All Phenotypes Tg(KRT14-cre)8Brn MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Tg(KRT14-cre)8Brn
transgene insertion 8, Anton Berns
MGI:2177243

Summary

37 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Rb1^tm2Brn/Rb1^tm2Brn Tg(KRT14-cre)8Brn/0 Tg(KRT5-Akt1*)Jmpa/0	involves: 129 * C57BL/6 * DBA/2 * DBA/2J * FVB/N	MGI:3842836
cn2	Acvr1b^tm1.1Gsu/Acvr1b^tm1.1Gsu Tg(KRT14-cre)8Brn/0	involves: 129 * C57BL/6J * FVB	MGI:5000109
cn3	Acvr1b^tm1.1Gsu/Acvr1b^tm1.1Gsu Tg(KRT14-cre)8Brn/Tg(KRT14-cre)8Brn	involves: 129 * C57BL/6J * FVB	MGI:5000110
cn4	Trp53^tm1.1Brn/Trp53^tm3Tyj Tg(KRT14-cre)8Brn/?	involves: 129P2/OlaHsd * 129S4/SvJae * FVB/N * SKH1	MGI:3716946
cn5	Brca1^tm1Brn/Brca1^tm1Brn Trp53^tm1Brn/Trp53⁺ Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * BALB/cJ * FVB/N	MGI:3762187
cn6	Brca1^tm1Brn/Brca1^tm1Brn Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * BALB/cJ * FVB/N	MGI:3762188
cn7	Brca1^tm1Brn/Brca1^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * BALB/cJ * FVB/N	MGI:3762189
cn8	Brca1^tm1Brn/Brca1⁺ Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * BALB/cJ * FVB/N	MGI:3762186
cn9	Pten^tm1Mro/Pten^tm1Mro Tg(KRT14-cre)8Brn/0 Trp53^tm1Brn/Trp53^tm1Brn	involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * DBA/2J * FVB/N	MGI:3842835
cn10	Tg(KRT14-cre)8Brn/0 Tg(KRT5-Akt1*)Jmpa/0 Trp53^tm1Brn/Trp53^tm1Brn	involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * DBA/2J * FVB/N	MGI:3842833
cn11	Brca1^tm1Brn/Brca1^tm1.1Jjon Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * C57BL/6J * FVB/N	MGI:5307256
cn12	Brca1^tm1Brn/Brca1^tm1Brn Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * C57BL/6J * FVB/N	MGI:5307257
cn13	Gata3^tm3Gsv/Gata3^tm3Gsv Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3697461
cn14	Itgb4^tm2Son/Itgb4^tm2Son Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3574283
cn15	Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3695270
cn16	Cdh1^tm1Jjon/Cdh1^tm1Jjon Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3695271
cn17	Cdh1^tm1Jjon/Cdh1^tm1Jjon Trp53^tm1Brn/Trp53⁺ Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3695272
cn18	Cdh1^tm1Jjon/Cdh1⁺ Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3695273
cn19	Cdh1^tm1Jjon/Cdh1^tm1Jjon Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3695274
cn20	Brca2^tm1Brn/Brca2^tm1Brn Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3831430
cn21	Brca2^tm1Brn/Brca2⁺ Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3831431
cn22	Brca2^tm1Brn/Brca2^tm1Brn Trp53^tm1Brn/Trp53⁺ Tg(KRT14-cre)8Brn/0	involves: 129P2/OlaHsd * FVB/N	MGI:3831432
cn23	Dcc^tm1Nki/Dcc^tm1Nki Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/?	involves: 129P2/OlaHsd * FVB/N	MGI:5308805
cn24	Trp53^tm1.1Brn/Trp53⁺ Tg(KRT14-cre)8Brn/?	involves: 129P2/OlaHsd * FVB/N * SKH1	MGI:3716948
cn25	Trp53^tm1.1Brn/Trp53^tm1.1Brn Tg(KRT14-cre)8Brn/?	involves: 129P2/OlaHsd * FVB/N * SKH1	MGI:3716947
cn26	Gba1^tm2Karl/Gba1^tm2Karl Tg(KRT14-cre)8Brn/?	involves: 129S1/Sv * 129X1/SvJ * FVB/N	MGI:3764515
cn27	Jun^tm1Rsjo/Jun^tm1Rsjo Tg(KRT14-cre)8Brn/0	involves: 129S1/Sv * 129X1/SvJ * FVB/N	MGI:2673712
cn28	Grhl3^tm1Jane/Grhl3^tm3.1Jane Tg(KRT14-cre)8Brn/0	involves: 129S1/Sv * C57BL/6 * FVB/N	MGI:5306659
cn29	Grhl1^tm1Jane/Grhl1^tm1Jane Grhl3^tm1Jane/Grhl3^tm3.1Jane Tg(KRT14-cre)8Brn/0	involves: 129S1/Sv * C57BL/6 * FVB/N	MGI:5896359
cn30	Grhl3^tm1Jane/Grhl3^tm3.1Jane Tgm5^{tm2a(KOMP)Wtsi}/Tgm5^{tm2a(KOMP)Wtsi} Tg(KRT14-cre)8Brn/0	involves: 129S1/Sv * C57BL/6N * FVB/N	MGI:5896358
cn31	Rb1^tm3Tyj/Rb1^tm3Tyj Tg(KRT14-cre)8Brn/0 Tg(KRT14-HPV16E7)2304Plam/0	involves: 129S4/SvJae * C57BL/6 * FVB	MGI:3607134
cn32	Rb1^tm3Tyj/Rb1^tm3Tyj Tg(KRT14-cre)8Brn/0	involves: 129S4/SvJae * C57BL/6 * FVB	MGI:3607133
cn33	Trp53^tm3Tyj/Trp53⁺ Tg(KRT14-cre)8Brn/?	involves: 129S4/SvJae * FVB/N * SKH1	MGI:3716945
cn34	Trp63^tm1Elrf/Trp63^tm1Elrf Tg(KRT14-cre)8Brn/0	involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NCr * FVB/N	MGI:4355553
cn35	Apc^tm2Rak/Apc^tm2Rak Tg(KRT14-cre)8Brn/0	involves: 129/Sv * C57BL/6J * FVB/N * SJL	MGI:3688736
cn36	Ptch1^tm1Bjw/Ptch1^tm1Bjw Tg(KRT14-cre)8Brn/0	involves: 129T2/SvEms * FVB/N	MGI:5925369
cn37	Rala^tm1.2Cjm/Rala^tm1.2Cjm Tg(KRT14-cre)8Brn/0	involves: C57BL/6 * C57BL/6J * FVB/N	MGI:5505294

Allelic Composition	Rb1^tm2Brn/Rb1^tm2Brn Tg(KRT14-cre)8Brn/0 Tg(KRT5-Akt1*)Jmpa/0
Genetic Background	involves: 129 * C57BL/6 * DBA/2 * DBA/2J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1^tm2Brn mutation (3 available); any Rb1 mutation (106 available)
Tg(KRT14-cre)8Brn mutation (4 available)
Tg(KRT5-Akt1*)Jmpa mutation (0 available)

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

neoplasm

increased tumor incidence ( J:144831 )

• pathologic characteristics of oral lesions and tumor development rate are the same as in Tg(KRT5-Akt1*)Jmpa mice

craniofacial

abnormal oral mucosa morphology ( J:144831 )

• pathologic characteristics of oral lesions and tumor development rate are the same as in Tg(KRT5-Akt1*)Jmpa mice

digestive/alimentary system

abnormal oral mucosa morphology ( J:144831 )

• pathologic characteristics of oral lesions and tumor development rate are the same as in Tg(KRT5-Akt1*)Jmpa mice

growth/size/body

abnormal oral mucosa morphology ( J:144831 )

• pathologic characteristics of oral lesions and tumor development rate are the same as in Tg(KRT5-Akt1*)Jmpa mice

Allelic Composition	Acvr1b^tm1.1Gsu/Acvr1b^tm1.1Gsu Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129 * C57BL/6J * FVB

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvr1b^tm1.1Gsu mutation (1 available); any Acvr1b mutation (36 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

skeleton

abnormal incisor color ( J:171766 )

