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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(tetO-Kras2)12Hev
transgene insertion 12, Harold E Varmus
MGI:2179992
Summary 9 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N MGI:5569002
cn2
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
Trp53tm1Tyj/Trp53+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N MGI:5569005
cx3
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-Kras2)12Hev/0
involves: 129 * C57BL/6 * FVB/N MGI:5912341
cx4
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-Kras2)12Hev/0
involves: 129 * C57BL/6J * FVB/N * SJL MGI:5912294
cx5
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-Kras2)12Hev/0
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 * FVB/N MGI:5912344
cx6
Tg(MMTV-Myc)141-3Led/0
Tg(MMTV-rtTA)1Lach/0
Tg(tetO-Kras2)12Hev/0
involves: C57BL/6J * CD-1 * FVB/N MGI:5827760
cx7
Tg(MMTV-rtTA)1Lach/0
Tg(tetO-Kras2)12Hev/0
Tg(tetO-MYC)1Lach/0
involves: FVB/N MGI:5827758
cx8
Tg(MMTV-rtTA)1Lach/0
Tg(tetO-Kras2)12Hev/0
involves: FVB/N MGI:5827756
tg9
Tg(tetO-Kras2)12Hev/0 involves: FVB/N MGI:5912342


Genotype
MGI:5569002
cn1
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 1 of 2 mice treated with doxycycline (dox) at 4-6 weeks of age show frank adenocarcinoma by 23 weeks on dox
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction
• mice treated with doxycycline (dox) at 4-6 weeks of age to induce Kras2 expression begin to show low-grade pancreatic intraepithelial neoplasia (PanIN) beginning at 3 weeks after dox treatment
• mice treated with dox at 4-6 weeks of age show PanIN, surrounded by areas of fibrosis and embedded in the acinar parenchyma after 18 weeks on dox and by 23 weeks, large areas of the pancreatic parenchyma are substituted with PanIN lesions of different grade, with frank adenocarcinoma seen in 1 of 2 mice
• mice kept on dox for 23 weeks show reversion of PanINs when dox is removed for 2 weeks
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein, to induce acute pancreatitis, develop low- and high-grade PanIN lesions at 5 weeks after induction
• mice treated with dox 72 hours prior to induction of pancreatitis also show reversion of PanINs when dox is removed for 2 weeks

homeostasis/metabolism
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show impaired recovery from pancreatitis, showing acinar-ductal metaplasia with progressive accumulation of fibrotic stroma at 1 week after induction, replacement of the whole pancreatic parenchyma with ductal structures and signs of PanINs at 3 weeks after induction, and low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction compared to adult mice without dox which show completely resolved damage
• mice kept on dox for 5 weeks prior to induction of pancreatitis and then dox removal for 2 weeks show incomplete repair process resulting in a small, fibrotic pancreas with fewer acini; after 5 weeks of dox removal, no PanINs are observed however, the pancreas appears fibrotic and is small

endocrine/exocrine glands
• mice kept on dox for 5 weeks following pancreatitis induction show an increase in apoptotic cells and small pancreas size upon removal of dox
• 1 of 2 mice treated with doxycycline (dox) at 4-6 weeks of age show frank adenocarcinoma by 23 weeks on dox
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction
• mice treated with doxycycline (dox) at 4-6 weeks of age to induce Kras2 expression begin to show low-grade pancreatic intraepithelial neoplasia (PanIN) beginning at 3 weeks after dox treatment
• mice treated with dox at 4-6 weeks of age show PanIN, surrounded by areas of fibrosis and embedded in the acinar parenchyma after 18 weeks on dox and by 23 weeks, large areas of the pancreatic parenchyma are substituted with PanIN lesions of different grade, with frank adenocarcinoma seen in 1 of 2 mice
• mice kept on dox for 23 weeks show reversion of PanINs when dox is removed for 2 weeks
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein, to induce acute pancreatitis, develop low- and high-grade PanIN lesions at 5 weeks after induction
• mice treated with dox 72 hours prior to induction of pancreatitis also show reversion of PanINs when dox is removed for 2 weeks
• mice treated with dox at 4-6 weeks of age begin to show acinar-ductal metaplasia beginning at 3 weeks after dox treatment




Genotype
MGI:5569005
cn2
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die between 8 and 18 weeks after doxycycline (dox) treatment to induce Kras2 expression due to pancreatic ductal adenocarinoma

neoplasm
• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion
• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant
• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma

homeostasis/metabolism
• adult mice treated with dox for 5 weeks prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis exhibit a small, translucent remnant of pancreatic tissue, without fibrosis or PanIN lesions
• when dox is removed after pancreatitis induction, mice show show normal acini interspersed with dilated ducts and acinar-ductal metaplasia, fibrosis and occasional lipomatosis, but with minimal inflammatory infiltrate, and reduced proliferation

endocrine/exocrine glands
• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion
• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant
• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:184378




