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Expression of B-RAF V600E in Type II Pneumocytes Causes Abnormalities in Alveolar Formation, Airspace Enlargement and Tumor Formation in Mice

Please always quote using this URN: urn:nbn:de:bvb:20-opus-137061
  • Growth factor induced signaling cascades are key regulatory elements in tissue development, maintenance and regeneration. Perturbations of these cascades have severe consequences, leading to developmental disorders and neoplastic diseases. As a major function in signal transduction, activating mutations in RAF family kinases are the cause of human tumorigenesis, where B-RAF V600E has been identified as the prevalent mutant. In order to address the oncogenic function of B-RAF V600E, we have generated transgenic mice expressing the activatedGrowth factor induced signaling cascades are key regulatory elements in tissue development, maintenance and regeneration. Perturbations of these cascades have severe consequences, leading to developmental disorders and neoplastic diseases. As a major function in signal transduction, activating mutations in RAF family kinases are the cause of human tumorigenesis, where B-RAF V600E has been identified as the prevalent mutant. In order to address the oncogenic function of B-RAF V600E, we have generated transgenic mice expressing the activated oncogene specifically in lung alveolar epithelial type II cells. Constitutive expression of B-RAF V600E caused abnormalities in alveolar epithelium formation that led to airspace enlargements. These lung lesions showed signs of tissue remodeling and were often associated with chronic inflammation and low incidence of lung tumors. The inflammatory cell infiltration did not precede the formation of the lung lesions but was rather accompanied with late tumor development. These data support a model where the continuous regenerative process initiated by oncogenic B-RAF-driven alveolar disruption provides a tumor-promoting environment associated with chronic inflammation.show moreshow less

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Metadaten
Author: Emanuele Zanucco, Rudolf Götz, Tamara Potapenko, Irene Carraretto, Semra Ceteci, Fatih Ceteci, Werner Seeger, Rajkumar Savai, Ulf R. Rapp
URN:urn:nbn:de:bvb:20-opus-137061
Document Type:Journal article
Faculties:Medizinische Fakultät / Institut für Medizinische Strahlenkunde und Zellforschung
Language:English
Parent Title (English):PLOS ONE
Year of Completion:2011
Volume:6
Issue:12
Pagenumber:e29093
Source:PLoS ONE 6(12): e29093. doi:10.1371/journal.pone.0029093
DOI:https://doi.org/10.1371/journal.pone.0029093
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Tag:activation; epithelial-cells; inflammation; kinase; lung-cancer; mouse models; obstructive pulmonary-disease; pathway; protein; somatic mutations
Release Date:2018/10/16
Licence (German):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung