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 122 and 180 days resulted in diminution of lung opacities on MRI at 9 and 2 days afterward; histologic examination of the second mouse immediately after MRI found tumors present, whereas examination of the first mouse 31 days after deinduction revealed that the tumors had regressed completely, 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 all mice on at least 12.5 mg kg-1 d-1 erlotinib 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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• 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
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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 122 and 180 days resulted in diminution of lung opacities on MRI at 9 and 2 days afterward; histologic examination of the second mouse immediately after MRI found tumors present, whereas examination of the first mouse 31 days after deinduction revealed that the tumors had regressed completely, 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 all mice on at least 12.5 mg kg-1 d-1 erlotinib 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 | |
