Activity Detail
Seminar
The role of inflammation in lung cancer: MyD88 as the key player
Irati Garmendia
Lung cancer is the most common form of cancer and the leading cause of cancer-related mortality worldwide. Although survival rates are improving every decade, currently only one out of five patients survives five years after the diagnosis, underscoring the urgent need for better diagnostic and prognostic tools as well as more effective therapeutic strategies. The lung tumor microenvironment (TME) is highly complex and heterogeneous across patients, and it represents a promising target to impair tumor progression. It is shaped by multiple intrinsic and extrinsic factors, including chronic inflammation, the lung microbiome and respiratory pathogens. In previous studies, we demonstrated that acute influenza A virus (IAV) infection results in a long-term pro-tumoral effect in lung cancer growth by modulating cellular and molecular players in the TME. Specifically, IAV impairs tumor-specific T cell responses and leads to the exhaustion of memory CD8+ T cells. In addition, IAV infection induces a transcriptional module in tumor cells that is also present in patients with lung adenocarcinoma and is associated with poor overall survival. Our present studies at Biogipuzkoa HRI aim to identify the key mediators involved in the tumor-promoting effects of several inflammatory signals. Deciphering crucial mechanisms orchestrating the crosstalk between tumor cells and the surrounding inflammatory microenvironment will unravel new targets to maximize the efficacy of precision immunotherapies for this deadly disease.