Phenotypes associated with this allele

• Allele Symbol: Tg(tetO-MYC)36aBop
• Allele Name: transgene insertion 36a, J Michael Bishop
• Allele ID: MGI:3039697
• Summary: 5 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Rb1^tm3Tyj/Rb1^tm3Tyj Tg(tetO-MYC)36aBop/0 Tg(Cebpb-tTA)5Bjd/0	involves: FVB/N * NMRI	MGI:5008419
cx2	Trp53bp2^tm1Cdlo/Trp53bp2^+ Tg(EmuSR-tTa)83Bop/0 Tg(tetO-MYC)36aBop/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N	MGI:3839868
cx3	Tg(Pax8-rtTA2S*M2)1Koes/0 Tg(tetO-MYC)36aBop/0	involves: C57BL/6 * DBA * FVB/N	MGI:3815300
cx4	Tg(Ggt1-tTA)#Agoc/0 Tg(tetO-MYC)36aBop/0	involves: FVB/N	MGI:5705536
cx5	Tg(tetO-MYC)36aBop/0 Tg(Cebpb-tTA)5Bjd/0	involves: FVB/N * NMRI	MGI:4358091

Genotype
MGI:5008419

cn1

• Allelic Composition: Rb1^tm3Tyj/Rb1^tm3Tyj; Tg(tetO-MYC)36aBop/0; Tg(Cebpb-tTA)5Bjd/0
• Genetic Background: involves: FVB/N * NMRI

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

Increase in ploidy in hepatocytes of tamoxifen-treated Rb1^tm3Tyj/Rb1^tm3Tyj Tg(tetO-MYC)36aBop/0 Tg(Cebpb-tTA)5Bjd/0 mice

mortality/aging

decreased tumor-free survival time ( J:172430 )

• median survival of mutants is 27 weeks following withdrawal of doxycycline and intrasplenic injection of adenovirus expressing Cre recombinase

• median survival of mutants with tumors is 16.5 weeks following withdrawal of doxycycline and intrasplenic injection of adenovirus expressing Cre recombinase

liver/biliary system

increased liver tumor incidence ( J:172430 )

• following withdrawal of doxycycline and intrasplenic injection of adenovirus expressing Cre recombinase, some mice develop liver tumors composed of multiple fleshy vascular nodules

increased hepatocellular carcinoma incidence ( J:172430 )

• tumors of mice injected with adenovirus expressing Cre recombinase and without doxycycline to induce MYC expression are composed of hepatocellular neoplasms characterized by sheets of cells with occasional mitotic figure, slightly pleomorphic nuclei, and prominent nucleoli

• tumors show a range of differentiation between well- and moderately-differentiated hepatocellular carcinoma

cellular

polyploidy ( J:172430 )

• following withdrawal of doxycycline and intrasplenic injection of adenovirus expressing Cre recombinase, adult liver cells exhibit an increase in polyploidy

neoplasm

increased liver tumor incidence ( J:172430 )

• following withdrawal of doxycycline and intrasplenic injection of adenovirus expressing Cre recombinase, some mice develop liver tumors composed of multiple fleshy vascular nodules

increased hepatocellular carcinoma incidence ( J:172430 )

• tumors of mice injected with adenovirus expressing Cre recombinase and without doxycycline to induce MYC expression are composed of hepatocellular neoplasms characterized by sheets of cells with occasional mitotic figure, slightly pleomorphic nuclei, and prominent nucleoli

• tumors show a range of differentiation between well- and moderately-differentiated hepatocellular carcinoma

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
hepatocellular carcinoma		DOID:684	OMIM:114550	J:172430

Genotype
MGI:3839868

cx2

• Allelic Composition: Trp53bp2^tm1Cdlo/Trp53bp2⁺; Tg(EmuSR-tTa)83Bop/0; Tg(tetO-MYC)36aBop/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N

neoplasm

increased T cell derived lymphoma incidence ( J:146764 )

• incidence of T cell lymphomas is similar to that in transgenic mice wild-type for Trp53bp2

endocrine/exocrine glands

increased T cell derived lymphoma incidence ( J:146764 )

• incidence of T cell lymphomas is similar to that in transgenic mice wild-type for Trp53bp2

Genotype
MGI:3815300

cx3

• Allelic Composition: Tg(Pax8-rtTA2S*M2)1Koes/0; Tg(tetO-MYC)36aBop/0
• Genetic Background: involves: C57BL/6 * DBA * FVB/N

renal/urinary system

kidney cyst ( J:140925 )

• following induction with doxycycline, mice develop glomerular cysts

polycystic kidney ( J:140925 )

• following induction with doxycycline, mice develop multiple renal cysts in all renal tubular compartments

increased renal carcinoma incidence ( J:140925 )

• following induction with doxycycline

kidney failure ( J:140925 )

• 3 to 4 months following induction with doxycycline

neoplasm

increased adenoma incidence ( J:140925 )

• following induction with doxycycline, mice develop renal adenomas

increased renal carcinoma incidence ( J:140925 )

• following induction with doxycycline

growth/size/body

kidney cyst ( J:140925 )

• following induction with doxycycline, mice develop glomerular cysts

polycystic kidney ( J:140925 )

• following induction with doxycycline, mice develop multiple renal cysts in all renal tubular compartments

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
cystic kidney disease		DOID:2975		J:140925

Genotype
MGI:5705536

cx4

• Allelic Composition: Tg(Ggt1-tTA)#Agoc/0; Tg(tetO-MYC)36aBop/0
• Genetic Background: involves: FVB/N

renal/urinary system

enlarged kidney ( J:222943 )

• removal of doxycycline (dox) results in increased kidney size

increased renal carcinoma incidence ( J:222943 )

• removal of dox results in the development of rapidly progressing of renal cell carcinoma

• marker analysis indicates that tumor subtype is of the collecting-duct carcinoma which exhibits a distinct lipid signature

• treatment with dox reverses tumor and results in regression of the renal cell carcinoma

• initiation of renal cell carcinoma is associated with the activation of glutaminolysis

• treatment with dox to suppress MYC protein expression results in regression of the renal cell carcinoma due to inhibition of proliferation accompanied by the persistence of apoptosis

• treatment with an inhibitor of kidney type glutaminase BPTES slows progression of renal cell carcinoma tumors, reduces neoplastic cells, and decreases kidney cell proliferation

neoplasm

increased renal carcinoma incidence ( J:222943 )

• removal of dox results in the development of rapidly progressing of renal cell carcinoma

• marker analysis indicates that tumor subtype is of the collecting-duct carcinoma which exhibits a distinct lipid signature

• treatment with dox reverses tumor and results in regression of the renal cell carcinoma

• initiation of renal cell carcinoma is associated with the activation of glutaminolysis

• treatment with dox to suppress MYC protein expression results in regression of the renal cell carcinoma due to inhibition of proliferation accompanied by the persistence of apoptosis

• treatment with an inhibitor of kidney type glutaminase BPTES slows progression of renal cell carcinoma tumors, reduces neoplastic cells, and decreases kidney cell proliferation

growth/size/body

enlarged kidney ( J:222943 )

• removal of doxycycline (dox) results in increased kidney size

Genotype
MGI:4358091

cx5

• Allelic Composition: Tg(tetO-MYC)36aBop/0; Tg(Cebpb-tTA)5Bjd/0
• Genetic Background: involves: FVB/N * NMRI

mortality/aging

premature death ( J:93899 )

• following withdrawal of doxycycline, all mice succumb to liver tumors within 2 weeks

decreased tumor-free survival time ( J:172430 )

• median survival of mutants is 31 weeks following doxycycline withdrawal to induce MYC expression

• median survival of mutants with tumors is 27 weeks following doxycycline withdrawal to induce MYC expression

neoplasm

increased liver tumor incidence ( J:93899 , J:172430 )

• following withdrawal of doxycycline, mice develop tumors with a latency of 12 weeks and all mice succumb to liver tumors within 2 weeks (J:93899)

• liver tumors that develop in mice after doxycycline withdrawal are invasive and metastasis into the thoracic cavity and lung parenchyma (J:93899)

• however, re-establishment of doxycycline-treatment produces rapid and sustained tumor regression (J:93899)

• repeated withdrawal and treatment with doxycyclineinduces and represses, respectively, tumor formation (J:93899)

increased hepatoblastoma incidence ( J:93899 )

• liver tumors that develop in mice after doxycycline withdrawal resemble hepatocellular carcinomas and/or hepatoblastomas

increased hepatocellular carcinoma incidence ( J:93899 , J:172430 , J:186226 , J:190067 )

• liver tumors that develop in mice after doxycycline withdrawal resemble hepatocellular carcinomas and/or hepatoblastomas (J:93899)

• tumors that form in mice after doxycycline withdrawal are composed of hepatocellular neoplasms characterized by sheets of cells with occasional mitotic figure, slightly pleomorphic nuclei, and prominent nucleoli (J:172430)

• tumors show a range of differentiation between well- and moderately-differentiated hepatocellular carcinoma (J:172430)

• mice develop multifocal hepatocellular carcinoma within 5-8 weeks of age when doxycycline is removed at birth, showing invasive tumor cells in glandular and solid pattern infiltrating adjacent normal liver tissue (J:186226)

• in doxycycline-treated mice (J:190067)

• however, treatment with adeno-associated virus-expressing Mir122 suppresses tumorigenesis (J:190067)

decreased tumor growth/size ( J:190067 )

• doxycycline-treated mice infected with an adeno-associated virus-expressing Mir122 exhibit suppression of tumorigenesis tumor cell proliferation compared with control mice

liver/biliary system

increased liver tumor incidence ( J:93899 , J:172430 )

• following withdrawal of doxycycline, mice develop tumors with a latency of 12 weeks and all mice succumb to liver tumors within 2 weeks (J:93899)

• liver tumors that develop in mice after doxycycline withdrawal are invasive and metastasis into the thoracic cavity and lung parenchyma (J:93899)

• however, re-establishment of doxycycline-treatment produces rapid and sustained tumor regression (J:93899)

• repeated withdrawal and treatment with doxycyclineinduces and represses, respectively, tumor formation (J:93899)

increased hepatoblastoma incidence ( J:93899 )

• liver tumors that develop in mice after doxycycline withdrawal resemble hepatocellular carcinomas and/or hepatoblastomas

increased hepatocellular carcinoma incidence ( J:93899 , J:172430 , J:186226 , J:190067 )

• liver tumors that develop in mice after doxycycline withdrawal resemble hepatocellular carcinomas and/or hepatoblastomas (J:93899)

• tumors that form in mice after doxycycline withdrawal are composed of hepatocellular neoplasms characterized by sheets of cells with occasional mitotic figure, slightly pleomorphic nuclei, and prominent nucleoli (J:172430)

• tumors show a range of differentiation between well- and moderately-differentiated hepatocellular carcinoma (J:172430)

• mice develop multifocal hepatocellular carcinoma within 5-8 weeks of age when doxycycline is removed at birth, showing invasive tumor cells in glandular and solid pattern infiltrating adjacent normal liver tissue (J:186226)

• in doxycycline-treated mice (J:190067)

• however, treatment with adeno-associated virus-expressing Mir122 suppresses tumorigenesis (J:190067)

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:190067
hepatocellular carcinoma		DOID:684	OMIM:114550	J:93899 , J:172430 , J:186226