• in mice with severe hair loss

abnormal lower incisor morphology ( J:171766 )

• mice with severe hair loss also show incisor abnormalities including absence of a lower incisor and overextending or shortening of one lower incisor

integument

abnormal skin sebaceous gland morphology ( J:171766 )

• at P24 and 6 months of age

• increase in the number of sebaceous glands at 5 months of age

enlarged sebaceous gland ( J:171766 )

• enlarged skin sebaceous glands at P24 and 6 months of age

abnormal hair growth ( J:171766 )

alopecia ( J:171766 )

• all pups born with hair show increased hair loss with age

• completely alopecic at 5 months of age

hairless ( J:171766 )

• about 25% of pups are hairless

abnormal hair follicle morphology ( J:171766 )

• mice with gross alopecia at P5 show hair follicle abnormalities

• the least affected mice show striking defects in hair follicle morphology at P24 (telogen phase) and P32 (anagen phase) but only slight defects at earlier times

dilated hair follicle ( J:171766 )

• at 5 months of age remaining hair follicles are dilated forming large cysts containing keratinaceous debris

abnormal skin adnexa physiology ( J:171766 )

• expression analysis indicates hair differentiation is disrupted when the hair cycle is deregulated

• increase in proliferation in the remaining hair follicles that had not completely disintegrated into cysts at 5 months of age

abnormal hair cycle ( J:171766 )

• in the least affected mice at P17 some follicles are delayed in their entry into catagen phase

• at P32 in the least affected mice the hair cycle appears completely deregulated

abnormal hair follicle regression ( J:171766 )

• in the least affected mice at P24 hair follicles remain in catagen rather than starting to enter anagen as in controls

abnormal epidermal layer morphology ( J:171766 )

epidermal cyst ( J:171766 )

• at 5 months of age remaining hair follicles are dilated forming large cysts containing keratinaceous debris

thick epidermis stratum basale ( J:171766 )

• at 5 months of age the skin has 3-5 more basal layers of epithelial cells compared to the skin of littermate controls

thick epidermis ( J:171766 )

• at 5 months of age

abnormal skin physiology ( J:171766 )

• increase in proliferation in the basal layer of the epidermis at 5 months of age but not from P11 to P32

growth/size/body

abnormal incisor color ( J:171766 )

• in mice with severe hair loss

abnormal lower incisor morphology ( J:171766 )

• mice with severe hair loss also show incisor abnormalities including absence of a lower incisor and overextending or shortening of one lower incisor

epidermal cyst ( J:171766 )

• at 5 months of age remaining hair follicles are dilated forming large cysts containing keratinaceous debris

postnatal growth retardation ( J:171766 )

• stunted growth by P5

craniofacial

abnormal incisor color ( J:171766 )

• in mice with severe hair loss

abnormal lower incisor morphology ( J:171766 )

• mice with severe hair loss also show incisor abnormalities including absence of a lower incisor and overextending or shortening of one lower incisor

reproductive system

reproductive system phenotype ( J:171766 )

N	• despite cre expression in the mammary gland females are fertile and able to nurse pups

digestive/alimentary system

digestive/alimentary phenotype ( J:171766 )

N	• despite cre expression in the tongue and esophagus no gross abnormalities are detected in these tissues

endocrine/exocrine glands

abnormal skin sebaceous gland morphology ( J:171766 )

• at P24 and 6 months of age

• increase in the number of sebaceous glands at 5 months of age

enlarged sebaceous gland ( J:171766 )

• enlarged skin sebaceous glands at P24 and 6 months of age

Allelic Composition	Acvr1b^tm1.1Gsu/Acvr1b^tm1.1Gsu Tg(KRT14-cre)8Brn/Tg(KRT14-cre)8Brn
Genetic Background	involves: 129 * C57BL/6J * FVB

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvr1b^tm1.1Gsu mutation (1 available); any Acvr1b mutation (36 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

integument

alopecia ( J:171766 )

• all pups born with hair show increased hair loss with age

• alopecia is more severe in mice homozygous for the cre transgene compared to mice hemizygous for the transgene

growth/size/body

postnatal growth retardation ( J:171766 )

• stunted growth by P5

• stunting is more severe in mice homozygous for the cre transgene compared to mice hemizygous for the transgene

Allelic Composition	Trp53^tm1.1Brn/Trp53^tm3Tyj Tg(KRT14-cre)8Brn/?
Genetic Background	involves: 129P2/OlaHsd * 129S4/SvJae * FVB/N * SKH1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1.1Brn mutation (0 available); any Trp53 mutation (232 available)
Trp53^tm3Tyj mutation (3 available); any Trp53 mutation (232 available)

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

neoplasm

increased skin tumor incidence ( J:121734 )

• skin tumors develop between 200 and 300 days

• whether spontaneous or induced, mice develop epithelial, proliferative lesions forming a continuum from nonneoplastic squamous keratosis and acanthosis to squamous cell papillomas, actinic keratosis and keratoacanthoma with increasing degrees of atypia and dysplasia, carcinoma in situ, up to invasive squamous cell carcinoma

increased lymphoma incidence ( J:121734 )

• developed in one mouse

cellular

decreased cellular sensitivity to ultraviolet irradiation ( J:121734 )

• fewer CASP3+ cells area found following UVB treatment when compared to wild-type mice

• the reduction in apoptotic cells is slightly greater in homozygotes than in heterozygotes

integument

increased skin tumor incidence ( J:121734 )

• skin tumors develop between 200 and 300 days

Allelic Composition	Brca1^tm1Brn/Brca1^tm1Brn Trp53^tm1Brn/Trp53⁺ Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * BALB/cJ * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1^tm1Brn mutation (2 available); any Brca1 mutation (113 available)
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (232 available)

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

neoplasm

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland with a latency of 407 days

integument

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland with a latency of 407 days

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland with a latency of 407 days

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:126551

Allelic Composition	Brca1^tm1Brn/Brca1^tm1Brn Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * BALB/cJ * FVB/N

Find Mice

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

neoplasm

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland with a latency of 213 days

• 80% of mice develop tumors compared to 63% of Trp53^tm1Jjon/Trp53^tm1Jjon Tg(KRT14-cre)8Jjon mice

• mice develop mammary types of carcinoma (91%), biphasic carcinoma that is poorly defined (3%) and biphasic carcinoma that is well defined (6%)

integument

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland with a latency of 213 days

• 80% of mice develop tumors compared to 63% of Trp53^tm1Jjon/Trp53^tm1Jjon Tg(KRT14-cre)8Jjon mice

• mice develop mammary types of carcinoma (91%), biphasic carcinoma that is poorly defined (3%) and biphasic carcinoma that is well defined (6%)

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland with a latency of 213 days

• 80% of mice develop tumors compared to 63% of Trp53^tm1Jjon/Trp53^tm1Jjon Tg(KRT14-cre)8Jjon mice

• mice develop mammary types of carcinoma (91%), biphasic carcinoma that is poorly defined (3%) and biphasic carcinoma that is well defined (6%)

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:126551

Allelic Composition	Brca1^tm1Brn/Brca1^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * BALB/cJ * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1^tm1Brn mutation (2 available); any Brca1 mutation (113 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

neoplasm

neoplasm ( J:126551 )

N	• mice fail to develop mammary gland tumors over 800 days of observation

Allelic Composition	Brca1^tm1Brn/Brca1⁺ Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * BALB/cJ * FVB/N

Find Mice

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

neoplasm

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland with a latency of 332 days

integument

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland with a latency of 332 days

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland with a latency of 332 days

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:126551

Allelic Composition	Pten^tm1Mro/Pten^tm1Mro Tg(KRT14-cre)8Brn/0 Trp53^tm1Brn/Trp53^tm1Brn
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * DBA/2J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pten^tm1Mro mutation (1 available); any Pten mutation (81 available)
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (232 available)

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

mortality/aging

premature death ( J:144831 )

• mice die by 20 weeks of age of unknown cause

neoplasm

increased carcinoma incidence ( J:144831 )

• all mice develop malignant carcinomas in the oral cavity or lips by 18 weeks of age

• tumors are similar to those that develop in Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn Tg(KRT5-Akt1*)Jmpa mice

behavior/neurological

weakness ( J:144831 )

• mice display a progressive weakening

Allelic Composition	Tg(KRT14-cre)8Brn/0 Tg(KRT5-Akt1*)Jmpa/0 Trp53^tm1Brn/Trp53^tm1Brn
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * DBA/2J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-cre)8Brn mutation (4 available)
Tg(KRT5-Akt1*)Jmpa mutation (0 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (232 available)

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

neoplasm

abnormal tumor morphology ( J:144831 )

• proliferation is increased in oral tumors compared to in Tg(KRT5-Akt1*)Jmpa oral tumors

• the number of blood vessels is enhanced in dysplasias and tumors compared to normal oral epithelia in Tg(KRT5-Akt1*)Jmpa mice

increased carcinoma incidence ( J:144831 )

• mice develop malignant carcinomas in the oral cavity affecting the palate, ventral side of the tongue, and the external and internal sides of the lips unlike in wild-type mice

• mice develop tumors earlier than in mice expressing Trp53

• mice develop lymph node metastases and lung micrometastases from undifferentiated highly aggressive primary tumors

increased squamous cell carcinoma incidence ( J:144831 )

cellular

increased cell proliferation ( J:144831 )

• cell proliferation of nonlesion oral epithelia is greater than in wild-type and Tg(KRT5-Akt1*)Jmpa mice

increased keratinocyte proliferation ( J:144831 )

• oral keratinocyte proliferation is greater than in wild-type cells

integument

increased keratinocyte proliferation ( J:144831 )

• oral keratinocyte proliferation is greater than in wild-type cells

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
head and neck squamous cell carcinoma		DOID:5520	OMIM:275355	J:144831

Allelic Composition	Brca1^tm1Brn/Brca1^tm1.1Jjon Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1^tm1.1Jjon mutation (0 available); any Brca1 mutation (113 available)
Brca1^tm1Brn mutation (2 available); any Brca1 mutation (113 available)
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (232 available)

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

neoplasm

decreased mammary gland tumor incidence ( J:178595 )

• compared to KB1P littermate controls homozygous

• most mammary tumors are poorly differentiated solid carcinomas

• a small percentage of tumors are classified as carcinosarcomas or lumen forming carcinomas

decreased skin tumor incidence ( J:178595 )

• markedly lower incidence compared to KB1P littermate controls

abnormal tumor pathology ( J:178595 )

• in transplanted tumors response to olaparib treatment is impaired compared to KB1P littermate controls but better than in KP mice

• transplanted tumors develop resistance to cisplatin and survival of transplanted mice is worse than that of mice transplanted with tumors from KB1P mice

abnormal tumor morphology ( J:178595 )

• increased genomic instability in tumors compared to mice homozygous for Trp53^tm1Brn and carrying Tg(KRT14-cre)8Brn (KP mice)

decreased tumor latency ( J:178595 )

• median latency is 197 days compared to 236 days in littermate controls homozygous for Brca1^tm1Brn Trp53^tm1Brn and carrying Tg(KRT14-cre)8Brn (KB1P)

• however, no difference in the latency of mammary tumor development

integument

decreased mammary gland tumor incidence ( J:178595 )

• compared to KB1P littermate controls homozygous

• most mammary tumors are poorly differentiated solid carcinomas

• a small percentage of tumors are classified as carcinosarcomas or lumen forming carcinomas

decreased skin tumor incidence ( J:178595 )

• markedly lower incidence compared to KB1P littermate controls

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:178595 )

• compared to KB1P littermate controls homozygous

• most mammary tumors are poorly differentiated solid carcinomas

• a small percentage of tumors are classified as carcinosarcomas or lumen forming carcinomas

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:178595

Allelic Composition	Brca1^tm1Brn/Brca1^tm1Brn Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J * FVB/N

Find Mice

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

neoplasm

increased mammary gland tumor incidence ( J:178595 )

• compared to KB1C61GP littermate controls

• most mammary tumors are poorly differentiated solid carcinomas

• a small percentage of tumors are classified as carcinosarcomas or lumen forming carcinomas

increased skin tumor incidence ( J:178595 )

• compared to KB1C61GP littermate controls

abnormal tumor pathology ( J:178595 )

• in transplanted tumors response to olaparib treatment is improved compared to KB1C61GP littermate controls and KP mice

• transplanted tumors never develop resistance to cisplatin unlike tumors from KP mice

abnormal tumor morphology ( J:178595 )

• increased genomic instability in tumors compared to mice homozygous for Trp53^tm1Brn and carrying Tg(KRT14-cre)8Brn (KP mice)

increased tumor latency ( J:178595 )

• median latency is 236 days compared to 197 days in littermate controls heterozygous for Brca1^tm1Brn and Brca1^tm1.1Jjon, homozygous for Trp53^tm1Brn and carrying Tg(KRT14-cre)8Brn (KB1C61GP)

integument

increased mammary gland tumor incidence ( J:178595 )

• compared to KB1C61GP littermate controls

• most mammary tumors are poorly differentiated solid carcinomas

• a small percentage of tumors are classified as carcinosarcomas or lumen forming carcinomas

increased skin tumor incidence ( J:178595 )

• compared to KB1C61GP littermate controls

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:178595 )

• compared to KB1C61GP littermate controls

• most mammary tumors are poorly differentiated solid carcinomas

• a small percentage of tumors are classified as carcinosarcomas or lumen forming carcinomas

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:178595

Allelic Composition	Gata3^tm3Gsv/Gata3^tm3Gsv Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata3^tm3Gsv mutation (0 available); any Gata3 mutation (31 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

endocrine/exocrine glands

absent nipple ( J:117058 )

• absence of visible nipples

enlarged sebaceous gland ( J:117058 )

• from P7 onwards

growth/size/body

decreased body size ( J:117058 )

weight loss ( J:117058 )

• during the first month of life

postnatal growth retardation ( J:117058 )

• apparent from P2 onwards

adipose tissue

absent subcutaneous adipose tissue ( J:117058 )

• reduced amount of subcutaneous adipose tissue

vision/eye

narrow eye opening ( J:117058 )

• eyes appear half-opened throughout life

hematopoietic system

decreased T cell number ( J:117058 )

• decrease in the number of CD3+ T cells and MHC class II cells in the skin

immune system

decreased T cell number ( J:117058 )

• decrease in the number of CD3+ T cells and MHC class II cells in the skin

homeostasis/metabolism

impaired skin barrier function ( J:117058 )

• slight delay in the development of skin barrier function at E16.5, E17.5, and E18.5

pigmentation

abnormal hair follicle melanin granule morphology ( J:117058 )

• pigment deposition is irregular and lacks the air spaces seen in wild-type hair

integument

absent subcutaneous adipose tissue ( J:117058 )

• reduced amount of subcutaneous adipose tissue

absent nipple ( J:117058 )

• absence of visible nipples

enlarged sebaceous gland ( J:117058 )

• from P7 onwards

impaired skin barrier function ( J:117058 )

• slight delay in the development of skin barrier function at E16.5, E17.5, and E18.5

abnormal hair growth ( J:117058 )

delayed hair appearance ( J:117058 )

• mice remain bald at P10

progressive hair loss ( J:117058 )

• gradual loss of abdominal hair

• anterior to posterior shedding in the head area with limited hair regeneration

short hair ( J:117058 )

• hair that does grow is short and stubby

sparse hair ( J:117058 )

• sparse hair growth around the head and neck starting from P12

abnormal hair texture ( J:117058 )

• remaining hairs are irregular with a short, thick, and hard appearance and a rounded tip

abnormal hair follicle morphology ( J:117058 )

• in some follicles small cysts develop by 5 months of age

• increase in the number of cells expressing stem cell markers in distal hair follicles

• the hair follicle and epidermal stem cell marker expression domains are connected rather than separate as in wild-type mice

• expanded precortex and cortex

• a decrease in the number of proliferating cells close to the hair bulb

abnormal hair follicle melanin granule morphology ( J:117058 )

• pigment deposition is irregular and lacks the air spaces seen in wild-type hair

abnormal hair follicle inner root sheath morphology ( J:117058 )

• absence of the companion layer that normally separates AE15+ and K14+ cells in inner root sheath cells

• absence of Huxley's layer and cuticle of the inner root sheath

abnormal hair follicle orientation ( J:117058 )

• grow at a wider angle, often parallel to the skin surface

• however, the overall hair follicle number is not reduced

abnormal hair follicle outer root sheath morphology ( J:117058 )

• increase in the number of proliferating cells in the outer root sheath

thick hair follicle outer root sheath ( J:117058 )

• the outer root sheath is about twice as thick as in wild-type mice

short vibrissae ( J:117058 )

• short and thick

abnormal hair cycle ( J:117058 )

• catagen is prolonged lasting for 6 days after which hair follicles enter telogen where in most cases the proximal end of the follicle fails to reform

abnormal skin morphology ( J:117058 )

• decrease in the number of apoptotic cells

thin dermal layer ( J:117058 )

abnormal epidermal layer morphology ( J:117058 )

• increase in the number of cells expressing stem cell markers

• the hair follicle and epidermal stem cell marker expression domains are connected rather than separate as in wild-type mice

abnormal epidermis stratum basale morphology ( J:117058 )

• increase in the number of proliferating cells at P7 and P11-15

hyperkeratosis ( J:117058 )

epidermal hyperplasia ( J:117058 )

• pronounced hyperplasia beginning at P3

thick epidermis ( J:117058 )

• gradual, pronounce epidermal thickening that involves the basal and suprabasal layers

• the basal epidermal layer is about twice as thick as in wild-type

scaly skin ( J:117058 )

• squames cover the skin wrinkles

wrinkled skin ( J:117058 )

• develops after onset of epidermal hyperplasia

abnormal skin condition ( J:117058 )

Allelic Composition	Itgb4^tm2Son/Itgb4^tm2Son Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itgb4^tm2Son mutation (0 available); any Itgb4 mutation (107 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

immune system

ear inflammation ( J:96543 )

• 16% of adult mutants developed an inflammation of the ear that might have been caused by repeated detachment of the epidermis

hearing/vestibular/ear

ear inflammation ( J:96543 )

• 16% of adult mutants developed an inflammation of the ear that might have been caused by repeated detachment of the epidermis

integument

abnormal keratinocyte morphology ( J:96543 )

• some areas of the skin had basal keratinocytes lacking hemidesmosomes that had detached from the dermis, however the regions of the skin where adhesion of the epidermis to the dermis is not compromised, keratinocytes were normal

blistering ( J:96543 )

• skin from newborn mutants exhibited small blisters in some areas of the epithelium, however organization of the skin, epidermal differentiation, epidermal proliferation, epidermal survival and formation of hair follicles and their epidermal branching was normal

Allelic Composition	Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (232 available)

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

neoplasm

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland and skin tumors with a latency of 299 days

• mice develop mammary types of carcinoma (38%), biphasic carcinoma that is poorly defined (48%) and biphasic carcinoma that is well defined (14%)

increased mammary adenocarcinoma incidence ( J:116152 )

• mice develop mostly single mammary carcinomas and carcinosarcomas with a median latency of 330 days

• most tumors are intermediate grade adenocarcinomas or high-grade solid carcinomas characterized by expansive growth pattern with large epithelial cells forming solid nest or irregular glands

• some tumors have a carcinosarcoma phenotype (elements of carcinoma and sarcoma) involving epithelial and mesenchymal elements with a metaphasic and biphasic histology

increased skin tumor incidence ( J:116152 , J:126551 )

• small numbers of skin carcinomas develop with latency of 330 days develop (J:116152)

• may be classified as pilomatriculomas or squamous cell carcinomas, without metastasis (J:116152)

• mice develop mammary gland and skin tumors with a latency of 299 days (J:126551)

increased pilomatricoma incidence ( J:116152 )

increased squamous cell carcinoma incidence ( J:116152 )

• develop in ~25% of females

integument

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland and skin tumors with a latency of 299 days

• mice develop mammary types of carcinoma (38%), biphasic carcinoma that is poorly defined (48%) and biphasic carcinoma that is well defined (14%)

increased mammary adenocarcinoma incidence ( J:116152 )

• mice develop mostly single mammary carcinomas and carcinosarcomas with a median latency of 330 days

• most tumors are intermediate grade adenocarcinomas or high-grade solid carcinomas characterized by expansive growth pattern with large epithelial cells forming solid nest or irregular glands

• some tumors have a carcinosarcoma phenotype (elements of carcinoma and sarcoma) involving epithelial and mesenchymal elements with a metaphasic and biphasic histology

increased skin tumor incidence ( J:116152 , J:126551 )

• small numbers of skin carcinomas develop with latency of 330 days develop (J:116152)

• may be classified as pilomatriculomas or squamous cell carcinomas, without metastasis (J:116152)

• mice develop mammary gland and skin tumors with a latency of 299 days (J:126551)

increased pilomatricoma incidence ( J:116152 )

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:126551 )

• mice develop mammary gland and skin tumors with a latency of 299 days

• mice develop mammary types of carcinoma (38%), biphasic carcinoma that is poorly defined (48%) and biphasic carcinoma that is well defined (14%)

increased mammary adenocarcinoma incidence ( J:116152 )

• mice develop mostly single mammary carcinomas and carcinosarcomas with a median latency of 330 days

• most tumors are intermediate grade adenocarcinomas or high-grade solid carcinomas characterized by expansive growth pattern with large epithelial cells forming solid nest or irregular glands

• some tumors have a carcinosarcoma phenotype (elements of carcinoma and sarcoma) involving epithelial and mesenchymal elements with a metaphasic and biphasic histology

Allelic Composition	Cdh1^tm1Jjon/Cdh1^tm1Jjon Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1^tm1Jjon mutation (1 available); any Cdh1 mutation (171 available)
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (232 available)

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

neoplasm

abnormal tumor vascularization ( J:116152 )

• mammary tumors show large numbers of uniformly distributed blood vessels

• a 3-fold increase in vasculature is observed compared to mutants homozygous for Cdh1 deletion and heterozygous for Trp53 deletion

increased mammary adenocarcinoma incidence ( J:116152 )

• develop at accelerated rate compared to single conditional Trp53 mutant females

• multiple tumors develop with median latency of 214 days

• shift towards invasive from expansive carcinoma is observed with tumors classified as invasive lobulocarcinoma (ILC) developing multifocally in several mammary glands

• carcinosarcomas (having elements of carcinoma and sarcoma) develop, having spindle shaped cell morphology with large cells with pleomorphic nuclei; these display both expansive and invasive growth

increased skin tumor incidence ( J:116152 )

• develop at accelerated rate compared to single conditional Trp53 mutant females

• multiple tumors develop with median latency of 214 days

• often show phenotypic change from expansive to invasive growth

• tumors may invade subcutaneous fat or carnous muscle in irregular strands and nest with polymorphic cell with dyskeratosis

increased metastatic potential ( J:116152 )

• in females presenting carcinomas ~1 cm in diameter, majority of tumors show extensive local invasion with ~50% demonstrating metastasis to draining and distant lymph nodes

• minority of animals show dissociated or loosely clustered lobulocarcinoma (ILC) cells in lungs, liver, gastrointestinal and urogenital tracts, and pancreas, or diffusely throughout peritoneal cavity

cardiovascular system

abnormal tumor vascularization ( J:116152 )

• mammary tumors show large numbers of uniformly distributed blood vessels

• a 3-fold increase in vasculature is observed compared to mutants homozygous for Cdh1 deletion and heterozygous for Trp53 deletion

integument

increased mammary adenocarcinoma incidence ( J:116152 )

• develop at accelerated rate compared to single conditional Trp53 mutant females

• multiple tumors develop with median latency of 214 days

• shift towards invasive from expansive carcinoma is observed with tumors classified as invasive lobulocarcinoma (ILC) developing multifocally in several mammary glands

increased skin tumor incidence ( J:116152 )

