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The current state of knowledge on small cell and non-small cell lung cancer and the position of durvalumab immunotherapy in lung cancer treatment

100%

Poboży K., Domańska J., Domański P.

OncoReview

2022

vol. 12

issue 4

75-82

Lung cancer is the second most frequently diagnosed cancer and the leading cause of cancer-related deaths in the world. These statistics make lung cancer one of the most important targets for modern medicine. The identification of multiple risk factors, including tobacco smoking, has been fundamental in understanding the disease. Late-stage detection is a significant contributor to the high mortality rate of lung cancer. Nonetheless, the role of screening is still debatable. The selection of therapy is primarily based on distinguishing between small-cell and non-small cell lung cancer. Despite the major differences in treatment, in both types in specific situations the treatment involves durvalumab – a monoclonal antibody targeting the programmed cell death ligand 1 molecule, which is often present on tumor cells and protects them against the patient’s immune system. The efficacy of durvalumab has been demonstrated in two randomized, multicenter clinical trials. The aim of this study is to summarize the current state of knowledge about lung cancer and durvalumab. Despite the current 5-year survival rate of 19% in lung cancer, the development of immunotherapeutics such as durvalumab may be the key to improving the unfavorable prognosis of lung cancer in the future.

Epigenetic Rewiring of Immune Checkpoints in Pollution-Driven Lung Adenocarcinoma: An In Vitro and In Vivo Translational Study

84%

Ekpo E. B., Ekanem P.

World News of Natural Sciences

2025

vol. 63

issue 2

385-393

Air pollution has been increasingly recognized as a major risk factor for lung adenocarcinoma, yet the molecular mechanisms linking exposure to carcinogenesis remain unclear. Recent studies suggest that fine particulate matter (PM2.5) can alter epigenetic landscapes, particularly through DNA methylation and histone modification, thereby influencing immune regulation. This study investigated how pollution exposure can induce epigenetic rewiring of the immune checkpoint gene PD-L1, leading to impaired immune recognition and tumor progression. Lung adenocarcinoma cell lines were exposed to PM2.5 extracts, and methylation patterns were analyzed using bisulfite sequencing. The expression of PD-L1 and related immune genes was quantified by qPCR, and reactivation assays using histone deacetylase (HDAC) inhibitors were performed. Complementary in vivo studies were conducted in Wistar rats exposed to PM2.5 for six weeks to assess tissue-level alterations. Results demonstrated that PM2.5 exposure significantly increased DNA methylation at CpG islands within the PD-L1 promoter, reducing gene expression and T-cell activation capacity. Treatment with epidrugs such as valproic acid reversed methylation changes and restored immune function. The findings provide mechanistic insight into how environmental pollutants contribute to immune evasion in cancer and suggest potential therapeutic intervention through epigenetic modulation.

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1 OncoReview

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1 Ekanem P.

1 Ekpo E. B.

1 Poboży K.

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The current state of knowledge on small cell and non-small cell lung cancer and the position of durvalumab immunotherapy in lung cancer treatment

Epigenetic Rewiring of Immune Checkpoints in Pollution-Driven Lung Adenocarcinoma: An In Vitro and In Vivo Translational Study