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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(tetO-EGFR*delta19)11Hev
transgene insertion 11, Harold E Varmus
MGI:3690457
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
cx1
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-EGFR*delta19)11Hev/0
involves: C57BL/6 * CBA MGI:3690458


Genotype
MGI:3690458
cx1
Allelic
Composition
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-EGFR*delta19)11Hev/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Scgb1a1-rtTA)1Jaw mutation (3 available)
Tg(tetO-EGFR*delta19)11Hev mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• a bitransgenic mouse examined after 13 days on doxycycline exhibited scattered thickening of the alveolar walls due to proliferation of abnormal pneumocytes, with a lepidic growth pattern similar to human bronchioalveolar carcinoma (BAC); animals examined after 28 days or longer on doxycycline exhibited BAC-like lesions at the lung periphery
• mice on doxycycline 28 days or longer exhibit multifocal, frondiform tumors radiating from bronchioalveolar duct junctions (BADJ) into the surrounding, BAC-free parenchyma; more advanced tumors form compact papilliform masses
• discontinuation of doxycycline treatment in two mice after 99 and 168 days resulted in partial remission of lung opacities on MRI at 6 and 4 days, respectively; histologic examination 4 days after deinduction found tumors still present, but at 31 days revealed that the tumors had regressed completely, leaving scar tissue
• treatment of two tumor-bearing bitransgenic mice (the second heterozygous for a Trp53-inactivating mutation) with the tyrosine kinase inhibitor erlotinib, while the mice continued receiving doxycycline, resulted in partial disappearance of opacities on MRI at 4 and 14 days and, after 4 days and 4 weeks on erlotinib, respectively, nearly complete histological regression of the tumors (i.e., some residual tumor cells remained)
• a bitransgenic mouse examined histologically 8 days after initiation of doxycycline exhibited proliferative lung lesions characteristic of early atypical adenomatous hyperplasia (AHH) at the lung periphery
• immunohistochemical analysis demonstrates that the tumors induced 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
• bitransgenic mice on doxycycline 28 days or longer exhibit multifocal, frondiform tumors arising and radiating from bronchioalveolar duct junctions (BADJ) into the surrounding, BAC-free parenchyma; more advanced tumors form compact papilliform masses

neoplasm
• a bitransgenic mouse examined after 13 days on doxycycline exhibited scattered thickening of the alveolar walls due to proliferation of abnormal pneumocytes, with a lepidic growth pattern similar to human bronchioalveolar carcinoma (BAC); animals examined after 28 days or longer on doxycycline exhibited BAC-like lesions at the lung periphery
• mice on doxycycline 28 days or longer exhibit multifocal, frondiform tumors radiating from bronchioalveolar duct junctions (BADJ) into the surrounding, BAC-free parenchyma; more advanced tumors form compact papilliform masses
• discontinuation of doxycycline treatment in two mice after 99 and 168 days resulted in partial remission of lung opacities on MRI at 6 and 4 days, respectively; histologic examination 4 days after deinduction found tumors still present, but at 31 days revealed that the tumors had regressed completely, leaving scar tissue
• treatment of two tumor-bearing bitransgenic mice (the second heterozygous for a Trp53-inactivating mutation) with the tyrosine kinase inhibitor erlotinib, while the mice continued receiving doxycycline, resulted in partial disappearance of opacities on MRI at 4 and 14 days and, after 4 days and 4 weeks on erlotinib, respectively, nearly complete histological regression of the tumors (i.e., some residual tumor cells remained)

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





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory