Overview

Also Known As:C3(1)-TAg , C3(1)/Tag

Stock No. 013591: The C3(1)-TAg transgenic strain is a model for the study of multistage oncogenesis in the prostate and mammary glands.

Of note, a subline was identified with transgene rearrangement/deletion to only one copy (or a partial copy) in the original chromosome 6 locus - resulting in retained tolerance to SV40 TAg but no spontaneous cancer phenotype. The new subline, called C3(1)/TAg-REAR, is available as Stock No. 030386.

Donating Investigator

Jeffrey E Green, National Cancer Institute, National Institutes of Health (NIH/NCI)

Cryopreservation Cryopreservation, TJL

Genetic overview

Genetic Background	Generation
	?+pN2F5 (2020-01-10 00:00:00)

Tg(C3-1-TAg)cJeg

Allele Type
Transgenic (Inserted expressed sequence)

View Genetics

Research Applications

Research Tools
Cancer Research
Reproductive Biology Research

View All Research Applications

Base Price

Starting at:

$255.00 Domestic price for female 4-week

333.51 Domestic price for breeder pair

View Price List

Details

Detailed Description

The C3(1)/TAg founder line C originally contained ~six transgene copies at a single locus in the telomeric portion of chromosome 6 (which contains the Ki-ras proto-oncogene) - resulting in multistage oncogenesis in prostate and mammary gland. The published details are described in detail below.

Male hemizygous transgenic mice develop prostatic hyperplasia in early life that progresses to adenoma or adenocarcinoma in about half of the animals which survive longer 7 months of age. Some transgenic male hemizygotes develop adenocarcinomas of the urethral/periurethral and bulbourethral glands (10-20% of hemizygous males) and submandibular gland (10% of hemizygous males 8 months of age). In female transgenic mice, the transgene is expressed primarily in the distal mammary ductal
epithelium and terminal ductal lobular unit. Female hemizygous animals generally develop mammary intraepithelial neoplasia with similarities to DCIS by 3 months of age with subsequent development of mammary adenocarcinoma by 6 months of age in 100% of the animals. About 10-15% of hemizygous female mice develop lung metastases. Direct invasion of adjacent lymph nodes, skeletal muscle, salivary glands and tissues as well as mammary tumor metastases in liver, adrenal and heart have also been observed. Bone, brain and regional lymph node metastases have not been observed. Tumors of the sweat glands have been observed in both male and female transgenic animals. The phenotype for this transgene has been most extensively studied in the FVB/N background. While homozygotes are viable and fertile, pups born to homozygous mothers need foster mothers because of lactation difficulties.

Of note, in 2016, 6-7 week old mice from this Jackson Laboratory colony were observed to display gait abnormalities. While the expected phenotype of this transgenic line might conceivably lead to gait abnormalities, the expected pathology in the eccrine sweat glands of the foot pads seems not to be the cause. Histologic analysis indicates that these mice have significant changes in the cartilage of the stifle and hip joints, with variable pathology that is sometimes severe. Cartilage is severely thickened and hyperplastic, with multifocal acellular regions and multifocal cartilage necrosis and loss.
Further, routine screening of the donating investigator’s C3(1)/TAg founder line C colony identified female transgenic mice that retained tolerance to SV40 TAg but did not develop the expected phenotype (mammary tumors) - a result of transgene rearrangement/deletion to only one copy (or a partial copy) in the original chromosome 6 locus. The newer subline, called C3(1)/TAg-REAR, is available as Stock No. 030386.

Development

A transgenic construct containing the simian virus 40 early-region transforming sequences under the regulatory control of the rat prostatic steroid binding protein C3(1) gene was microinjected into FVB/N fertilized oocytes. Founder line c was subsequently established. Upon arrival at The Jackson Laboratory, the mice were crossed to FVB/NJ (Stock No. 001800) at least once to establish the colony.

Expression Data

Expressed Gene	TAg, SV40 large T-antigen, SV40
Site of Expression

Control Suggestions

Noncarrier

Approximate Controls

001800 FVB/NJ

Additional Information

Considerations for Choosing Controls

Selected References

Maroulakou IG; Anver M; Garrett L; Green JE. 1994. Prostate and mammary adenocarcinoma in transgenic mice carrying a rat C3(1) simian virus 40 large tumor antigen fusion gene. Proc Natl Acad Sci U S A 91(23):11236-40PubMed: 7972041 MGI: J:52786

View All References

Genetics

Tg(C3-1-TAg)cJeg

Allele Symbol: Tg(C3-1-TAg)cJeg

Allele Name	transgene insertion c, Jeffrey E Green
Allele Type	Transgenic (Inserted expressed sequence)
Allele Synonym(s)	C3(1)/SV40; C3(1)/SV40T; C3(1)/T antigen (Tag); C3(1)/T(AG); C3(1)/TAg; C3(1)-SV40 T antigen; C3(1)-Tag; C3Tag; C3-TAg; Large T; Tg(Scgb2a2-TAg)cJeg
Gene Symbol and Name	Tg(C3-1-TAg)cJeg, transgene insertion c, Jeffrey E Green
Gene Synonym(s)
Promoter	C3(1), C3(1), rat
Expressed Gene	TAg, SV40 large T-antigen, SV40
Strain of Origin	FVB/N
Chromosome	UN
Molecular Note	This transgene contains the rat prostatic binding protein C3 promoter (Pbpc3) and the wild-type allele of the SV40 large tumor antigen (TAg) gene. Founder c carried 6 copies of the transgene. Founders f, g, i, j, k, and l were also generated. Two transgenic lines (c and l) were produced.
Mutations Made By	Jeffrey Green, National Cancer Institute, National Institutes of Health (NIH/NCI)

Disease/Phenotype

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Research Tools
- Cancer Research
  - tumor immunology
Cancer Research
- Increased Tumor Incidence
  - Prostate Tumors
  - Gonadal Tumors
  - Mammary Gland Tumors
- Other
  - tumor metastasis
Reproductive Biology Research
- Gonadal Tumors
- Prostate Tumors

Mammalian Phenotype Terms by Genotype

The following phenotype relates to a compound genotype created using this strain

Genotype: Tg(C3-1-TAg)cJeg/0
FVB/N-Tg(C3-1-TAg)cJeg

endocrine/exocrine gland phenotype

increased prostate gland tumor incidence

increased prostate intraepithelial neoplasia incidence
- PIN is higher in the ventral lobe compared to in the dorsal lobe
- mice develop prostate intraepithelial neoplasia (PIN) unlike wild-type mice

neoplasm

increased prostate gland tumor incidence

increased prostate intraepithelial neoplasia incidence
- mice develop prostate intraepithelial neoplasia (PIN) unlike wild-type mice
- PIN is higher in the ventral lobe compared to in the dorsal lobe

reproductive system phenotype

increased prostate gland tumor incidence

increased prostate intraepithelial neoplasia incidence
- PIN is higher in the ventral lobe compared to in the dorsal lobe
- mice develop prostate intraepithelial neoplasia (PIN) unlike wild-type mice

Genotype: Tg(C3-1-TAg)cJeg/0
involves: FVB/N

integument phenotype

mammary gland alveolar hyperplasia
- acini lesions resemble hyperplastic alveolar nodules
- 2/3 of females develop atypical hyperplasia in the ducts and acini of mammary glands by 3 months of age

increased mammary adenocarcinoma incidence
- by 6 months of age female mice develop multiple mammary ductular adenocarcinomas unlike in wild-type mice
- adenocarcinomas are classified as Dunn type B tumors nonporous females typically develop mammary adenocarcinoma at about 4 months of age while females that become pregnant show accelerated adenocarcinoma development
- adenocarcinoma cells exhibit increased rates of apoptosis compared to cells in wild-type mice
- adenocarcinomas are classified as Dunn type B tumors
- at 6 months, 10% of female mice exhibit lung metastasis

mammary gland hyperplasia
- at 2 months of age, female mice exhibit atypical ductal hyperplasias unlike in wild-type mice
- hyperplastic cells exhibit increased rates of apoptosis compared to cells in wild-type mice

mammary gland duct hyperplasia
- 2/3 of females develop atypical hyperplasia in the ducts and acini of mammary glands by 3 months of age

mortality/aging

premature death
- survival of males is longer than females, with 50% survival at around 4 months of age for females and 8 months of age for males
- all females die by 5-6 months of age, while all males die by 11 months of age

neoplasm

increased bulbourethral gland adenocarcinoma incidence
- at 7 months, 10% to 20% male mice develop adenocarcinomas of the bulbourethral glands unlike in wild-type mice

increased mammary adenocarcinoma incidence
- adenocarcinoma cells exhibit increased rates of apoptosis compared to cells in wild-type mice
- at 6 months, 10% of female mice exhibit lung metastasis
- adenocarcinomas are classified as Dunn type B tumors
- by 6 months of age female mice develop multiple mammary ductular adenocarcinomas unlike in wild-type mice
- adenocarcinomas are classified as Dunn type B tumors nonporous females typically develop mammary adenocarcinoma at about 4 months of age while females that become pregnant show accelerated adenocarcinoma development

increased prostate gland adenocarcinoma incidence
- at 7 months of age, 19% of mice exhibit carcinomas in the ventral lobe and 3% in the dorsolateral lobe unlike in wild-type mice
- at 7 months in the ventral prostate and 11 months in the dorsolateral prostate
- Normal - however, no metastasis is observed
- the number of apoptotic cells in the prostate is greater than in wild-type mice
- after 8 months, 40% of mice exhibit carcinomas in the ventral lobe and 13% in the dorsolateral lobe unlike in wild-type mice

increased prostate intraepithelial neoplasia incidence
- low-grade PIN is observed in 83% and 100% of the ventral prostate at 2 to 3 months and 4 to 12 months, respectively, unlike wild-type mice
- at 5 months, high-grade PIN is observed in both lobes unlike in wild-type mice
- at 5 months, ventral and dorsolateral lobes exhibit high grade PIN unlike in wild-type mice
- high-grade PIN is observed on 88% and 100% of mice at 5 to 8 months and more than 8 months, respectively, unlike in wild-type mice
- the number of apoptotic cells in the prostate is greater than in wild-type mice
- numbers of PIN lesions increase with age in the ventral and dorsolateral lobes unlike wild-type mice
- PIN lesions increase with age
- at 2 to 3 months, low-grade prostate intraepithelial neoplasia (PIN) is observed in the ventral and dorsolateral prostates unlike in wild-type mice
- at 5 to 6 months, mice develop low to high grade prostate intraepithelial neoplasia (PIN) unlike wild-type mice

increased urethral gland adenocarcinoma incidence
- at 7 months, 10% to 20% male mice develop adenocarcinomas of the urethral glands unlike in wild-type mice

increased tumor incidence
- some mice exhibit mixed tumors of the sweat glands and occasional nasal proliferative or neoplastic lesions develop from the nasal turbinate epithelium unlike in wild-type mice

endocrine/exocrine gland phenotype

increased mammary adenocarcinoma incidence
- at 6 months, 10% of female mice exhibit lung metastasis
- adenocarcinomas are classified as Dunn type B tumors nonporous females typically develop mammary adenocarcinoma at about 4 months of age while females that become pregnant show accelerated adenocarcinoma development
- by 6 months of age female mice develop multiple mammary ductular adenocarcinomas unlike in wild-type mice
- adenocarcinomas are classified as Dunn type B tumors
- adenocarcinoma cells exhibit increased rates of apoptosis compared to cells in wild-type mice

increased prostate intraepithelial neoplasia incidence
- at 5 months, high-grade PIN is observed in both lobes unlike in wild-type mice
- the number of apoptotic cells in the prostate is greater than in wild-type mice
- low-grade PIN is observed in 83% and 100% of the ventral prostate at 2 to 3 months and 4 to 12 months, respectively, unlike wild-type mice
- numbers of PIN lesions increase with age in the ventral and dorsolateral lobes unlike wild-type mice
- PIN lesions increase with age
- at 2 to 3 months, low-grade prostate intraepithelial neoplasia (PIN) is observed in the ventral and dorsolateral prostates unlike in wild-type mice
- at 5 to 6 months, mice develop low to high grade prostate intraepithelial neoplasia (PIN) unlike wild-type mice
- high-grade PIN is observed on 88% and 100% of mice at 5 to 8 months and more than 8 months, respectively, unlike in wild-type mice
- at 5 months, ventral and dorsolateral lobes exhibit high grade PIN unlike in wild-type mice

increased prostate gland adenocarcinoma incidence
- at 7 months of age, 19% of mice exhibit carcinomas in the ventral lobe and 3% in the dorsolateral lobe unlike in wild-type mice
- at 7 months in the ventral prostate and 11 months in the dorsolateral prostate
- Normal - however, no metastasis is observed
- after 8 months, 40% of mice exhibit carcinomas in the ventral lobe and 13% in the dorsolateral lobe unlike in wild-type mice
- the number of apoptotic cells in the prostate is greater than in wild-type mice

mammary gland alveolar hyperplasia
- acini lesions resemble hyperplastic alveolar nodules
- 2/3 of females develop atypical hyperplasia in the ducts and acini of mammary glands by 3 months of age

increased bulbourethral gland adenocarcinoma incidence
- at 7 months, 10% to 20% male mice develop adenocarcinomas of the bulbourethral glands unlike in wild-type mice

mammary gland hyperplasia
- at 2 months of age, female mice exhibit atypical ductal hyperplasias unlike in wild-type mice
- hyperplastic cells exhibit increased rates of apoptosis compared to cells in wild-type mice

prostate gland epithelial hyperplasia
- hyperplastic changes in the epithelium of the dorsal/ventral regions of the prostate are seen as early as 3 months of age

abnormal prostate gland physiology
- prostate cells exhibit increased proliferation and apoptosis rates compared to in wild-type mice according to their degree of prostate intraepithelial neoplasia

mammary gland duct hyperplasia
- 2/3 of females develop atypical hyperplasia in the ducts and acini of mammary glands by 3 months of age

renal/urinary system phenotype

increased bulbourethral gland adenocarcinoma incidence
- at 7 months, 10% to 20% male mice develop adenocarcinomas of the bulbourethral glands unlike in wild-type mice

increased urethral gland adenocarcinoma incidence
- at 7 months, 10% to 20% male mice develop adenocarcinomas of the urethral glands unlike in wild-type mice

reproductive system phenotype

prostate gland epithelial hyperplasia
- hyperplastic changes in the epithelium of the dorsal/ventral regions of the prostate are seen as early as 3 months of age

increased prostate intraepithelial neoplasia incidence
- numbers of PIN lesions increase with age in the ventral and dorsolateral lobes unlike wild-type mice
- at 5 to 6 months, mice develop low to high grade prostate intraepithelial neoplasia (PIN) unlike wild-type mice
- the number of apoptotic cells in the prostate is greater than in wild-type mice
- at 2 to 3 months, low-grade prostate intraepithelial neoplasia (PIN) is observed in the ventral and dorsolateral prostates unlike in wild-type mice
- at 5 months, high-grade PIN is observed in both lobes unlike in wild-type mice
- at 5 months, ventral and dorsolateral lobes exhibit high grade PIN unlike in wild-type mice
- high-grade PIN is observed on 88% and 100% of mice at 5 to 8 months and more than 8 months, respectively, unlike in wild-type mice
- low-grade PIN is observed in 83% and 100% of the ventral prostate at 2 to 3 months and 4 to 12 months, respectively, unlike wild-type mice
- PIN lesions increase with age

increased prostate gland adenocarcinoma incidence
- at 7 months in the ventral prostate and 11 months in the dorsolateral prostate
- at 7 months of age, 19% of mice exhibit carcinomas in the ventral lobe and 3% in the dorsolateral lobe unlike in wild-type mice
- Normal - however, no metastasis is observed
- the number of apoptotic cells in the prostate is greater than in wild-type mice
- after 8 months, 40% of mice exhibit carcinomas in the ventral lobe and 13% in the dorsolateral lobe unlike in wild-type mice

abnormal prostate gland physiology
- prostate cells exhibit increased proliferation and apoptosis rates compared to in wild-type mice according to their degree of prostate intraepithelial neoplasia

References

Maroulakou IG; Anver M; Garrett L; Green JE. 1994. Prostate and mammary adenocarcinoma in transgenic mice carrying a rat C3(1) simian virus 40 large tumor antigen fusion gene. Proc Natl Acad Sci U S A 91(23):11236-40PubMed: 7972041 MGI: J:52786

Additional - Tg(C3-1-TAg)cJeg related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Probe:Generic SV40 TAg 1 Probe
- QPCR:Generic SV40 TAg 1
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, transgene carrier mice may be bred with wildtype mice from the colony or with FVB/NJ (Stock No. 001800) mice. While homozygotes are viable and fertile, pups born to homozgyous mothers need foster mothers because of lactation difficulties. Female hemizygous animals generally develop mammary intraepithelial neoplasia with similarities to DCIS by 3 months of age with subsequent development of mammary adenocarcinoma by 6 months of age in 100% of the animals. Male hemizygous transgenic mice develop prostatic hyperplasia in early life that progresses to adenoma or adenocarcinoma in about half of the animals which survive longer 7 months of age.
- Additional Breeding and Husbandry Support
Mating System
- Noncarrier x Hemizygote
Citation
When using the C3(1)-TAg , C3(1)/Tag mouse strain in a publication, please cite the originating article(s) and include JAX stock #013591 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX12 (Maximum)

Pricing & Availability

Available

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Breeder Pair

Sex

Genotype

Price

Female
Male

Cryorecovery - Pricing

Service/Product	Description	Price
	Hemizygous or Non carrier for Tg(C3-1-TAg)cJeg

Related Products and Services

Frozen Mouse Embryo	FVB-Tg(C3-1-TAg)cJeg/JegJ Frozen Embryo	$2595.00
Frozen Mouse Embryo	FVB-Tg(C3-1-TAg)cJeg/JegJ Frozen Embryo	$2595.00
Frozen Mouse Embryo	FVB-Tg(C3-1-TAg)cJeg/JegJ Frozen Embryo	$3373.50
Frozen Mouse Embryo	FVB-Tg(C3-1-TAg)cJeg/JegJ Frozen Embryo	$3373.50

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:C3(1)-TAg , C3(1)/Tag

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Expression Data

Control Suggestions

Approximate Controls

Additional Information

Selected References

Tg(C3-1-TAg)cJeg

Allele Symbol: Tg(C3-1-TAg)cJeg

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Mammalian Phenotype Terms by Genotype

Genotype: Tg(C3-1-TAg)cJeg/0FVB/N-Tg(C3-1-TAg)cJeg

endocrine/exocrine gland phenotype

neoplasm

reproductive system phenotype

Genotype: Tg(C3-1-TAg)cJeg/0involves: FVB/N

integument phenotype

mortality/aging

neoplasm

endocrine/exocrine gland phenotype

renal/urinary system phenotype

reproductive system phenotype

References

Additional - Tg(C3-1-TAg)cJeg related

Genotyping Protocols

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Breeder Pair

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Genotype: Tg(C3-1-TAg)cJeg/0
FVB/N-Tg(C3-1-TAg)cJeg

Genotype: Tg(C3-1-TAg)cJeg/0
involves: FVB/N