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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(tetO-MYC)36Bop
transgene insertion 36, J Michael Bishop
MGI:4459898
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Cdkn2atm1Rdp/Cdkn2a+
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw/0
Tg(Pdx1-cre)6Tuv/0
Tg(tetO-MYC)36Bop/0
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * FVB/N * SJL MGI:5521487
cn2
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw/0
Tg(Pdx1-cre)6Tuv/0
Tg(tetO-MYC)36Bop/0
involves: 129P2/OlaHsd * FVB/N MGI:5521486
cx3
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-MYC)36Bop/0
involves: 129 * C57BL/6 MGI:4946282
cx4
Tg(SFTPC-rtTA)5Jaw/0
Tg(tetO-MYC)36Bop/0
Not Specified MGI:4946284


Genotype
MGI:5521487
cn1
Allelic
Composition
Cdkn2atm1Rdp/Cdkn2a+
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw/0
Tg(Pdx1-cre)6Tuv/0
Tg(tetO-MYC)36Bop/0
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Rdp mutation (6 available); any Cdkn2a mutation (51 available)
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw mutation (1 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Tg(tetO-MYC)36Bop mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop pancreatic tumors with a similar tumor latency as in mutants with wild-type Cdkn2a, however mice show an increase in the occurrence of more aggressive primary pancreatic ductal adenocarcinomas (PDACs) that quickly metastasized to the liver
• mutants show an increase in the occurrence of more aggressive primary pancreatic ductal adenocarcinomas
• 77% of mice show invasive PDAC and 85% show poorly differentiated adenocarcinoma

neoplasm
• mutants develop pancreatic tumors with a similar tumor latency as in mutants with wild-type Cdkn2a, however mice show an increase in the occurrence of more aggressive primary pancreatic ductal adenocarcinomas (PDACs) that quickly metastasized to the liver
• mutants show an increase in the occurrence of more aggressive primary pancreatic ductal adenocarcinomas
• 77% of mice show invasive PDAC and 85% show poorly differentiated adenocarcinoma
• primary pancreatic ductal adenocarcinomas quickly metastasize to the liver
• 67% incidence of metastases to the liver, 18% incidence to the lung, and 15% incidence to the thymus

mortality/aging
• due to pancreatic tumors




Genotype
MGI:5521486
cn2
Allelic
Composition
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw/0
Tg(Pdx1-cre)6Tuv/0
Tg(tetO-MYC)36Bop/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw mutation (1 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Tg(tetO-MYC)36Bop mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice develop pancreatic tumors as early as 14 days post partum
• all mice develop pancreatic neoplasms in less than 5 months
• 43% of mutants develop only ductal lesions, 46% of mutants have both ductal lesions and poorly differentiated carcinomas, and 11% of mutants exhibit only poorly differentiated adenocarcinomas
• 40-50 day old mutants with palpable pancreatic neoplasms treated with doxycycline for 7 days show cancer regression, however tumor-associated stroma does not remodel/regress
• 43% of mutants develop only ductal lesions that include pancreatic intraepithelial neoplasia (PanINs) and invasive pancreatic ductal adenocarcinomas (PDACs) with sporadic metastasis to the liver
• 11% of mutants exhibit exclusively poorly differentiated adenocarcinomas that can metastasize to the liver, diaphragm, and lung
• 46% of mutants have both ductal lesions and poorly differentiated carcinomas, with a few mutants having moderately differentiated lesions that have an acinar-like appearance
• 43% of mutants develop only ductal lesions that include pancreatic intraepithelial neoplasia (PanINs) and invasive pancreatic ductal adenocarcinoma (PDACs) with sporadic metastasis to the liver

mortality/aging
• mutants become moribund before they develop large tumors

neoplasm
• mice develop pancreatic tumors as early as 14 days post partum
• all mice develop pancreatic neoplasms in less than 5 months
• 43% of mutants develop only ductal lesions, 46% of mutants have both ductal lesions and poorly differentiated carcinomas, and 11% of mutants exhibit only poorly differentiated adenocarcinomas
• 40-50 day old mutants with palpable pancreatic neoplasms treated with doxycycline for 7 days show cancer regression, however tumor-associated stroma does not remodel/regress
• 43% of mutants develop only ductal lesions that include pancreatic intraepithelial neoplasia (PanINs) and invasive pancreatic ductal adenocarcinomas (PDACs) with sporadic metastasis to the liver
• 11% of mutants exhibit exclusively poorly differentiated adenocarcinomas that can metastasize to the liver, diaphragm, and lung
• 46% of mutants have both ductal lesions and poorly differentiated carcinomas, with a few mutants having moderately differentiated lesions that have an acinar-like appearance
• 43% of mutants develop only ductal lesions that include pancreatic intraepithelial neoplasia (PanINs) and invasive pancreatic ductal adenocarcinoma (PDACs) with sporadic metastasis to the liver
• pancreatic ductal adenocarcinomas metastasize to the liver, diaphragm, and lung

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:197052




Genotype
MGI:4946282
cx3
Allelic
Composition
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-MYC)36Bop/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Scgb1a1-rtTA)1Jaw mutation (3 available)
Tg(tetO-MYC)36Bop mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• 100% of tumors show activating Kras mutations
• mice treated with DOX develop papillary adenomas
• 23.8% penetrance of adenocarcionomas in untreated mice and 56.7% penetrance in DOX treated mice

mortality/aging
• mice fed a diet supplemented with DOX to stimulate transactivating function of the rtTA protein and induce MYC expression exhibit reduced lifespan

neoplasm
• 16.7% of DOX treated mice exhibit metastases
• 100% of tumors show activating Kras mutations
• mice treated with DOX develop papillary adenomas
• 23.8% penetrance of adenocarcionomas in untreated mice and 56.7% penetrance in DOX treated mice




Genotype
MGI:4946284
cx4
Allelic
Composition
Tg(SFTPC-rtTA)5Jaw/0
Tg(tetO-MYC)36Bop/0
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(SFTPC-rtTA)5Jaw mutation (3 available)
Tg(tetO-MYC)36Bop mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice fed a diet supplemented with DOX to stimulate transactivating function of the rtTA protein and induce MYC expression exhibit reduced lifespan
• treatment of non-DOX treated mutants with the mutagen N-methyl-N-nitrosourea (MNU) accelerates the rate of demise

respiratory system
• 100% of tumors show activating Kras mutations
• mice treated with DOX develop papillary adenomas
• 31.6% penetrance of adenocarcionomas in untreated mice and 57.9% penetrance in DOX treated mice
• mice treated with DOX develop alveolar hyperplasia
• alveolar hyperplasia forms as clusters of cells that expand the alveolar septa, reaches a maximum after 4 days of DOX treatment and then resolves due to apoptosis of the hyperplastic cells

neoplasm
• 5.9% of DOX treated mice exhibit metastases
• 100% of tumors show activating Kras mutations
• mice treated with DOX develop papillary adenomas
• 31.6% penetrance of adenocarcionomas in untreated mice and 57.9% penetrance in DOX treated mice
• mutants treated with DOX and then MNU have significantly lower number of tumors compared to mutagenized mice not treated with DOX





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
01/07/2020
MGI 6.14
The Jackson Laboratory