Phenotypes Associated with This Genotype

Genotype
MGI:4946284

• Allelic Composition: Tg(SFTPC-rtTA)5Jaw/0; Tg(tetO-MYC)36Bop/0
• Genetic Background: Not Specified

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

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