Abstract
Abstract Lung adenocarcinoma (AC) induced by carcinogen inhalation never came close to the human counterpart. This has changed with the creation of genetically engineered models. Different types of mouse AC were studied, some of them with a KRAS codon12 mutation background, others with HRAS mutants inserted; in most additional hits were introduced (ATG5, PTEN, PI3K, p53). Development of AC was followed for 28 weeks. Human lung AC subtypes and precursor lesions served for comparison. AC in mice starts with papillary growth at the bronchoalveolar junction (baJ). Tumor spreads into the alveolar periphery. Due to different cell to alveolar size alveoli are filled almost completely, simulating solid growth. At a certain size hypoxic necrosis is seen in centers, followed by neoangiogenesis and desmoplastic stroma formation. Finally invasion of tumor cells into stroma occur. Metastasis is rare, due to high tumor load, causing early death. Vascular invasion is seen, if second carcinogenic hits are applied. Dissimilarities with human precursor and AC types are: AC in mice are all non-mucinous, they are predominant papillary or solid, often with a high degree of signet ring cell formation; in addition there seems to be a requirement of large tumor size before invasion and metastasis occur. To understand AC development knowledge of the anatomy and histology of mouse and human lung is necessary, but these models open a new way of investigating lung AC. Citation Format: Helmut H. Popper, Beatrice Grabner, Emilio Casanova, Robert Eferl, Rao Shuan, Josef Penninger. Comparison of lung adenocarcinoma development in genetically engineered mouse and in humans - similarities and differences. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1209. doi:10.1158/1538-7445.AM2014-1209
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