• develop at accelerated rate compared to single conditional Trp53 mutant females

• multiple tumors develop with median latency of 214 days

• often show phenotypic change from expansive to invasive growth

• tumors may invade subcutaneous fat or carnous muscle in irregular strands and nest with polymorphic cell with dyskeratosis

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:116152 )

• develop at accelerated rate compared to single conditional Trp53 mutant females

• multiple tumors develop with median latency of 214 days

• shift towards invasive from expansive carcinoma is observed with tumors classified as invasive lobulocarcinoma (ILC) developing multifocally in several mammary glands

Allelic Composition	Cdh1^tm1Jjon/Cdh1^tm1Jjon Trp53^tm1Brn/Trp53⁺ Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

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

neoplasm

abnormal tumor vascularization ( J:116152 )

• mammary tumors show less vascularization, especially in periphery compared to double conditional null mice

increased mammary adenocarcinoma incidence ( J:116152 )

• mice show longer tumor latency periods (495 days) compared to double conditional knockouts (214 days)

• shift towards invasive from expansive carcinoma is observed with tumors classified as invasive lobulocarcinoma (ILC) developing multifocally in several mammary glands

• carcinosarcomas (having elements of carcinoma and sarcoma) develop, having spindle shaped cell morphology with large cells with pleomormphic nuclei; these display both expansive and invasive growth

• massive central necrosis is observed

increased skin tumor incidence ( J:116152 )

• mice show longer tumor latency periods (495 days) compared to double conditional knockouts (214 days)

• often show phenotypic change from expansive to invasive growth

• tumors may invade subcutaneous fat or carnous muscle in irregular strands and nest with polymorphic cell with dyskeratosis

increased metastatic potential ( J:116152 )

• in females presenting carcinomas ~1 cm in diameter, majority of tumors show extensive local invasion with ~50% demonstrating metastasis to draining and distant lymph nodes

cardiovascular system

abnormal tumor vascularization ( J:116152 )

• mammary tumors show less vascularization, especially in periphery compared to double conditional null mice

integument

increased mammary adenocarcinoma incidence ( J:116152 )

• mice show longer tumor latency periods (495 days) compared to double conditional knockouts (214 days)

• shift towards invasive from expansive carcinoma is observed with tumors classified as invasive lobulocarcinoma (ILC) developing multifocally in several mammary glands

• massive central necrosis is observed

increased skin tumor incidence ( J:116152 )

• mice show longer tumor latency periods (495 days) compared to double conditional knockouts (214 days)

• often show phenotypic change from expansive to invasive growth

• tumors may invade subcutaneous fat or carnous muscle in irregular strands and nest with polymorphic cell with dyskeratosis

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:116152 )

• mice show longer tumor latency periods (495 days) compared to double conditional knockouts (214 days)

• shift towards invasive from expansive carcinoma is observed with tumors classified as invasive lobulocarcinoma (ILC) developing multifocally in several mammary glands

• massive central necrosis is observed

Allelic Composition	Cdh1^tm1Jjon/Cdh1⁺ Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

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

neoplasm

increased mammary adenocarcinoma incidence ( J:116152 )

• mice show longer tumor latency periods (330 days) compared to double conditional knockouts (214 days)

• most tumors are intermediate grade adenocarcinomas or high-grade solid carcinomas characterized by expansive growth pattern with large epithelial cells forming solid nest or irregular glands

• some tumors have a carcinosarcoma phenotype (elements of carcinoma and sarcoma) involving epithelial and mesenchymal elements with a metaphasic and biphasic histology

increased skin tumor incidence ( J:116152 )

• small numbers of skin carcinomas develop with latency of 330 days develop

• may be classified as pilomatriculomas or squamous cell carcinomas, without metastasis

increased pilomatricoma incidence ( J:116152 )

increased squamous cell carcinoma incidence ( J:116152 )

integument

increased mammary adenocarcinoma incidence ( J:116152 )

• mice show longer tumor latency periods (330 days) compared to double conditional knockouts (214 days)

• most tumors are intermediate grade adenocarcinomas or high-grade solid carcinomas characterized by expansive growth pattern with large epithelial cells forming solid nest or irregular glands

• some tumors have a carcinosarcoma phenotype (elements of carcinoma and sarcoma) involving epithelial and mesenchymal elements with a metaphasic and biphasic histology

increased skin tumor incidence ( J:116152 )

• small numbers of skin carcinomas develop with latency of 330 days develop

• may be classified as pilomatriculomas or squamous cell carcinomas, without metastasis

increased pilomatricoma incidence ( J:116152 )

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:116152 )

• mice show longer tumor latency periods (330 days) compared to double conditional knockouts (214 days)

• most tumors are intermediate grade adenocarcinomas or high-grade solid carcinomas characterized by expansive growth pattern with large epithelial cells forming solid nest or irregular glands

• some tumors have a carcinosarcoma phenotype (elements of carcinoma and sarcoma) involving epithelial and mesenchymal elements with a metaphasic and biphasic histology

Allelic Composition	Cdh1^tm1Jjon/Cdh1^tm1Jjon Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1^tm1Jjon mutation (1 available); any Cdh1 mutation (171 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

normal phenotype

no abnormal phenotype detected ( J:116152 )

• virgin, pregnant, or parous females show no abnormalities in ductal or alveolar development

• dams are able to nurse litters normally

• mice show no predisposition to skin or mammary tumor development

Allelic Composition	Brca2^tm1Brn/Brca2^tm1Brn Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2^tm1Brn mutation (5 available); any Brca2 mutation (132 available)
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (232 available)

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

neoplasm

increased tumor incidence ( J:73028 )

• mice develop tumors with a short median latency period of 181 days

• tumors exhibit expansive growth pattern, a high nuclear grade, and a high mitotic index

increased mammary gland tumor incidence ( J:73028 )

• in 72% of mice

increased mammary adenocarcinoma incidence ( J:73028 )

increased skin tumor incidence ( J:73028 )

• mice develop skin carcinomas

integument

increased mammary gland tumor incidence ( J:73028 )

• in 72% of mice

increased mammary adenocarcinoma incidence ( J:73028 )

increased skin tumor incidence ( J:73028 )

• mice develop skin carcinomas

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:73028 )

• in 72% of mice

increased mammary adenocarcinoma incidence ( J:73028 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:73028

Allelic Composition	Brca2^tm1Brn/Brca2⁺ Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

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

neoplasm

increased tumor incidence ( J:73028 )

• mice develop tumors with a short median latency period of 298 days

• tumors exhibit expansive growth pattern, a high nuclear grade, and a high mitotic index

increased mammary gland tumor incidence ( J:73028 )

• in 55% of mice

increased mammary adenocarcinoma incidence ( J:73028 )

increased skin tumor incidence ( J:73028 )

• mice develop skin carcinomas

integument

increased mammary gland tumor incidence ( J:73028 )

• in 55% of mice

increased mammary adenocarcinoma incidence ( J:73028 )

increased skin tumor incidence ( J:73028 )

• mice develop skin carcinomas

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:73028 )

• in 55% of mice

increased mammary adenocarcinoma incidence ( J:73028 )

Allelic Composition	Brca2^tm1Brn/Brca2^tm1Brn Trp53^tm1Brn/Trp53⁺ Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

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

neoplasm

increased tumor incidence ( J:73028 )

• mice develop tumors with a short median latency period of 360 days

• tumors exhibit expansive growth pattern, a high nuclear grade, and a high mitotic index

increased mammary gland tumor incidence ( J:73028 )

• in 31% of mice

increased mammary adenocarcinoma incidence ( J:73028 )

increased skin tumor incidence ( J:73028 )

• mice develop skin carcinomas

integument

increased mammary gland tumor incidence ( J:73028 )

• in 31% of mice

increased mammary adenocarcinoma incidence ( J:73028 )

increased skin tumor incidence ( J:73028 )

• mice develop skin carcinomas

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:73028 )

• in 31% of mice

increased mammary adenocarcinoma incidence ( J:73028 )

Allelic Composition	Dcc^tm1Nki/Dcc^tm1Nki Trp53^tm1Brn/Trp53^tm1Brn Tg(KRT14-cre)8Brn/?
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dcc^tm1Nki mutation (0 available); any Dcc mutation (76 available)
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (232 available)

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

neoplasm

increased metastatic potential ( J:181090 )

• metastasis is much more frequent (6 out of 14 cases) than when Dcc is un-mutated or mutation is heterozygous

• metastases are found in draining lymph nodes and/or lungs

increased tumor incidence ( J:181090 )

• high tumor incidence (80%) of mammary tumors regardless of presence or zygosity of Dcc mutation

• single or multiple independent tumors

increased classified tumor incidence ( J:181090 )

• solid tumors with clear demarcations

increased mammary adenocarcinoma incidence ( J:181090 )

increased spindle cell carcinoma incidence ( J:181090 )

• in mammary glands

abnormal tumor latency ( J:181090 )

• tumor latency of mammary tumors is not modified by the presence or zygosity of Dcc mutation

cellular

decreased apoptosis ( J:181090 )

• tumor cells in culture cannot be induced to apoptosis

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:181090 )

integument

increased mammary adenocarcinoma incidence ( J:181090 )

Allelic Composition	Trp53^tm1.1Brn/Trp53⁺ Tg(KRT14-cre)8Brn/?
Genetic Background	involves: 129P2/OlaHsd * FVB/N * SKH1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1.1Brn mutation (0 available); any Trp53 mutation (232 available)

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

neoplasm

increased skin tumor incidence ( J:121734 )

• skin tumors develop between 500 and 600 days

• UVB exposure results in 2.4+/-0.6 tumors at day 100 compared to 6.5+/-1.4 in Trp53^tm3Tyj Tg(KRT14-cre)8Brn heterozygotes and 0.6+/-0.2 in wild-type mice

cellular

decreased cellular sensitivity to ultraviolet irradiation ( J:121734 )

• fewer CASP3+ cells area found following UVB treatment when compared to wild-type mice

• the reduction in apoptotic cells is slightly greater in homozygotes than in heterozygotes

integument

increased skin tumor incidence ( J:121734 )

• skin tumors develop between 500 and 600 days

• UVB exposure results in 2.4+/-0.6 tumors at day 100 compared to 6.5+/-1.4 in Trp53^tm3Tyj Tg(KRT14-cre)8Brn heterozygotes and 0.6+/-0.2 in wild-type mice

Allelic Composition	Trp53^tm1.1Brn/Trp53^tm1.1Brn Tg(KRT14-cre)8Brn/?
Genetic Background	involves: 129P2/OlaHsd * FVB/N * SKH1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm1.1Brn mutation (0 available); any Trp53 mutation (232 available)

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

neoplasm

increased skin tumor incidence ( J:121734 )

• skin tumors develop between 200 and 300 days

cellular

decreased cellular sensitivity to ultraviolet irradiation ( J:121734 )

• fewer CASP3+ cells area found following UVB treatment when compared to wild-type mice

• the reduction in apoptotic cells is slightly greater in homozygotes than in heterozygotes

integument

increased skin tumor incidence ( J:121734 )

• skin tumors develop between 200 and 300 days

Allelic Composition	Gba1^tm2Karl/Gba1^tm2Karl Tg(KRT14-cre)8Brn/?
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gba1^tm2Karl mutation (1 available); any Gba1 mutation (43 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

Gba1^tm2Karl/Gba1^tm2Karl Tg(KRT14-cre)8Brn/? mice display a severe and rapidly progressive neurological disease

mortality/aging

postnatal lethality ( J:127108 )

nervous system

seizures ( J:127108 )

abnormal brain morphology ( J:127108 )

• brain cellularity is reduced particularly in the cortex and thalamus

• the cerebellum and nuclei of the pons and medulla exhibit lose of cellularity that is associated with abundant pyknotic cells

• apoptotic cells are observed in the thalamus, dendate gyrus of the hippocampus and cerebellum

decreased brain size ( J:127108 )

abnormal neuron morphology ( J:127108 )

• large neurons are surrounded by ameboid-shaped cells (microglia-like) and those in the motor trigeminal nuclei and pons regions have huge vacuoles likely due to lipid accumulation

hippocampal neuron degeneration ( J:127108 )

• neurons in the CA3 and dendate gyrus undergo degeneration

• however, neurons in the CA1 are unaffected

decreased cerebral cortex pyramidal cell number ( J:127108 )

• pyramidal neurons are lost from the cortical layer

decreased Purkinje cell number ( J:127108 )

• the number of Purkinje cells in the cerebellum is decreased compared to in wild-type mice and those present exhibit a profound swelling in their axons

behavior/neurological

abnormal gait ( J:127108 )

• mice develop a rapidly progressing neurological disease beginning at day 10 with abnormal gait, hyperextension of the neck and seizure

paralysis ( J:127108 )

• at 2 weeks of age mice develop end-stage paralysis

seizures ( J:127108 )

hematopoietic system

abnormal macrophage morphology ( J:127108 )

• visceral Gaucher cells (macrophages with lipid accumulation observed in Gaucher disease) are present in the spleen and liver

homeostasis/metabolism

abnormal lipid homeostasis ( J:127108 )

• glucosylceramide accumulates in the brain, spleen and liver unlike in wild-type mice

immune system

abnormal macrophage morphology ( J:127108 )

• visceral Gaucher cells (macrophages with lipid accumulation observed in Gaucher disease) are present in the spleen and liver

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Gaucher's disease type II		DOID:0110958	OMIM:230900	J:127108

Allelic Composition	Jun^tm1Rsjo/Jun^tm1Rsjo Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * FVB/N

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Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Jun^tm1Rsjo mutation (0 available); any Jun mutation (12 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

vision/eye

increased incidence of corneal inflammation ( J:84743 )

• mutant mice develop severe corneal inflammation shortly after birth due to a lack of protection by the abnormal eyelids

abnormal eyelid development ( J:84743 )

• mutant embryos show no formation of eyelid protrusive tips at E14.5

• no extension of the upper or lower eyelids is observed at E15.5

failure of eyelid fusion ( J:84743 )

• although rudimentary eyelid tips may be observed at E16.5, they extend only slightly and do not cover the entire cornea even by E19.5

microphthalmia ( J:84743 )

• the eyes of adult mutant mice are often smaller than normal

eyelids open at birth ( J:84743 )

• mutant mice are born with a wide oval gap between the eyelids due to a failure of eyelid epithelial migration around E15

eye opacity ( J:84743 )

• the eyes of adult mutant mice are often opaque

homeostasis/metabolism

delayed wound healing ( J:84743 )

• whereas wild-type full-thickness skin wounds typically require 11 days for full closure, those in mutant mice are fully closed after 14 days due to impaired reepithelialization

impaired wound healing ( J:84743 )

• at 4 days after cutaneous wounding, the mutant leading edge epidermis is clearly malformed and fails to migrate or invade into the fibrin clot properly, despite normal keratinocyte proliferation

• impaired reepithelialization is associated with decreased expression levels of keratin-6 and PTK2 protein tyrosine kinase 2 (FAK), and a large reduction in activation of the EGF receptor at the leading edge of mutant wounds

immune system

increased incidence of corneal inflammation ( J:84743 )

• mutant mice develop severe corneal inflammation shortly after birth due to a lack of protection by the abnormal eyelids

integument

abnormal keratinocyte morphology ( J:84743 )

• in an in vitro scratch assay, mutant keratinocytes appear less elongated and show a striking fragmentation of actin stress fibers at the leading edge of the wound, unlike wild-type cells where stress fibers accumulate in the anterior lamellipodia towards the wound

abnormal keratinocyte physiology ( J:84743 )

• in vitro, mutant keratinocytes cultured in the presence of mitomycin C fail to migrate or elongate properly at the border of scratch assays, unlike wild-type keratinocytes which migrate into the gap in an EGF-dependent manner and achieve wound closure within 14 hrs

• in an in vitro scratch assay, mutant keratinocytes show no EGF receptor activation and display significantly less focal adhesions than wild-type keratinocytes at the front of leading edge cells

• addition of HB-EGF (an EGF ligand) into the mutant cell growth medium rescues the keratinocyte migration defect and induces phosphorylation of EGF receptor

decreased keratinocyte proliferation ( J:84743 )

• in culture, primary keratinocytes isolated from newborn mutant mice display significantly reduced EGF-induced proliferation relative to wild-type controls

cellular

decreased keratinocyte proliferation ( J:84743 )

• in culture, primary keratinocytes isolated from newborn mutant mice display significantly reduced EGF-induced proliferation relative to wild-type controls

Allelic Composition	Grhl3^tm1Jane/Grhl3^tm3.1Jane Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129S1/Sv * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Grhl3^tm1Jane mutation (1 available); any Grhl3 mutation (53 available)
Grhl3^tm3.1Jane mutation (1 available); any Grhl3 mutation (53 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

integument

integument phenotype ( J:178952 , J:233531 )

N	• from E18.5 through 8 weeks, mice exhibit normal skin barrier formation (J:178952) • no overt skin barrier defect or abnormality of the cornified envelope of the stratum corneum from birth to 6 weeks of age (J:233531)

epidermal hyperplasia ( J:178952 )

• in aged mice

increased skin papilloma incidence ( J:178952 )

• spontaneously in aged mice affecting the snout and neck

• in 4 weeks after DMBA/TPA treatment

increased skin squamous cell carcinoma incidence ( J:178952 )

• spontaneously in aged mice affecting the snout and neck

• in 4 weeks after DMBA/TPA treatment

neoplasm

increased incidence of tumors by chemical induction ( J:178952 )

• 4 weeks after DMBA/TPA treatment, mice develop skin papillomas many which progress to squamous cell carcinomas unlike control mice

increased skin papilloma incidence ( J:178952 )

• spontaneously in aged mice affecting the snout and neck

• in 4 weeks after DMBA/TPA treatment

increased skin squamous cell carcinoma incidence ( J:178952 )

• spontaneously in aged mice affecting the snout and neck

• in 4 weeks after DMBA/TPA treatment

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:178952 )

• 4 weeks after DMBA/TPA treatment, mice develop skin papillomas many which progress to squamous cell carcinomas unlike control mice

Allelic Composition	Grhl1^tm1Jane/Grhl1^tm1Jane Grhl3^tm1Jane/Grhl3^tm3.1Jane Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129S1/Sv * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Grhl1^tm1Jane mutation (1 available); any Grhl1 mutation (33 available)
Grhl3^tm1Jane mutation (1 available); any Grhl3 mutation (53 available)
Grhl3^tm3.1Jane mutation (1 available); any Grhl3 mutation (53 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

mortality/aging

postnatal lethality, complete penetrance ( J:233531 )

• present in expected numbers at E18.5 but all died by P3 with most lost during the first 48 hours after birth

integument

impaired skin barrier function ( J:233531 )

• at P2 excessive fluid loss and regression of skin barrier function leads to dehydration and death

abnormal corneocyte envelope morphology ( J:233531 )

• loss of cornified envelope integrity by P2

homeostasis/metabolism

impaired skin barrier function ( J:233531 )

• at P2 excessive fluid loss and regression of skin barrier function leads to dehydration and death

Allelic Composition	Grhl3^tm1Jane/Grhl3^tm3.1Jane Tgm5^{tm2a(KOMP)Wtsi}/Tgm5^{tm2a(KOMP)Wtsi} Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129S1/Sv * C57BL/6N * FVB/N

Find Mice

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

mortality/aging

mortality/aging ( J:233531 )

N	• present in expected numbers at E18.5 and 6 weeks of age

integument

integument phenotype ( J:233531 )

N	• no evidence of skin barrier dysfunction was seen

Allelic Composition	Rb1^tm3Tyj/Rb1^tm3Tyj Tg(KRT14-cre)8Brn/0 Tg(KRT14-HPV16E7)2304Plam/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * FVB

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1^tm3Tyj mutation (10 available); any Rb1 mutation (106 available)
Tg(KRT14-cre)8Brn mutation (4 available)
Tg(KRT14-HPV16E7)2304Plam mutation (1 available)

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

integument

abnormal epidermis stratum granulosum morphology ( J:101623 )

• thickness of the granular layer is increased to a greater extent than in conditional RB1 mice that lack Tg(KRT14-HPV16E7)2304Plam

abnormal epidermis suprabasal layer morphology ( J:101623 )

• thickness of the spinous suprabasal layer is increased

epidermal hyperplasia ( J:101623 )

• epidermal hyperplasia is increased compared to conditional RB1 mice that lack Tg(KRT14-HPV16E7)2304Plam

Allelic Composition	Rb1^tm3Tyj/Rb1^tm3Tyj Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * FVB

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1^tm3Tyj mutation (10 available); any Rb1 mutation (106 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

integument

abnormal epidermis stratum granulosum morphology ( J:101623 )

• thickness of the granular layer is increased

abnormal epidermis suprabasal layer morphology ( J:101623 )

• thickness of the spinous suprabasal layer is increased

epidermal hyperplasia ( J:101623 )

Allelic Composition	Trp53^tm3Tyj/Trp53⁺ Tg(KRT14-cre)8Brn/?
Genetic Background	involves: 129S4/SvJae * FVB/N * SKH1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53^tm3Tyj mutation (3 available); any Trp53 mutation (232 available)

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

neoplasm

increased skin tumor incidence ( J:121734 )

• skin tumors develop between 500 and 600 days

• UVB exposure results in 6.5+/-1.4 tumors at day 100 compared to 0.6+/-0.2 in wild-type mice

increased hemangioma incidence ( J:121734 )

• one mouse developed a hemangiosarcoma in the intestine

increased lymphoma incidence ( J:121734 )

• developed in one mouse

cellular

decreased cellular sensitivity to ultraviolet irradiation ( J:121734 )

• fewer CASP3+ cells area found following UVB treatment when compared to wild-type mice

• the reduction in apoptotic cells is slightly greater in homozygotes than in heterozygotes

integument

increased skin tumor incidence ( J:121734 )

• skin tumors develop between 500 and 600 days

• UVB exposure results in 6.5+/-1.4 tumors at day 100 compared to 0.6+/-0.2 in wild-type mice

Allelic Composition	Trp63^tm1Elrf/Trp63^tm1Elrf Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NCr * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-cre)8Brn mutation (4 available)
Trp63^tm1Elrf mutation (1 available); any Trp63 mutation (60 available)

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

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:151638 )

N	• mice exhibit normal wound healing

integument

integument phenotype ( J:151638 )

N	• under normal conditions, mice have normal skin • colony formation capabilities and proliferation of epidermal cells are normal

Allelic Composition	Apc^tm2Rak/Apc^tm2Rak Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129/Sv * C57BL/6J * FVB/N * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apc^tm2Rak mutation (1 available); any Apc mutation (154 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

Stunted growth, short whiskers, sparse hair coat and abnormal tooth development in the Apc^tm2Rak/Apc^tm2Rak Tg(KRT14-cre)8Brn/0 mouse

mortality/aging

postnatal lethality, complete penetrance ( J:114152 )

• some pups have died by P8-10 and none survive to weaning; time of death is variable with some dying within 1-2 days of birth, while some survive almost to weaning

growth/size/body

absent upper incisors ( J:114152 )

• maxillary incisors are often absent or underdeveloped

abnormal tooth development ( J:114152 )

• initiation of ectopic tooth buds is evident by E15.5

absent teeth ( J:114152 )

• at time of death, animals are toothless

increased forehead pigmentation ( J:114152 )

• at E17.5-18.5 mutants display a patch of dark pigmentation on the forehead

abnormal ear shape ( J:114152 )

• external ears or pinnae are shriveled in appearance

increased ear pigmentation ( J:114152 )

• external ears or pinnae are pigmented compared to littermates

decreased body size ( J:114152 )

• by P8-10, mutant pups are considerably smaller than wild-type

weight loss ( J:114152 )

• mutants start to lose weight from P10 onwards

cellular

abnormal keratinocyte differentiation ( J:114152 )

• mutants show aberrant proliferation and differentiation of keratinocytes leading to massive squamous metaplasia, rather than forming medullary or cortical thymic epithelial cells

abnormal cell proliferation ( J:114152 )

• in skin, proliferating cells are observed in cells in bulbs at base of hair cells and in bulb-like structures budding from outer root sheaths of existing hair follicles

behavior/neurological

lethargy ( J:114152 )

• by P16-17, mice are lethargic

craniofacial

absent upper incisors ( J:114152 )

• maxillary incisors are often absent or underdeveloped

abnormal tooth development ( J:114152 )

• initiation of ectopic tooth buds is evident by E15.5

absent teeth ( J:114152 )

• at time of death, animals are toothless

increased forehead pigmentation ( J:114152 )

• at E17.5-18.5 mutants display a patch of dark pigmentation on the forehead

abnormal ear shape ( J:114152 )

• external ears or pinnae are shriveled in appearance

increased ear pigmentation ( J:114152 )

• external ears or pinnae are pigmented compared to littermates

endocrine/exocrine glands

salivary gland epithelial hyperplasia ( J:114152 )

• hyperplasia in salivary gland squamous epithelium is observed

abnormal thymus morphology ( J:114152 )

• at P12-17, thymi frequently contain black deposits within the tissue

• in more severely affected mutants, by P3, distinct thymic epithelial compartments are lost as well as most lymphocytes

• at P10-13, thymus consists of numerous enlarged Hassall's corpuscle-like structures surrounding large keratin deposits, and show large numbers of infiltrating neutrophils and macrophages in response to keratins

abnormal Hassall's corpuscle morphology ( J:114152 )

• numerous enlarged Hassall's corpuscle-like structures surrounding large keratin deposits

small thymus ( J:114152 )

• thymi are inconspicuous and small for pups' age; this is evident by P3

decreased thymocyte number ( J:114152 )

• no thymocytes are detectable at P10-13

Harderian gland hyperplasia ( J:114152 )

• hyperplasia in squamous epithelium is observed

digestive/alimentary system

salivary gland epithelial hyperplasia ( J:114152 )

• hyperplasia in salivary gland squamous epithelium is observed

small stomach ( J:114152 )

• stomach is small at time of death, and contains no solid food

pigmentation

abnormal skin pigmentation ( J:114152 )

• at E17.5-18.5 mutants display patch of dark pigmentation on forehead and a dark median line running caudally from head to tail

increased forehead pigmentation ( J:114152 )

• at E17.5-18.5 mutants display a patch of dark pigmentation on the forehead

increased ear pigmentation ( J:114152 )

• external ears or pinnae are pigmented compared to littermates

hematopoietic system

abnormal thymus morphology ( J:114152 )

• at P12-17, thymi frequently contain black deposits within the tissue

• in more severely affected mutants, by P3, distinct thymic epithelial compartments are lost as well as most lymphocytes

abnormal Hassall's corpuscle morphology ( J:114152 )

• numerous enlarged Hassall's corpuscle-like structures surrounding large keratin deposits

small thymus ( J:114152 )

• thymi are inconspicuous and small for pups' age; this is evident by P3

decreased thymocyte number ( J:114152 )

• no thymocytes are detectable at P10-13

immune system

abnormal thymus morphology ( J:114152 )

• at P12-17, thymi frequently contain black deposits within the tissue

• in more severely affected mutants, by P3, distinct thymic epithelial compartments are lost as well as most lymphocytes

abnormal Hassall's corpuscle morphology ( J:114152 )

• numerous enlarged Hassall's corpuscle-like structures surrounding large keratin deposits

small thymus ( J:114152 )

• thymi are inconspicuous and small for pups' age; this is evident by P3

decreased thymocyte number ( J:114152 )

• no thymocytes are detectable at P10-13

skeleton

absent upper incisors ( J:114152 )

• maxillary incisors are often absent or underdeveloped

abnormal tooth development ( J:114152 )

• initiation of ectopic tooth buds is evident by E15.5

absent teeth ( J:114152 )

• at time of death, animals are toothless

vision/eye

cornea epithelium hyperplasia ( J:114152 )

• hyperplasia in squamous epithelium of cornea occurs

blepharoptosis ( J:114152 )

• by P17, animals hardly keep eyes open

hearing/vestibular/ear

abnormal ear shape ( J:114152 )

• external ears or pinnae are shriveled in appearance

increased ear pigmentation ( J:114152 )

• external ears or pinnae are pigmented compared to littermates

integument

abnormal keratinocyte differentiation ( J:114152 )

• mutants show aberrant proliferation and differentiation of keratinocytes leading to massive squamous metaplasia, rather than forming medullary or cortical thymic epithelial cells

delayed hair appearance ( J:114152 )

• at ~P8, mutants are hairless while normal littermates have a smooth thin coat

short hair ( J:114152 )

• around P10-12, mice display short, shaggy coats

abnormal hair follicle morphology ( J:114152 )

• at P3, follicles are often irregularly spaced and seen as disoriented and clamped invaginations that become more noticeable at P12

• clusters of dysplastic follicular structures are frequently observed throughout the epidermis, while other regions display gaps with no follicles

abnormal hair follicle bulb morphology ( J:114152 )

• bulbs are often bent and irregularly angled to one another, with variable size and location

abnormal hair follicle development ( J:114152 )

• ectopic hair follicle morphogenesis is observed in epithelium of cornea, oral, salivary, and Harderian glands

underdeveloped hair follicles ( J:114152 )

• at P12, some hair follicles are not properly formed or shorter than normal

abnormal hair follicle orientation ( J:114152 )

short vibrissae ( J:114152 )

• around P10-12, mutants display short and misshapen vibrissae

scaly skin ( J:114152 )

• ridged skin regions look scaly

skin ridges ( J:114152 )

• at P17, development of thick ridges in the skin around the ears, eyelids, forehead, nose and paws becomes noticeable

wrinkled skin ( J:114152 )

• mutants have wrinkled skin at P8

abnormal skin pigmentation ( J:114152 )

• at E17.5-18.5 mutants display patch of dark pigmentation on forehead and a dark median line running caudally from head to tail

increased forehead pigmentation ( J:114152 )

• at E17.5-18.5 mutants display a patch of dark pigmentation on the forehead

increased ear pigmentation ( J:114152 )

• external ears or pinnae are pigmented compared to littermates

Allelic Composition	Ptch1^tm1Bjw/Ptch1^tm1Bjw Tg(KRT14-cre)8Brn/0
Genetic Background	involves: 129T2/SvEms * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptch1^tm1Bjw mutation (2 available); any Ptch1 mutation (115 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

endocrine/exocrine glands

thymus hypoplasia ( J:231264 )

growth/size/body

postnatal growth retardation ( J:231264 )

• severe growth deficiency such that mice do not progress beyond 49% of control weight, with differences first seen around P19

hematopoietic system

thymus hypoplasia ( J:231264 )

homeostasis/metabolism

decreased circulating insulin-like growth factor I level ( J:231264 )

• serum Igf1 levels are reduced

• however, serum growth hormone levels are normal

immune system

thymus hypoplasia ( J:231264 )

integument

skin lesions ( J:231264 )

• hyperproliferative lesions first develop in the skin around P19

increased basal cell carcinoma incidence ( J:231264 )

• mice show rapid development basal cell carcinoma

neoplasm

increased basal cell carcinoma incidence ( J:231264 )

• mice show rapid development basal cell carcinoma

reproductive system

infertility ( J:231264 )

• mice do not breed successfully

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
basal cell carcinoma		DOID:2513		J:231264

Allelic Composition	Rala^tm1.2Cjm/Rala^tm1.2Cjm Tg(KRT14-cre)8Brn/0
Genetic Background	involves: C57BL/6 * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rala^tm1.2Cjm mutation (2 available); any Rala mutation (26 available)
Tg(KRT14-cre)8Brn mutation (4 available)

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

neoplasm

neoplasm ( J:199742 )

N	• DMBA-TPA-treated mice exhibit normal tumor formation

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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