Phenotypes associated with this allele

• Allele Symbol: Tg(tetO-MYC)36Bop
• Allele Name: transgene insertion 36, J Michael Bishop
• Allele ID: MGI:4459898
• Summary: 4 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw/0 Tg(Pdx1-cre)6Tuv/0 Tg(tetO-MYC)36Bop/0	involves: 129P2/OlaHsd * FVB/N	MGI:5521486
cn2	Cdkn2a^tm1Rdp/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
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:5521486

cn1

• 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

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

mortality/aging

decreased tumor-free survival time ( J:197052 )

• mutants become moribund before they develop large tumors

neoplasm

increased pancreas tumor incidence ( J:197052 )

• 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

increased pancreatic ductal adenocarcinoma incidence ( J:197052 )

• 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

increased pancreatic intraepithelial neoplasia incidence ( J:197052 )

• 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

increased metastatic potential ( J:197052 )

• pancreatic ductal adenocarcinomas metastasize to the liver, diaphragm, and lung

endocrine/exocrine glands

increased pancreas tumor incidence ( J:197052 )

• 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

increased pancreatic ductal adenocarcinoma incidence ( J:197052 )

• 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

increased pancreatic intraepithelial neoplasia incidence ( J:197052 )

• 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

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

Genotype
MGI:5521487

cn2

• Allelic Composition: Cdkn2a^tm1Rdp/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

neoplasm

increased pancreas tumor incidence ( J:197052 )

• 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

increased pancreatic ductal adenocarcinoma incidence ( J:197052 )

• 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

increased metastatic potential ( J:197052 )

• 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

endocrine/exocrine glands

increased pancreas tumor incidence ( J:197052 )

• 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

increased pancreatic ductal adenocarcinoma incidence ( J:197052 )

• 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

mortality/aging

decreased tumor-free survival time ( J:197052 )

• due to pancreatic tumors

Genotype
MGI:4946282

cx3

• Allelic Composition: Tg(Scgb1a1-rtTA)1Jaw/0; Tg(tetO-MYC)36Bop/0
• Genetic Background: involves: 129 * C57BL/6

mortality/aging

premature death ( J:169920 )

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

neoplasm

increased metastatic potential ( J:169920 )

• 16.7% of DOX treated mice exhibit metastases

increased lung tumor incidence ( J:169920 )

• 100% of tumors show activating Kras mutations

increased lung adenoma incidence ( J:169920 )

• mice treated with DOX develop papillary adenomas

increased lung adenocarcinoma incidence ( J:169920 )

• 23.8% penetrance of adenocarcionomas in untreated mice and 56.7% penetrance in DOX treated mice

respiratory system

increased lung tumor incidence ( J:169920 )

• 100% of tumors show activating Kras mutations

increased lung adenoma incidence ( J:169920 )

• mice treated with DOX develop papillary adenomas

increased lung adenocarcinoma incidence ( J:169920 )

• 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

mortality/aging

premature death ( J:169920 )

• 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

increased lung tumor incidence ( J:169920 )

• 100% of tumors show activating Kras mutations

increased lung adenoma incidence ( J:169920 )

• mice treated with DOX develop papillary adenomas

increased lung adenocarcinoma incidence ( J:169920 )

• 31.6% penetrance of adenocarcionomas in untreated mice and 57.9% penetrance in DOX treated mice

abnormal pulmonary alveolar system morphology ( J:169920 )

• 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

increased metastatic potential ( J:169920 )

• 5.9% of DOX treated mice exhibit metastases

increased lung tumor incidence ( J:169920 )

• 100% of tumors show activating Kras mutations

increased lung adenoma incidence ( J:169920 )

• mice treated with DOX develop papillary adenomas

increased lung adenocarcinoma incidence ( J:169920 )

• 31.6% penetrance of adenocarcionomas in untreated mice and 57.9% penetrance in DOX treated mice

decreased tumor incidence ( J:169920 )

• mutants treated with DOX and then MNU have significantly lower number of tumors compared to mutagenized mice not treated with DOX