Search Criteria: Research Area is "Cancer Research: Increased Tumor Incidence (Mammary Gland Tumors)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002020 | C57BL/6J-ApcMin/J | Level 3 |
| The C57BL/6J-ApcMin/J strain is highly susceptible to spontaneous intestinal adenoma formation. Homozygous mice are not viable. It was initially reported that one hundred percent of the C57BL/6J-ApcMin heterozygous mice raised on a high fat diet develop in excess of 30 adenomas throughout the intestinal tract and most die by 120 days of age. Heterozygotes also develop anemia. (Moser et al., 1990, Su et al., 1992). A small number of C57BL/6J-ApcMin heterozygous female mice develop mammary tumors. A subsequent publication indicates that this strain may carry a dominant modifier (Mom2) gene that reduces the number and incidence of polyp formation in C57BL/6J-ApcMin heterozygous mice (Silverman et al., 2002). | ||
| 002376 | FVB/N-Tg(MMTVneu)202Mul/J | Level 3 |
| Mice homozygous for the MMTVneu (rat) transgene are viable and fertile. There is no phenotypic effect in males. The transgene is expressed at low levels in normal mammary epithelium, salivary gland, and lung. Higher expression is detected in tumor tissue. Focal mammary tumors first appear at 4 months, with a median incidence of 205 days. Both virgin and breeder mice develop tumors. Tumors arise as foci in hyperplastic, dysplastic mammary glands. Seventy-two percent of tumor-bearing mice that live to 8 months or longer develop metastatic disease to the lung. The phenotype of MMTV/unactivated neu transgenic mice differs from that of the MMTV/activated neu produced by Phil Leder, in which multifocal tumors involving the entire mammary epithelium arise. | ||
| 000689 | SWR/J | Level 3 |
| SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominant pronuclei with good resistance to l
..... For more information please see the full descriiption on the strain data sheet | ||
| 006132 | DDD.GR-Mtv2a/JmsJ | Repository- Live |
| 005038 | FVB-Tg(MMTV-Erbb2)NK1Mul/J | Repository- Live |
| These transgenic mice express the activated rat Erbb2 (c-neu) oncogene under the direction of the mouse mammary tumor virus promoter. The activated, or transforming, version of the rat Erbb2 (c-neu) oncogene has a valine to glutamic acid substitution at acid 664, (Val664 to Glu664). Non-uniform and random transgene expression is detected by RNase protection assay in mammary gland epithelium from hemizygous mice. Tumor formation is multifocal, stochastic and matches the expression pattern of the transgene. While no transgene expression is detected at 5 and 8 weeks of age in normal mammary gland tissue, it is detected in adenocarcinomas from older (23 week old) mice. The donating investigator indicates that 50% of transgenic mice derived from the TG.NK founder line, develop tumors within 6-12 months of age. Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. This mutant mouse strain may be useful in studies of bre
..... For more information please see the full descriiption on the strain data sheet | ||
| 004363 | FVB.Cg-Tg(MMTV-vHaras)SH1Led/J | Repository- Live |
| These transgenic mice express the Harvey RAS (human) gene under the direction of the mouse mammary tumor virus promoter. The majority of expression of the transgene is detected in the mammary tissue and salivary glands. Both male and female transgenic mice develop malignant lymphoid tissue and mammary and salivary gland tumors as early as 5 weeks of age. Half of the female transgenic animals develop tumors by 6 months of age. Histological analysis of mammary tumors revealed most of the tumors were adenocarcinomas and were locally invasive with some cases of metastasis to liver and/or lung. The tumors were found to express the transgene transcript. Protein-tyrosine phosphatase epsilon mRNA and protein was found to be highly expressed only in mammary tumors. In 20% of the transgenic mice diffuse benign hyperplasia develops in the Harderian lacrimal gland causing bilateral exophthalmia. The donating investigator reports hemizygous females develop tumors by delivery of their first litter (
..... For more information please see the full descriiption on the strain data sheet | ||
| 002374 | FVB/N-Tg(MMTV-PyVT)634Mul/J | Repository- Live |
| Mice carrying the (MMTV-PyVT) transgene are viable, but show loss of lactational ability coincident with transgene expression. Female carriers develop palpable mammary tumors as early as 5 weeks of age. Adenocarcinomas arise in virgin and breeder females as well as males, which are multifocal, highly fibrotic, and involve the entire mammary fat pad. Males also develop adenocarcinoma of the seminal vesicles and hemangiomas. Pulmonary metastases are observed in 80-94% of tumor-bearing female mice. Transgene expression is detected at high levels in male and female mammary glands. Lower levels are detected in salivary gland, seminal vesicles, ovaries, and lungs (believed to be the result of pulmonary metastases). | ||
| 005221 | RIII/ImrNhsJ | Repository- Live |
| The original RIII strain was known for its high incidence of hormone-dependent mammary tumors transmissible by milk-born MMTV. The RIII/ImrNhsJ substrain is reported to show a pattern of virus expression and tumor incidence similar to the RIII strain (Sarkar, et al. 2004). RIII/ImrNhsJ mice carry the following endogenous MMTV loci: Mtv-6, 8, 14, 17 and possibly 21 (Popken-Harris, et al. 2001). Exogenous MMTV infection leads to the deletion of CD4+ Vbeta-2 and Vbeta-8 peripheral and central T cells (Uz-Zaman, et al. 2003). It is possible to modulate mammary tumor incidence using high and low calorie diets (Li, et al. 1994). RIII/ImrNhsJ mice infected with exogenous MMTV may be useful for studies of human breast cancer activated by insertional mutagenesis. NOTE: Mice distributed by The Jackson Laboratory are not infected with MMTV. Regrettably, we do not have a source for the virus. | ||
| 003382 | B10.D2-Tg(C3-1-TAg)cJeg/J | Repository-Cryopreserved |
| This transgenic strain is a model for the study of multistage oncogenesis in the prostate and mammary glands. Male 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. Female 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 female mice develop lung metastases, although lung metastases from prostate cancer is extremely rare. Bone metastases have not been observed. Please note that the phenotype description above was developed for this allele on an FVB background (stock number 3381). The mammary and prostate tumor phenotypes may be different on the C57BL/10 background in this strain. | ||
| 003180 | B6.129S-Cdh3tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Cdh3tm1Hyn targeted mutation (P-cadherin deficient) are viable and fertile with females able to nurse and maintain their litters. Virgin homozygous mutant females display precocious differentiation of the mammary gland. Aging mice develop hyperplasia and dysplasia of the mammary epithelium. In addition, mammary glands from P-cadherin deficient mice show abnormal lymphocyte infiltration. | ||
| 003380 | B6.FVB-Tg(C3-1-TAg)cJeg/J | Repository-Cryopreserved |
| TgN(C3-1-TAg)cJeg mice are transgenic for the SV-40 Large tumor antigen (TAg) driven by the rat prostatic steroid binding protein (C3(1))promoter. Male mice survive up to 11 months of age. They develop hyperplastic changes in the prostate epithelium which progress to prostate adenocarcinoma in the majority of mice after 8 months of age. Carcinogenic changes in female mice begin with development of hyperplasia of the mammary gland ducts and acini by 3 months of age and progress to multifocal mammary adenocarcinoma with death by 6 month of age. Homozygous mothers can bear offspring but pregnancy appears to accelerate tumor development and foster mothers are required for pups due to lactation difficulties. Evidence of pulmonary metastases has been seen in both male and female mice. These C3-1-TAg transgenic mice provide a model to study TAg-induced progression of hormone responsive tumors. Please note that the phenotype description above was developed for this allele on an FVB backgrou
..... For more information please see the full descriiption on the strain data sheet | ||
| 002459 | B6D2-Tg(MMTVTGFA)254Rjc/J | Repository-Cryopreserved |
| The phenotype of TgN(MMTVTGFA)254Rjc transgenic mice is very similar to that of B6D2-TgN(MMTVTGFA)29Rjc (Stock No. 002373). Mice are viable and fertile, but lactate insufficiently to support the litter. Virgin transgenic mice show no mammary gland abnormalities prepubertally, but adult virgin mice have considerable alveolar gland hyperplasia. Pregnant transgenic mice show marked proliferation of the stromal cells, and alveolar secretion is markedly increased compared to nontransgenic mice. After multiple pregnancies, isolated adenocarcinomas develop. There is no apparent phenotypic effect in males. In females transgene expression was localized to the small ducts and alveoli in both virgin and pregnant mice as evidenced by in situ hybridization and by immunohistochemistry. Immunostaining also revealed some stromal staining in the hyperplastic areas. Egfr mRNA expression was also increased in mammary tissues expressing high levels of the transgene. Crosses between TGFA transgenic
..... For more information please see the full descriiption on the strain data sheet | ||
| 002373 | B6D2-Tg(MMTVTGFA)29Rjc/J | Repository-Cryopreserved |
| Mice are viable and fertile, although mice of the most extensively studied line lactate insufficiently to support the litter. Virgin transgenic mice show no mammary gland abnormalities prepubertally, but adult virgin mice have considerable alveolar gland hyperplasia. Pregnant transgenic mice show marked proliferation of the stromal cells, and alveolar secretion is markedly increased compared to nontransgnic mice. After multiple pregnancies, isolated adenocarcinomas develop. There is no apparent phenotypic effect in males. In females, transgene expression is localized to the small ducts and alveoli in both virgin and pregnant mice as evidenced by in situ hybridization and by immunohistochemistry. Immunostaining also reveals some stromal staining in the hyperplastic areas. Egfr mRNA expression is also increased in mammary tissues expressing high levels of the transgene. Crosses between TGFA transgenic mice and TGFB1 transgenic mice demonstrate that these growth factors oppose each other'
..... For more information please see the full descriiption on the strain data sheet | ||
| 002870 | B6SJL-Tg(Wnt1)1Hev/J | Repository-Cryopreserved |
| Mammary glands from virgin hemizygous females carrying the (Wnt1)1Hev transgene resemble hormonally-stimulated glands from pregnant mice. There was a marked increase in numbers of terminal branches and alveoli, producing a diffuse lobular hyperplasia. Parous transgenic females were unable to lactate. Hemizygous transgenic male glands, while less developed, also were hyperplastic. Adenocarcinomas developed between 3 and 7 months in females and more rarely in males. Occasional metastatic lesions were observed in females. Salivary adenocarcinomas were also occasionally observed in both males and females. Tumors arose stochastically, indicating additional events are required for neoplasia. Subsequent work with Wnt1 transgenic mice includes infection with MMTV to identify contributing oncogenes and mating to transgenic mice bearing other oncogenes. | ||
| 006863 | C3Fe.B6-Mcm4chaos3/J | Repository-Cryopreserved |
| Mice homozygous for this ENU-induced F345I hypomorphic allele (Chaos3) are viable, fertile, and overtly indistinguishable from normal littermates. Homozygous, but not heterozygous, mice have slightly reduced wildtype protein levels in mouse embryonic fibroblasts (MEFs). Whereas Chaos3 heterozygotes show mildly elevated (2- to 5-fold) micronucleus frequencies compared with wildtype, homozygotes have an approximate 20-fold increase with over 7% of erythrocytes containing micronuclei. MEFs from homozygous mice exhibit mild defects (cell proliferation, S phase and G2/M populations), and are highly susceptible to chromosome breakage following treatment with the DNA replication inhibitor aphidicolin. On a congenic C3HeB/FeJ background, greater than 80% of homozygous females exhibit mammary adenocarcinomas with a mean latency of 12 months, while males have no tumor incidence. These Chaos3 mice provide a novel, non-transgenic model of breast cancer, and may be useful for s
..... For more information please see the full descriiption on the strain data sheet | ||
| 003381 | FVB-Tg(C3-1-TAg)cJeg/J | Repository-Cryopreserved |
| This transgenic strain is a model for the study of multistage oncogenesis in the prostate and mammary glands. Male 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. Female 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 female mice develop lung metastases, although lung metastases from prostate cancer is extremely rare. Bone metastases have not been observed. The phenotype for this transgene has been most extensively studied in the FVB/N background. | ||
| 002953 | FVB.Cg-Tg(MMTVTGFA)254Rjc/J | Repository-Cryopreserved |
