Interplay Between Lung Microbiome Dysbiosis and Driver Mutations in Oncogenic Pathways: Implications for Lung Cancer Development

Emerging evidence establishes the lung microbiota as a key regulator of lung cancer initiation, with mounting evidence of bidirectional interplay between microbial imbalance and oncogenic driver mutations. This review synthesizes recent advances on how altered microbial communities promote carcinogenesis through interrelated mechanisms of chronic inflammation, metabolite signaling, epigenetic modification, and direct DNA damage. Recent research illustrates that certain taxa of bacteria, specifically Streptococcus, Veillonella, Prevotella, and Granulicatella species, are remarkably enriched in lung cancer tissues and directly contribute to the acquisition and development of major driver mutations in critical genes (KRAS, EGFR, TP۵۳). The lung microbiome seems to regulate the tumor microenvironment by the production of inflammatory mediators, short-chain fatty acids, reactive oxygen species, and other bioactive metabolites with the ability to promote or suppress tumorigenesis in a context-dependent fashion. Emerging evidence indicates that the composition of the microbiome can affect treatment outcome, immune checkpoint inhibitor response, and patient prognosis, revealing new possibilities for offers new hope for prevention, earlier detection, and personalized treatments. Also, the gut-lung axis, Even gut bacteria problems can fuel lung cancer, introduces another level of complexity wherein intestinal dysbiosis may influence pulmonary carcinogenesis via systemic immune modulation and metabolite flux. Unraveling such complex host-microbe-cancer interactions introduces unprecedented opportunities for new prevention strategies, early detection biomarkers, and therapeutic targets for lung cancer. This review discusses the state of the art of the knowledge of lung microbiome dysbiosis in cancer development, mechanistic pathways between microbial communities and oncogenic processes, clinical implications for diagnosis and therapy, and future perspectives on translational research and clinical practice in precision oncology.

کلیدواژه ها:

dysbiosis ، Mutation ، lung Neoplasms ، Carcinogenesis ، Microbiota