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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ptentm2.1Ppp
targeted mutation 2.1, Pier Paolo Pandolfi
MGI:2679886
Summary 18 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Ptentm2.1Ppp/Ptentm2.1Ppp involves: 129S1/Sv MGI:5320164
cn2
Cdkn1btm1Ako/Cdkn1b+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
129S1.Cg-Cdkn1btm1Ako Ptentm2.1Ppp Tg(TPO-cre)1Shk MGI:4838319
cn3
Cdkn1btm1Ako/Cdkn1btm1Ako
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
129S1.Cg-Cdkn1btm1Ako Ptentm2.1Ppp Tg(TPO-cre)1Shk MGI:4838318
cn4
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
129S1.Cg-Ptentm2.1Ppp Tg(TPO-cre)1Shk MGI:4838317
cn5
Pik3cdtm1Tnr/Pik3cdtm1Tnr
Ptentm2.1Ppp/Ptentm2.1Ppp
Cd19tm1(cre)Cgn/Cd19+
involves: 129P2/OlaHsd * 129S1/Sv * 129S4/SvJae * C57BL/6 MGI:3796508
cn6
Ptentm2.1Ppp/Pten+
Spry1tm1Jdli/Spry1tm1.1Jdli
Spry2tm1Mrt/Spry2tm1.1Mrt
Tg(Osr1-cre)4Mrt/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N MGI:5467305
cn7
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(CAG-Bgeo,-Spry2,-ALPP)1Mrt/0
Tg(Osr1-cre)4Mrt/0
involves: 129P2/OlaHsd * 129S1/Sv * FVB/N MGI:5467306
cn8
Ptentm2.1Ppp/Ptentm2.1Ppp
Tnfrsf4tm2(cre)Nik/Tnfrsf4+
involves: 129S1/Sv * 129X1/SvJ MGI:4850096
cn9
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Osr1-cre)4Mrt/0
involves: 129S1/Sv * 129X1/SvJ MGI:5467307
cn10
Eif4etm1.1Lfur/Eif4etm1.1Lfur
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:4830313
cn11
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)8113ANg/0
involves: 129S1/Sv * C57BL/6 MGI:2679902
cn12
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(GFAP-TAg121)1Tvd/0
involves: 129S1/Sv * C57BL/6 * C57BL/6J * DBA/2 * FVB/N MGI:5286094
cn13
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key/Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * C57BL/6 * DBA/2 MGI:5524280
cn14
Ptentm2.1Ppp/Ptentm2.1Ppp
Trp53tm1Thl/Trp53tm1Thl
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * C57BL/6 * DBA/2 MGI:3603330
cn15
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * C57BL/6 * DBA/2 MGI:2679901
cn16
Ptentm2.1Ppp/Pten+
Tg(Cnp-EGFR)10Nrat/0
Tg(Dhh-cre)1Mejr/0
involves: 129S1/Sv * C57BL/6 * FVB/N * SJL MGI:5485415
cn17
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Dhh-cre)1Mejr/0
involves: 129S1/Sv * C57BL/6 * FVB/N * SJL MGI:5485416
cn18
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Cnp-EGFR)10Nrat/0
Tg(Dhh-cre)1Mejr/0
involves: 129S1/Sv * C57BL/6 * FVB/N * SJL MGI:5485414


Genotype
MGI:5320164
cn1
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Genetic
Background
involves: 129S1/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice injected with an adenovirus expressing Cre recombinase into the left auditory cortex exhibit neurons with increased dendritic total length and branch number
• mice injected with an adenovirus expressing Cre recombinase into the left auditory cortex exhibit neurons with increased density of dendritic spines
• mice injected with an adenovirus expressing Cre recombinase into the left auditory cortex have neurons that exhibit lower input resistance than nearby control neurons without adenovirus
• pyramidal neurons from mice injected with an adenovirus expressing Cre recombinase into the left auditory cortex receive stronger local inputs in the auditory cortex than control neurons without adenovirus; the increase is greatest for inputs arising from layer 2 but is present in all layers
• neurons from mice injected with an adenovirus expressing Cre recombinase into the left auditory cortex or the left auditory thalamus exhibit increased neuronal responses to auditory callosal and thalamic inputs as indicated by enhanced light-evoked EPSCs after channelrhodopsin-2 adenoviral expression (which allows for neurons to be excited to fire action potentials by flashing blue light)
• mice injected with an adenovirus expressing Cre recombinase into the left auditory cortex exhibit increased miniature spontaneous EPSC frequency and miniature EPSC amplitude

