Non-Small Cell Lung Cancer Coverage from Every Angle

Can Lung Microbiome Enrichment Improve Outcomes for Patients With Lung Cancer?

By: Joshua D. Madera, MS
Posted: Monday, January 25, 2021

For patients with advanced-stage lung cancer, administration of commensal microbes to enrich the lungs resulted in worse prognosis, advanced disease, and tumor progression, according to a study published in Cancer Discovery. These findings conflict with previous research that demonstrated microbes' role in immune activation and modulation of lung cancer pathogenesis, explained Leopoldo N. Segal, MD, of New York University School of Medicine, and colleagues.

“Given the results of our study, it is possible that changes to the lung microbiome could be used as a biomarker to predict prognosis or to stratify patients for treatment,” commented Dr. Segal in an American Association for Cancer Research press release.

A total of 83 patients with advanced-stage lung cancer were recruited for the study. All patients had untreated disease. Via clinical bronchoscopies, lung samples were collected to analyze the lung microbiome and gene expression.

The analysis revealed increased commensal enrichment in patients with advanced-stage lung disease compared with patients with early-stage disease. In addition, lung commensal enrichment was associated with decreased survival. The microorganisms Veillonella, Prevotella, and Streptococcus in the lung biome were associated with a poorer prognosis for patients. Moreover, Veillonella, Prevotella, Streptococcus, and Rothia in the lungs were associated with tumor progression. Furthermore, the activation of various oncoproteins in patients with early-stage lung cancer was associated with the enrichment of Veillonella, Prevotella, and Streptococcus.

In particular, a strain of the bacteria Veillonella was found to be associated with the expression of cytokines, interleukin-17, growth factors, and cell-adhesion molecules. Additionally, there was increased activation of Janus kinase/signal transducer and activator of transcription, tumor necrosis factor, and phosphoinositide 3-kinase-protein kinase B signaling pathways.

Disclosure: For full disclosures of the study authors, visit

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