Genotype
MGI:5912341
cx3
Allelic
Composition
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-Kras2)12Hev/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Scgb1a1-rtTA)1Jaw mutation (3 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• in doxycycline-treated mice
• however, tumors regress after doxycycline withdrawal due to apoptosis
• multiple large, solid-type adenomas in doxycycline-treated mice
• in doxycycline-treated mice

respiratory system
• in doxycycline-treated mice
• however, tumors regress after doxycycline withdrawal due to apoptosis
• multiple large, solid-type adenomas in doxycycline-treated mice
• in doxycycline-treated mice
• proliferative alveolar lesions and focal hyperplasia of type II pneumocytes in doxycycline-treated mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung adenocarcinoma DOID:3910 J:73468




Genotype
MGI:5912294
cx4
Allelic
Composition
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-Kras2)12Hev/0
Genetic
Background
involves: 129 * C57BL/6J * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Rdp mutation (6 available); any Cdkn2a mutation (67 available)
Tg(Scgb1a1-rtTA)1Jaw mutation (3 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• doxycycline-treated mice initiate lung tumors more rapidly than in Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice with a more malignant phenotype
• however, tumors regress after doxycycline withdrawal due to apoptosis
• more sooner in doxycycline-treated mice compared with Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice (J:73468)
• in doxycycline-treated mice (J:166963)

respiratory system
• doxycycline-treated mice initiate lung tumors more rapidly than in Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice with a more malignant phenotype
• however, tumors regress after doxycycline withdrawal due to apoptosis
• more sooner in doxycycline-treated mice compared with Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice (J:73468)
• in doxycycline-treated mice (J:166963)




Genotype
MGI:5912344
cx5
Allelic
Composition
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-Kras2)12Hev/0
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Scgb1a1-rtTA)1Jaw mutation (3 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• doxycycline-treated mice initiate lung tumors more rapidly than in Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice with a more malignant phenotype
• more sooner in doxycycline-treated mice compared with Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice

respiratory system
• doxycycline-treated mice initiate lung tumors more rapidly than in Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice with a more malignant phenotype
• more sooner in doxycycline-treated mice compared with Tg(Scgb1a1-rtTA)1Jaw Tg(tetO-Kras2)12Hev mice




Genotype
MGI:5827760
cx6
Allelic
Composition
Tg(MMTV-Myc)141-3Led/0
Tg(MMTV-rtTA)1Lach/0
Tg(tetO-Kras2)12Hev/0
Genetic
Background
involves: C57BL/6J * CD-1 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(MMTV-Myc)141-3Led mutation (1 available)
Tg(MMTV-rtTA)1Lach mutation (0 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice fed doxycycline develop tumors in all mammary glands within 10 weeks of induction, with a median latency between 6 and 8 weeks
• removal of doxycycline results in apoptosis and reduced proliferation of tumors after doxycycline withdrawal, almost all of the transformed mammary glands completely regress to a nonpalpable state, however, hyperplastic changes persist in the glands
• after doxycycline withdrawal, almost all of the transformed mammary glands completely regress to a nonpalpable state, however, hyperplastic changes persist in the glands
• mammary tumors develop after withdrawal of doxycycline at a median age of 33 weeks, indicating recurrent tumors
• tumor recurrence is associated with reactivation of oncogenic transgenes and somatic mutations in the rtTA transgene

integument
• mice fed doxycycline develop tumors in all mammary glands within 10 weeks of induction, with a median latency between 6 and 8 weeks
• removal of doxycycline results in apoptosis and reduced proliferation of tumors after doxycycline withdrawal, almost all of the transformed mammary glands completely regress to a nonpalpable state, however, hyperplastic changes persist in the glands
• after doxycycline withdrawal, almost all of the transformed mammary glands completely regress to a nonpalpable state, however, hyperplastic changes persist in the glands
• mammary tumors develop after withdrawal of doxycycline at a median age of 33 weeks, indicating recurrent tumors
• tumor recurrence is associated with reactivation of oncogenic transgenes and somatic mutations in the rtTA transgene

endocrine/exocrine glands
• mice fed doxycycline develop tumors in all mammary glands within 10 weeks of induction, with a median latency between 6 and 8 weeks
• removal of doxycycline results in apoptosis and reduced proliferation of tumors after doxycycline withdrawal, almost all of the transformed mammary glands completely regress to a nonpalpable state, however, hyperplastic changes persist in the glands
• after doxycycline withdrawal, almost all of the transformed mammary glands completely regress to a nonpalpable state, however, hyperplastic changes persist in the glands
• mammary tumors develop after withdrawal of doxycycline at a median age of 33 weeks, indicating recurrent tumors
• tumor recurrence is associated with reactivation of oncogenic transgenes and somatic mutations in the rtTA transgene