Mouse Models of Human Disease
OMIM ID Ref(s)
Autism 209850 J:181347




Genotype
MGI:4838319
cn2
Allelic
Composition
Cdkn1btm1Ako/Cdkn1b+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
Genetic
Background
129S1.Cg-Cdkn1btm1Ako Ptentm2.1Ppp Tg(TPO-cre)1Shk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn1btm1Ako mutation (0 available); any Cdkn1b mutation (15 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(TPO-cre)1Shk mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• no gender differences in development of adenomas
• no gender differences in development of carcinomas

mortality/aging
• mean survival is 58 weeks of age

neoplasm
• no gender differences in development of adenomas
• no gender differences in development of carcinomas




Genotype
MGI:4838318
cn3
Allelic
Composition
Cdkn1btm1Ako/Cdkn1btm1Ako
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
Genetic
Background
129S1.Cg-Cdkn1btm1Ako Ptentm2.1Ppp Tg(TPO-cre)1Shk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn1btm1Ako mutation (0 available); any Cdkn1b mutation (15 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(TPO-cre)1Shk mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival is 21 weeks and all mutants die by 6 months of age

endocrine/exocrine glands

respiratory system
• hyperplastic thyroids cause dyspnea and prevent feeding




Genotype
MGI:4838317
cn4
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
Genetic
Background
129S1.Cg-Ptentm2.1Ppp Tg(TPO-cre)1Shk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(TPO-cre)1Shk mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• females have a reduced lifespan compared to males, with a mean survival age of 73 weeks compared to 83 weeks in males
• mutants start to show signs of illness starting after 1 year of age

endocrine/exocrine glands
• enlarged thyroid
• ovariectomization of females results in reduced proliferative index of thyroids to a similar level seen in males
• 52% of females develop thyroid follicular adenomas between 8-12 months of age compared to 12% of males
• 50% of the females and 35% of males over one year of age develop invasive and often metastatic thyroid follicular carcinomas

homeostasis/metabolism
• aging mice exhibit suppression of thyroid-stimulating hormone
• thyroxine levels are slightly, but significantly, increased in all mice with adenomas

neoplasm
• 52% of females develop thyroid follicular adenomas between 8-12 months of age compared to 12% of males
• 50% of the females and 35% of males over one year of age develop invasive and often metastatic thyroid follicular carcinomas




Genotype
MGI:3796508
cn5
Allelic
Composition
Pik3cdtm1Tnr/Pik3cdtm1Tnr
Ptentm2.1Ppp/Ptentm2.1Ppp
Cd19tm1(cre)Cgn/Cd19+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd19tm1(cre)Cgn mutation (6 available); any Cd19 mutation (16 available)
Pik3cdtm1Tnr mutation (0 available); any Pik3cd mutation (20 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• unlike in Pten deficient mice, B1 B cell numbers are normal in the spleen and peritoneum
• defects in class switch recombination associated with Pten deficiency are partially reversed
• mice exhibit an increase in marginal zone B cells that is not as great as in Pten null mice but more than in wild-type mice

hematopoietic system
• defects in class switch recombination associated with Pten deficiency are partially reversed
• mice exhibit an increase in marginal zone B cells that is not as great as in Pten null mice but more than in wild-type mice




