Analysis Tools
respiratory system
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• as early as 2 weeks after initiation of doxycycline, lungs of bitransgenic mice exhibit scattered thickening of the alveolar walls due to proliferation of abnormal pneumocytes, with a lepidic growth pattern similar to human bronchioalveolar carcinoma (BAC), a subtype of lung adenocarcinoma; this wall thickening may be progressive, gradually compressing the air spaces
• after longer than 4 weeks on doxycycline, bitransgenic mice develop multifocal invasive adenocarcinoma of the lungs, with papilliform tumors of varying size embedded in the abnormal lung parenchyma; the adenocarcinoma cells have moderately pleomorphic nuclei with large nucleoli
• immunohistochemical analysis demonstrates that the tumors in these mice express the mutant human EGFR protein and that they are composed of cells that express surfactant protein C, characteristic of type II pneumocytes, but not Clara cell protein CC26
• discontinuation of doxycycline treatment in two mice after 43 and 55 days resulted in complete disappearance of lung opacities on MRI within a week; histologic examination at 32 and 169 days after deinduction revealed that the tumors had regressed completely, in one case leaving scar tissue
• treatment of tumor-bearing mice with the tyrosine kinase inhibitor erlotinib, while the mice continued receiving doxycycline, resulted in partial to complete disappearance of opacities on MRI in 2-8 days and, in mice examined after at least 4 days on erlotinib, complete or nearly complete (i.e., some residual tumor cells remained) histological regression of the tumors
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• after only 4 days' induction with doxycycline, lung tissue from doubly transgenic mice contained nearly 2-fold the number of type II pneumocytes, identified by staining with antibody against surfactant protein C, than control tissue
• immunohistochemical analysis demonstrates that the tumors induced by doxycycline in these mice express the mutant human EGFR protein and that they are composed of cells that express surfactant protein C, characteristic of type II pneumocytes, but not Clara cell protein CC26
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neoplasm
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• as early as 2 weeks after initiation of doxycycline, lungs of bitransgenic mice exhibit scattered thickening of the alveolar walls due to proliferation of abnormal pneumocytes, with a lepidic growth pattern similar to human bronchioalveolar carcinoma (BAC), a subtype of lung adenocarcinoma; this wall thickening may be progressive, gradually compressing the air spaces
• after longer than 4 weeks on doxycycline, bitransgenic mice develop multifocal invasive adenocarcinoma of the lungs, with papilliform tumors of varying size embedded in the abnormal lung parenchyma; the adenocarcinoma cells have moderately pleomorphic nuclei with large nucleoli
• immunohistochemical analysis demonstrates that the tumors in these mice express the mutant human EGFR protein and that they are composed of cells that express surfactant protein C, characteristic of type II pneumocytes, but not Clara cell protein CC26
• discontinuation of doxycycline treatment in two mice after 43 and 55 days resulted in complete disappearance of lung opacities on MRI within a week; histologic examination at 32 and 169 days after deinduction revealed that the tumors had regressed completely, in one case leaving scar tissue
• treatment of tumor-bearing mice with the tyrosine kinase inhibitor erlotinib, while the mice continued receiving doxycycline, resulted in partial to complete disappearance of opacities on MRI in 2-8 days and, in mice examined after at least 4 days on erlotinib, complete or nearly complete (i.e., some residual tumor cells remained) histological regression of the tumors
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| lung cancer | DOID:1324 |
OMIM:211980 OMIM:608935 OMIM:612571 OMIM:612593 OMIM:614210 |
J:109092 | |
