorphisms and smoking. Our findings suggest that IL-17F 7488G allele is associated with increased lung cancer risk in the Tunisian population.
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http://dx.doi.org/10.1016/j.cyto.2013.12.012 | DOI Listing |
Cancer Immunol Res
January 2025
Massachusetts Institute of Technology, Cambridge, MA, United States.
Tumor cell-intrinsic signaling pathways can drastically affect the tumor immune microenvironment, promoting tumor progression and resistance to immunotherapy by excluding immune-cell populations from the tumor. Several tumor cell-intrinsic pathways have been reported to modulate myeloid-cell and T-cell infiltration creating "cold" tumors. However, clinical evidence suggests that excluding cytotoxic T cells from the tumor core also mediates immune evasion.
View Article and Find Full Text PDFClin Cancer Res
January 2025
University Hospital Essen, Essen, Germany.
Antibodies targeting immune checkpoints, such as PD-1, PD-L1, or CTLA-4, have transformed the treatment of patients with lung cancers. Unprecedented rates of durable responses are achieved in an imperfectly characterized population of patients with metastatic disease. More recently, immune checkpoint inhibitors have been explored in patients with resectable non-small-cell lung cancers.
View Article and Find Full Text PDFTuberk Toraks
December 2024
Department of Thoracic Surgery, Hacettepe University Faculty of Medicine, Ankara, Türkiye.
Lung cancers associated with cystic airspaces (LCCAs) are a rare and relatively novel concept analyzed in various case reports and retrospective studies. In this review, it was our aim to investigate the morphologic, imaging, and clinicopathologic characteristics of this entity, as well as its natural course in light of the current literature. Literature search including the years 2000-2022 was conducted in PubMed.
View Article and Find Full Text PDFCancer Cytopathol
January 2025
Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Background: Telecytology-assisted rapid on-site evaluation (ROSE) offers a cost-effective method to enhance minimally invasive biopsies like fine needle aspiration and core biopsies with touch preparation. By reducing nondiagnostic sampling and the need for repeat procedures, ROSE via telecytology facilitates prompt triage for ancillary tests, improving patient management. This study examines cases initially deemed adequate for diagnosis during telecytology-assisted ROSE but later categorized as nondiagnostic at final evaluation (NDIS).
View Article and Find Full Text PDFJ Am Chem Soc
January 2025
Department of Pulmonary and Critical Care Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, West China Hospital, Sichuan University, Chengdu 610065, China.
Determining mutations in the kinase domain of the epidermal growth factor receptor (EGFR) is critical for the effectiveness of EGFR tyrosine kinase inhibitors (TKIs) in lung cancer. Yet, DNA-based sequencing analysis of tumor samples is time-consuming and only provides gene mutation information on EGFR, making it challenging to design effective EGFR-TKI therapeutic strategies. Here, we present a new image-based method involving the rational design of a quenched probe based on EGFR-TKI to identify mutant proteins, which permits specific and "no-wash" real-time imaging of EGFR in living cells only upon covalent targeting of the EGFR kinase.
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