Genotype
MGI:5467305
cn6
Allelic
Composition
Ptentm2.1Ppp/Pten+
Spry1tm1Jdli/Spry1tm1.1Jdli
Spry2tm1Mrt/Spry2tm1.1Mrt
Tg(Osr1-cre)4Mrt/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Spry1tm1.1Jdli mutation (0 available); any Spry1 mutation (3 available)
Spry1tm1Jdli mutation (1 available); any Spry1 mutation (3 available)
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (16 available)
Spry2tm1Mrt mutation (1 available); any Spry2 mutation (16 available)
Tg(Osr1-cre)4Mrt mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• evidence of invasion, including clusters of epithelial cells in the mesenchyme and vasculature and loss of the smooth muscle around ducts, is seen associated with high-grade PIN, indicating transition to invasive cancer
• prostates at 6 months of age show multiple, widely spaced areas with low-grade PIN and occasional ducts with high-grade PIN
• at 12-14 months of age, about 50% of ducts show low-grade PIN and about 15% show high-grade PIN compared to 5-10% of control ducts showing PIN
• ductal lumens are filled with atypical and dysplastic cells that distort the overall ductal architecture and are associated with areas of necrosis and abnormal intraepithelial vessels typical of high-grade PIN

reproductive system
• evidence of invasion, including clusters of epithelial cells in the mesenchyme and vasculature and loss of the smooth muscle around ducts, is seen associated with high-grade PIN, indicating transition to invasive cancer
• prostates at 6 months of age show multiple, widely spaced areas with low-grade PIN and occasional ducts with high-grade PIN
• at 12-14 months of age, about 50% of ducts show low-grade PIN and about 15% show high-grade PIN compared to 5-10% of control ducts showing PIN
• ductal lumens are filled with atypical and dysplastic cells that distort the overall ductal architecture and are associated with areas of necrosis and abnormal intraepithelial vessels typical of high-grade PIN

neoplasm
• evidence of invasion, including clusters of epithelial cells in the mesenchyme and vasculature and loss of the smooth muscle around ducts, is seen associated with high-grade PIN, indicating transition to invasive cancer
• prostates at 6 months of age show multiple, widely spaced areas with low-grade PIN and occasional ducts with high-grade PIN
• at 12-14 months of age, about 50% of ducts show low-grade PIN and about 15% show high-grade PIN compared to 5-10% of control ducts showing PIN
• ductal lumens are filled with atypical and dysplastic cells that distort the overall ductal architecture and are associated with areas of necrosis and abnormal intraepithelial vessels typical of high-grade PIN

Mouse Models of Human Disease
OMIM ID Ref(s)
Prostate Cancer 176807 J:192348




Genotype
MGI:5467306
cn7
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(CAG-Bgeo,-Spry2,-ALPP)1Mrt/0
Tg(Osr1-cre)4Mrt/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(CAG-Bgeo,-Spry2,-ALPP)1Mrt mutation (0 available)
Tg(Osr1-cre)4Mrt mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• PIN is seen in 15% of prostate ducts as early as 2 weeks of age, in 31% of ducts at 4 weeks, and 42% of ducts at 9 months of age

endocrine/exocrine glands
• PIN is seen in 15% of prostate ducts as early as 2 weeks of age, in 31% of ducts at 4 weeks, and 42% of ducts at 9 months of age

neoplasm
• PIN is seen in 15% of prostate ducts as early as 2 weeks of age, in 31% of ducts at 4 weeks, and 42% of ducts at 9 months of age




Genotype
MGI:4850096
cn8
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tnfrsf4tm2(cre)Nik/Tnfrsf4+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tnfrsf4tm2(cre)Nik mutation (1 available); any Tnfrsf4 mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• following immunization
• 3-fold following immunization
• following immunization, mice exhibit an increased in high-affinity antibody titers compared to in similarly treated wild-type mice

hematopoietic system
• following immunization
• 3-fold following immunization
• following immunization, mice exhibit an increased in high-affinity antibody titers compared to in similarly treated wild-type mice