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
breast cancer DOID:1612 OMIM:114480
J:133578




Genotype
MGI:5827758
cx7
Allelic
Composition
Tg(MMTV-rtTA)1Lach/0
Tg(tetO-Kras2)12Hev/0
Tg(tetO-MYC)1Lach/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(MMTV-rtTA)1Lach mutation (0 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
Tg(tetO-MYC)1Lach mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• diffuse mammary hyperplasia is seen at 7 days after doxycycline administration, numerous tumor nodules are seen throughout the glandular tree at 14 days and confluent tumors are present at 21 days
• removal of doxycycline results in apoptosis and reduced proliferation of tumors
• after doxycycline withdrawal, almost all of the transformed mammary glands completely regress to a nonpalpable state within 2 weeks
• solitary mammary tumors develop after withdrawal of doxycycline in 20 of 36 mice at a median age of 53 weeks, indicating recurrent tumors
• in the absence of doxycycline, only one of 31 mice develop a mammary tumor
• tumor recurrence is associated with reactivation of oncogenic transgenes and somatic mutations in the rtTA transgene

integument
• diffuse mammary hyperplasia is seen at 7 days after doxycycline administration, numerous tumor nodules are seen throughout the glandular tree at 14 days and confluent tumors are present at 21 days
• removal of doxycycline results in apoptosis and reduced proliferation of tumors
• after doxycycline withdrawal, almost all of the transformed mammary glands completely regress to a nonpalpable state within 2 weeks
• solitary mammary tumors develop after withdrawal of doxycycline in 20 of 36 mice at a median age of 53 weeks, indicating recurrent tumors
• in the absence of doxycycline, only one of 31 mice develop a mammary tumor
• tumor recurrence is associated with reactivation of oncogenic transgenes and somatic mutations in the rtTA transgene
• diffuse mammary hyperplasia is seen at 7 days after doxycycline administration

endocrine/exocrine glands
• diffuse mammary hyperplasia is seen at 7 days after doxycycline administration, numerous tumor nodules are seen throughout the glandular tree at 14 days and confluent tumors are present at 21 days
• removal of doxycycline results in apoptosis and reduced proliferation of tumors
• after doxycycline withdrawal, almost all of the transformed mammary glands completely regress to a nonpalpable state within 2 weeks
• solitary mammary tumors develop after withdrawal of doxycycline in 20 of 36 mice at a median age of 53 weeks, indicating recurrent tumors
• in the absence of doxycycline, only one of 31 mice develop a mammary tumor
• tumor recurrence is associated with reactivation of oncogenic transgenes and somatic mutations in the rtTA transgene
• diffuse mammary hyperplasia is seen at 7 days after doxycycline administration

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
breast cancer DOID:1612 OMIM:114480
J:114480




Genotype
MGI:5827756
cx8
Allelic
Composition
Tg(MMTV-rtTA)1Lach/0
Tg(tetO-Kras2)12Hev/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(MMTV-rtTA)1Lach mutation (0 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice fed doxycycline after weaning develop mammary gland hyperplasia, progress to hyperplastic alveolar nodules, and then palpable oligofocal mammary tumors with a median latency of 22 weeks

integument
• mice fed doxycycline after weaning develop mammary gland hyperplasia, progress to hyperplastic alveolar nodules, and then palpable oligofocal mammary tumors with a median latency of 22 weeks
• mice fed doxycycline after weaning develop mammary gland hyperplasia as early as one week after induction

endocrine/exocrine glands
• mice fed doxycycline after weaning develop mammary gland hyperplasia, progress to hyperplastic alveolar nodules, and then palpable oligofocal mammary tumors with a median latency of 22 weeks
• mice fed doxycycline after weaning develop mammary gland hyperplasia as early as one week after induction

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
breast cancer DOID:1612 OMIM:114480
J:133578




Genotype
MGI:5912342
tg9
Allelic
Composition
Tg(tetO-Kras2)12Hev/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(tetO-Kras2)12Hev mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• doxycycline-treated mice doe not develop lung lesions





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory