{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T15:40:01Z","timestamp":1787240401573,"version":"build-2736575974"},"reference-count":128,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,10,14]],"date-time":"2024-10-14T00:00:00Z","timestamp":1728864000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:p>The lungs are most often a preferential target organ for malignant spreading and growth. It is well known that chronic parenchymal inflammation and prolonged injuries represents an independent risk factor for cancer onset. Growing evidence supports the implication of lung microbiota in the pathogenesis of lung cancer. However, the full interplay between chronic inflammation, bacterial colonization, pathologic condition as bronchiectasis and malignant growth deserves better clarification. 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