Genotype
MGI:5467307
cn9
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Osr1-cre)4Mrt/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(Osr1-cre)4Mrt mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• PIN is seen in 31% of prostate ducts as early as 2 weeks of age, in 66% of ducts at 4 weeks, and 79% of ducts at 9 months of age show extensive high-grade PIN

endocrine/exocrine glands
• PIN is seen in 31% of prostate ducts as early as 2 weeks of age, in 66% of ducts at 4 weeks, and 79% of ducts at 9 months of age show extensive high-grade PIN

neoplasm
• PIN is seen in 31% of prostate ducts as early as 2 weeks of age, in 66% of ducts at 4 weeks, and 79% of ducts at 9 months of age show extensive high-grade PIN




Genotype
MGI:4830313
cn10
Allelic
Composition
Eif4etm1.1Lfur/Eif4etm1.1Lfur
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Eif4etm1.1Lfur mutation (0 available); any Eif4e mutation (30 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(Pbsn-cre)4Prb mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• at 7 months, mice exhibit fewer incidence of high grade prostate intraepithelial neoplasia due to delayed onset and decreased cell proliferation compared with Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice
• mice do not exhibit infiltrating adenocarcinoma in the prostate unlike Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice




Genotype
MGI:2679902
cn11
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)8113ANg/0
Genetic
Background
involves: 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(Pbsn-cre)8113ANg mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• complete penetrance of invasive and diffuse prostate cancer
• disruption of basement membrane and organ infiltration
• tumors were less diffuse than in homozygotes carrying Tg(Pbsn-cre)4Prb, variably differentiated, and only affected a single lobe

endocrine/exocrine glands
• focal areas of epithelial hyperplasia
• increased proliferation of epithelial cells
• enlargement of prostate, less pronounced than in homozygotes carrying Tg(Pbsn-cre)4Prb
• complete penetrance of invasive and diffuse prostate cancer
• disruption of basement membrane and organ infiltration
• tumors were less diffuse than in homozygotes carrying Tg(Pbsn-cre)4Prb, variably differentiated, and only affected a single lobe

reproductive system
• focal areas of epithelial hyperplasia
• increased proliferation of epithelial cells
• enlargement of prostate, less pronounced than in homozygotes carrying Tg(Pbsn-cre)4Prb
• complete penetrance of invasive and diffuse prostate cancer
• disruption of basement membrane and organ infiltration
• tumors were less diffuse than in homozygotes carrying Tg(Pbsn-cre)4Prb, variably differentiated, and only affected a single lobe




Genotype
MGI:5286094
cn12
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(GFAP-TAg121)1Tvd/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * C57BL/6J * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(GFAP-TAg121)1Tvd mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice infected with a cre-expression virus exhibit increased angiogenesis in the cerebral cortex compared to in control mice
• mice infected with a cre-expression virus exhibit astrocytmoa with increased invasiveness compared with mice expressing Tg(GFAP-TAg121)1Tvd
• mice infected with a cre-expression virus exhibit astrocytmoa with increased invasiveness compared with mice expressing Tg(GFAP-TAg121)1Tvd

neoplasm
• mice infected with a cre-expression virus exhibit astrocytmoa with increased invasiveness compared with mice expressing Tg(GFAP-TAg121)1Tvd

cardiovascular system
• mice infected with a cre-expression virus exhibit increased angiogenesis in the cerebral cortex compared to in control mice
• in cerebral cortex injected with cre-expressing virus

cellular
• mice infected with a cre-expression virus exhibit astrocytmoa with increased invasiveness compared with mice expressing Tg(GFAP-TAg121)1Tvd




Genotype
MGI:5524280
cn13
Allelic
Composition
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key/Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key mutation (1 available); any Gt(ROSA)26Sor mutation (313 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(Pbsn-cre)4Prb mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• shortened survival compared with Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice

reproductive system
• enlarged and hardened by 6 months
• invasive with small irregular glandular structures composed of malignant cells with large, pleiomorphic nuclei and pale cytoplasm by 8 weeks
• with a proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice
• proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice

neoplasm
• invasive with small irregular glandular structures composed of malignant cells with large, pleiomorphic nuclei and pale cytoplasm by 8 weeks
• with a proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice

renal/urinary system

growth/size/body
• increased abdominal girth

endocrine/exocrine glands
• enlarged and hardened by 6 months
• invasive with small irregular glandular structures composed of malignant cells with large, pleiomorphic nuclei and pale cytoplasm by 8 weeks
• with a proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice
• proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice




Genotype
MGI:3603330
cn14
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Trp53tm1Thl/Trp53tm1Thl
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(Pbsn-cre)4Prb mutation (3 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (139 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• invasive prostatic cancer is seen in all mutants by 10 weeks of age
• average tumor weight is increased 32-fold compared to mutants wild-type for Trp53 and these tumors encompass the entire genitourinary tract and pelvis
• no increase is seen in the number of senescent cells compared to wild-type prostates unlike in mutants wild-type for Trp53

endocrine/exocrine glands
• invasive prostatic cancer is seen in all mutants by 10 weeks of age
• average tumor weight is increased 32-fold compared to mutants wild-type for Trp53 and these tumors encompass the entire genitourinary tract and pelvis
• no increase is seen in the number of senescent cells compared to wild-type prostates unlike in mutants wild-type for Trp53

mortality/aging
• all mutants died by 7 months of age

neoplasm
• invasive prostatic cancer is seen in all mutants by 10 weeks of age
• average tumor weight is increased 32-fold compared to mutants wild-type for Trp53 and these tumors encompass the entire genitourinary tract and pelvis
• no increase is seen in the number of senescent cells compared to wild-type prostates unlike in mutants wild-type for Trp53
• by 11 weeks of age invasive adenocarcinoma develops

renal/urinary system
• bladder obstruction




Genotype
MGI:2679901
cn15
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(Pbsn-cre)4Prb mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• large, irregular cells, occasionally forming cryptic glandular structures
• prostate epithelial dysplasia
• focal areas of epithelial hyperplasia (J:86212)
• increased proliferation of epithelial cells (J:86212)
• mutant prostates contain a 20-fold increase in senescent epithelial cells compared to wild-type prostates (J:100683)
• massive enlargement of all prostatic lobes evident at 2 to 3 months of age, complete penetrance
• tumors were undifferentiated and often affected multiple lobes, suggesting multifocal origns (J:86212)
• complete penetrance of invasive and diffuse prostate cancer with disruption of basement membrane and signs of organ infiltration (J:86212)
• invasive prostatic cancer develops after a 4-6 month latency; however none of the mutants had died of prostatic cancer by 10 months of age (J:100683)
• tumors retain clearly defined urogenital organ boundaries (J:100683)
• high-grade prostatic intraepithelial neoplasia are seen in all 3 prostatic lobes in 9-week old mutants (J:100683)
(J:163589)
• that does not progress to grossly invasive disease (J:200002)

neoplasm
• tumors were undifferentiated and often affected multiple lobes, suggesting multifocal origns (J:86212)
• complete penetrance of invasive and diffuse prostate cancer with disruption of basement membrane and signs of organ infiltration (J:86212)
• invasive prostatic cancer develops after a 4-6 month latency; however none of the mutants had died of prostatic cancer by 10 months of age (J:100683)
• tumors retain clearly defined urogenital organ boundaries (J:100683)
• high-grade prostatic intraepithelial neoplasia are seen in all 3 prostatic lobes in 9-week old mutants (J:100683)
(J:163589)
• that does not progress to grossly invasive disease (J:200002)

endocrine/exocrine glands
• large, irregular cells, occasionally forming cryptic glandular structures
• prostate epithelial dysplasia
• focal areas of epithelial hyperplasia (J:86212)
• increased proliferation of epithelial cells (J:86212)
• mutant prostates contain a 20-fold increase in senescent epithelial cells compared to wild-type prostates (J:100683)
• massive enlargement of all prostatic lobes evident at 2 to 3 months of age, complete penetrance
• tumors were undifferentiated and often affected multiple lobes, suggesting multifocal origns (J:86212)
• complete penetrance of invasive and diffuse prostate cancer with disruption of basement membrane and signs of organ infiltration (J:86212)
• invasive prostatic cancer develops after a 4-6 month latency; however none of the mutants had died of prostatic cancer by 10 months of age (J:100683)
• tumors retain clearly defined urogenital organ boundaries (J:100683)
• high-grade prostatic intraepithelial neoplasia are seen in all 3 prostatic lobes in 9-week old mutants (J:100683)
(J:163589)
• that does not progress to grossly invasive disease (J:200002)




Genotype
MGI:5485415
cn16
Allelic
Composition
Ptentm2.1Ppp/Pten+
Tg(Cnp-EGFR)10Nrat/0
Tg(Dhh-cre)1Mejr/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(Cnp-EGFR)10Nrat mutation (0 available)
Tg(Dhh-cre)1Mejr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice display a similar peripheral nervous system phenotype as homozygous Ptentm2.1Ppp Tg(Dhh-cre)1Mejr/0 mice, except with a latency of 415 days
• 100% exhibit enlarged branchial plexi
• 20% exhibit enlarged sacral plexi
• enlarged peripheral nerves are graded as hyperplasia to low-grade grade peripheral nerve sheath tumors (PNSTs)
• 100% exhibit enlarged trigeminal nerves
• 80% exhibit enlarged sciatic nerves

neoplasm
• enlarged peripheral nerves are graded as hyperplasia to low-grade grade peripheral nerve sheath tumors (PNSTs)




Genotype
MGI:5485416
cn17
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Dhh-cre)1Mejr/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(Dhh-cre)1Mejr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival age is 247 days compared to conditional Pten heterozygotes that have a median survival age of 415 days

nervous system
• mutants exhibit a similar peripheral nervous system phenotype as triple homozygous Ptentm2.1Ppp Tg(Dhh-cre)1Mejr/0 Tg(Cnp-EGFR)10Nrat/0 mutants but with delayed latency and reduced tumor multiplicity
• 100% exhibit enlarged branchial plexi
• 10% exhibit enlarged sacral plexi
• enlarged peripheral nerves are low-grade peripheral nerve sheath tumors (PNSTs)
• 90% exhibit enlarged trigeminal nerves
• 80% exhibit enlarged sciatic nerves

neoplasm
• enlarged peripheral nerves are low-grade peripheral nerve sheath tumors (PNSTs)




Genotype
MGI:5485414
cn18
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Cnp-EGFR)10Nrat/0
Tg(Dhh-cre)1Mejr/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (40 available)
Tg(Cnp-EGFR)10Nrat mutation (0 available)
Tg(Dhh-cre)1Mejr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• rapid postnatal death, with a medial survival age of 26 days

nervous system
• mutants exhibit enlarged peripheral nerves: brachial plexi, sacral plexi, trigeminal and sciatic nerves
• 100% exhibit enlarged branchial plexi
• 50% exhibit enlarged lumbar sacral plexi
• mast cells are seen in enlarged peripheral nerves
• enlarged peripheral nerves are graded as high-grade grade peripheral nerve sheath tumors (PNSTs) resembling human sporatic malignant grade peripheral nerve sheath tumors
• 92% exhibit enlarged trigeminal nerves
• mutants exhibit multiple enlarged dorsal root ganglia
• 50% exhibit enlarged sciatic nerves

neoplasm
• enlarged peripheral nerves are graded as high-grade grade peripheral nerve sheath tumors (PNSTs) resembling human sporatic malignant grade peripheral nerve sheath tumors





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
07/19/2016
MGI 6.04
The Jackson Laboratory