| Mice carrying the (MMTVTGFA)254Rjc transgene are viable and fertile, but lactate insufficiently to support the litter. Virgin transgenic mice show no mammary gland abnormalities prepubertally, but adult virgin mice have considerable alveolar gland hyperplasia. Pregnant transgenic mice show marked proliferation of the stromal cells, and alveolar secretion is markedly increased compared to nontransgenic mice. After multiple pregnancies, isolated adenocarcinomas develop. There is no apparent phenotypic effect in males. In females transgene expression was localized to the small ducts and alveoli in both virgin and pregnant mice as evidenced by in situ hybridization and by immunohistochemistry. Immunostaining also revealed some stromal staining in the hyperplastic areas. Egfr mRNA expression was also increased in mammary tissues expressing high levels of the transgene. Crosses between TGFA transgenic mice and TGFB1 transgenic mice demonstrate that these growth factors oppose each oth
..... For more information please see the full descriiption on the strain data sheet | ||
| 002677 | FVB.Cg-Tg(WapMyc)212Bri/J | Repository-Cryopreserved |
| Female mice transgenic for the Tg(WapMyc)212Bri are viable and fertile but do not lactate. Mammary glands from pregnant transgenic mice showed enlarged and hyperplastic alveoli with poorly differentiated epithelial cells. Multiparous females develop observable mammary tumors at the average age of 6 months. The majority of tumors were of mixed histotypes with solid as well as glandular or papillary foci. Lung metastases were observed in 3 of 14 tumor-bearing mice. All tumors tested were transplantable into syngeneic mice. | ||
| 002678 | FVB.Cg-Tg(WapTgfa)215Bri/J | Repository-Cryopreserved |
| Transgenic females showed precocious mammary gland development during pregnancy. Involution was delayed beyond 8 days post-parturition. With successive pregnancies hyperplastic alveolar nodules increased in number. Mammary tumors, the majority of which were well-differentiated, were observed with variable latency, on average at 7-8 months of age in multiparious females. Fibroadenomas composed of neoplastic glandular alveolar epithelium surrounded by variable amounts of stroma were also observed. Metastasis to the lung was observed in 1 of 40 tumor-bearing mice. Virgin mice were tumor-free. | ||
| 002934 | FVB.Cg-Tg(Wnt1)1Hev/J | Repository-Cryopreserved |
| Mammary glands from virgin hemizygous females carrying the (Wnt1)1Hev transgene resemble hormonally-stimulated glands from pregnant mice. There was a marked increase in numbers of terminal branches and alveoli, producing a diffuse lobular hyperplasia. Parous transgenic females were unable to lactate. Hemizygous transgenic male glands, while less developed, also were hyperplastic. Adenocarcinomas developed between 3 and 7 months in females and more rarely in males. Occasional metastatic lesions were observed in females. Salivary adenocarcinomas were also occasionally observed in both males and females. Tumors arose stochastically, indicating additional events are required for neoplasia. Subsequent work with Wnt1 transgenic mice includes infection with MMTV to identify contributing oncogenes and mating to transgenic mice bearing other oncogenes. | ||
| 002437 | FVB/N-Tg(MMTV-Notch4)3Rnc/J | Repository-Cryopreserved |
| Male mice transgenic for the Notch4 gene (previously called Int3) are sterile, and females fail to lactate. Mammary tissue of females does not develop completely, exhibiting dramatic inhibition of alveolar-lobular development and reduced penetration of the mammary fat pad by ductal epithelium. Glandular epithelia of tissues expressing the activated form of Notch4 generally display severe ductal hyperplasia. Salivary glands fail to differentiate completely. Male transgenic mice exhibit severe epididymal hyperplasia, which is thought to be the cause of their sterility. Both male and female mice develop focal adenomas of the mammary and salivary glands. | ||
| 002421 | FVB/N-Tg(MtTGFA)100Lmb/J | Repository-Cryopreserved |
| In the CD1-TgN(MtTGFA)42Lmb line liver lesions develop in a progressive fashion, with neoplasia confirmed at autopsy (average age 13 months). Mammary ductal network was more densely developed in CD1-TgN(MtTGFA)42Lmb transgenic mice, with dividing cells in the subtending ducts as well as in the end bud region. Pancreas showed progressive hyperplasia of the stroma, tubular structures and ductular metaplasia. Penetrance was 100%. The mice were not diabetic. There was no obvious inflammatory reaction. Mice from the FVB/N-TgN(MtTGFA)100Lmb line exhibit a 60% mammary tumor incidence. | ||
| 002675 | FVB/N-Tg(MtTPRMET)243Lng/J | Repository-Cryopreserved |
| Mammary tumors developed at around a year of age in multiparous mice. Multiple tumors classified as independent arose in several mice. No metastases were observed. Hyperplastic alveolar nodules were identified in most multiparous mice and several also had foci of microscopic carcinoma. Tumors exhibited scirrhous, papillary, or nodular histologic patterns. Other tumor types seen included diffuse lymphoblastic lymphomas involving the mammary gland and lymph nodes, thymic lymphoma, spindle cell sarcoma, and orbital giant cell osteosarcoma. | ||
| 002775 | FVB/N-Tg(MtTPRMET)773Lng/J | Repository-Cryopreserved |
| Mammary tumors developed at around a year of age in multiparous mice. Multiple tumors classified as independent arose in several mice. No metastases were observed. Hyperplastic alveolar nodules were identified in most multiparous mice and several also had foci of microscopic carcinoma. Tumors exhibited scirrhous, papillary, or nodular histologic patterns. Other tumor types seen included diffuse lymphoblastic lymphomas involving the mammary gland and lymph nodes, thymic lymphoma, spindle cell sarcoma, and orbital giant cell osteosarcoma. | ||
| 006131 | GR/J | Repository-Cryopreserved |
| The inbred strain, GR carries the Mtv2a allele. This allele controls expression of endogenous MMTV and the early development of hormone-induced mammary tumors. Nearly all breeding females develop mammary tumors prior to one year of age (van Nie et al. 1977). Most females will exhibit small tumors by the day of first parturition (van Nie et al. 1971). These tumors are most often of the Dunn classification type B adenocarcinoma. MMTV is transmitted through both the milk and the germinal cells of both males and females. Foster nursing does not eliminate endogenous mammary tumor virus (Muhlbock 1965). MTV-antigens are detectable by immunodiffusion assay in the milk of the first lactation period. (van Nie et al. 1977). GR is used extensively to study endocrine regulation of mammary gland development and tumorigenesis. | ||
| 003690 | STOCK Tg(MMTV-Cdc37)1Stp/J | Repository-Cryopreserved |
| In wildtype mice Cdc37 is expressed primarily in proliferative tissues. These transgenic mice express Cdc37 under the direction of an MMTV promoter. As a result, levels of transgene mRNA are significantly higher than levels of endogenous Cdc37 in specific tissues (lacrimal, mammary, salivary glands, uterus and testis). Mice are born and develop normally. By 18 months of age females exhibit proliferative disorders including mammary tumors and lymphomas. By 22 months of age 100% of transgenic females develop mammary or lymphoid tumors. Histopathological examination indicates that mammary tumors are adenocarcinomas and adenosquamous carcinomas. Males expressing Cdc37 in mammary tissue develop a system of mammary ducts resembling that of virgin females, but do not develop tumors. Crosses with other MMTV-oncogene expressing mice indicate that Cdc37 can cooperate with myc in transformation of multiple tissues, and with Cyclin D1 in transformation of
..... For more information please see the full descriiption on the strain data sheet | ||
| 003337 | STOCK Tg(MMTV-PIP)1Shu/J | Repository-Cryopreserved |
| Transgenic transcripts are detected in mammary, salivary, lacrimal glands and lymph nodes. This strain exhibits no overt phenotype but has potential to be useful in studying processes involved in the transformation of mammary tissue cells. | ||
| 003153 | WLC.C-H2d.GR-Mtv2/MorJ | Repository-Cryopreserved |
| The GR strain carries five endogenous proviral copies of mouse mammary tumor virus (MMTV) including Mtv2. In GR, Mtv2 causes mammary carcinomas in 100% of breeding females prior to one year of age. Mtv2 deletes T cells carrying V beta 14 in the presence of MHC class II I-E (Ferrick 1992). This double congenic carries the GR Mtv2 locus in an exogenous and endogenous MMTV-free genetic background (WLC/MorJ, Stock No. 002600) and in an H2d background. This congenic represents a model for studying MMTV-induced mammary tumorigenesis in the absence of multiple endogenous proviruses (Morris 1986). Mammary tumor incidence has not been confirmed at The Jackson Laboratory. | ||
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