Silica-mediated airway chronic inflammation promotes lung carcinogenesis through the activation of preneoplastic lesions in the context of an immunosuppressive microenvirontment

ABSTRACT: Basic studies on preneoplastic lesions are important to determine the molecular alterations that take place in early steps of lung carcinogenesis. Little is known about the molecular events preceding the development of lung cancer in the context of an inflammatory environment. In this study we report the generation of a chemical-induced lung carcinogenesis mouse model in the presence of silicotic chronic inflammation. Silica-induced lung inflammation, strongly promoted incidence of lung cancer in mice treated with NDMA, a carcinogen found in tobacco smoke. Histological and molecular analysis revealed that permanent inflammation contributed to lung tumorigenesis through the adquisition of preneoplastic changes in lung epithelial cells. Inflammatory milieu increased the expression of PDCD1,

ORGANISM(S): Mus musculus

SUBMITTER: Daniel Ajona 

PROVIDER: E-GEOD-43453 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress