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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(KRT14-Snai1)1Efu
transgene insertion 1, Elaine Fuchs
MGI:3774670
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Krt14tm1.1(cre)Wbm/Krt14+
Tg(KRT14-Snai1)1Efu/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * CD-1 MGI:6196149
tg2
Tg(KRT14-Snai1)1Efu/0 involves: CD-1 MGI:3774672


Genotype
MGI:6196149
cn1
Allelic
Composition
Krt14tm1.1(cre)Wbm/Krt14+
Tg(KRT14-Snai1)1Efu/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krt14tm1.1(cre)Wbm mutation (1 available); any Krt14 mutation (36 available)
Tg(KRT14-Snai1)1Efu mutation (0 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• sebaceous gland carcinoma

integument
• mice develop skin tumors more rapidly than single Tg(KRT14-Snai1)1Efu expressing mice, with a median latency of 176 days
• however, mice do not develop more tumors than Tg(KRT14-Snai1)1Efu mice alone
• tumors include basal cell carcinoma, squamous cell carcinoma, and sebaceous gland carcinoma and more aggressive carcinosarcomas characterized by the biphasic appearance of intermixed epithelial and mesenchymal elements

neoplasm
• sebaceous gland carcinoma
• mice develop skin tumors more rapidly than single Tg(KRT14-Snai1)1Efu expressing mice, with a median latency of 176 days
• however, mice do not develop more tumors than Tg(KRT14-Snai1)1Efu mice alone
• tumors include basal cell carcinoma, squamous cell carcinoma, and sebaceous gland carcinoma and more aggressive carcinosarcomas characterized by the biphasic appearance of intermixed epithelial and mesenchymal elements




Genotype
MGI:3774672
tg2
Allelic
Composition
Tg(KRT14-Snai1)1Efu/0
Genetic
Background
involves: CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype

Tg(KRT14-Snai1)1Efu/0 mice are small, have short tails and flaky skin, and exhibit epidermal hyperproliferation

cellular
• keratinocytes are more resistant to chemotoxic stress
• keratinocytes form more and larger colonies than wild-type cells
• treatment of isolated keratinocytes from newborns with 2,4-dimethoxybenzaldehyde (DMBA) results in enhanced proliferation and a survival advantage
• isolated keratinocytes treated with the chemotherapeutic drug doxorubicin show a survival advantage

growth/size/body
• progressively poor health

endocrine/exocrine glands
• sebaceous gland cells are hyperproliferative and lack terminal differentiation
• in adults, the Mts24+progenitor population that gives rise to the sebaceous gland cells is expanded
• clonogenic potential of Mts24+ progenitor cells is enhanced
• sebaceous gland cells start to accumulate and several glands per hair follicle are formed, with this disorganization becoming worse over time and leading to sebaceous gland hyperplasia and carcinoma
• 40% incidence of sebaceous gland carcinoma
• sebaceous gland carcinoma is often mixed with squamous cell carcinoma implying an early progenitor population that becomes transformed but still retains some differentiation characteristics

behavior/neurological
• reduction in food intake

neoplasm
• 40% incidence of sebaceous gland carcinoma
• sebaceous gland carcinoma is often mixed with squamous cell carcinoma implying an early progenitor population that becomes transformed but still retains some differentiation characteristics
• mice start to develop spontaneous skin tumors at 5 months of age, with a median latency of 282 days
• tumors include basal cell carcinoma, squamous cell carcinoma, sebaceous gland carcinoma, and mixed tumors (40%)
• 6.67% incidence of basal cell carcinoma
• 13.33% incidence of squamous cell carcinoma
• sebaceous gland carcinomas are highly metastatic, with draining lymph nodes of 59% of mice with sebaceous gland carcinomas containing carcinoma cells with sebaceous differentiation
• mice show lung metastasis displaying features of terminal skin differentiation in mice with squamous cell carcinoma

limbs/digits/tail

integument
• keratinocytes form more and larger colonies than wild-type cells
• treatment of isolated keratinocytes from newborns with 2,4-dimethoxybenzaldehyde (DMBA) results in enhanced proliferation and a survival advantage
• isolated keratinocytes treated with the chemotherapeutic drug doxorubicin show a survival advantage
• sebaceous gland cells are hyperproliferative and lack terminal differentiation
• in adults, the Mts24+progenitor population that gives rise to the sebaceous gland cells is expanded
• clonogenic potential of Mts24+ progenitor cells is enhanced
• sebaceous gland cells start to accumulate and several glands per hair follicle are formed, with this disorganization becoming worse over time and leading to sebaceous gland hyperplasia and carcinoma
• epidermis is hyperproliferative and exhibits differentiation defects
• with age, epidermal folds and undulations develop in the epithelium
• adults exhibit alteration of the basement membrane that separates the epidermis from the dermis
• mice start to develop spontaneous skin tumors at 5 months of age, with a median latency of 282 days
• tumors include basal cell carcinoma, squamous cell carcinoma, sebaceous gland carcinoma, and mixed tumors (40%)
• 6.67% incidence of basal cell carcinoma
• 13.33% incidence of squamous cell carcinoma

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
skin cancer DOID:4159 J:229072





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory