Search Criteria: Research Area is "Cancer Research: Increased Tumor Incidence (Skin Cancers: Induced)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 006238 | B6;129S4-Thbs2tm1Bst/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. Multiple analyses has confirmed the absence of protein in embryonic and adult tissue of homozygous mice. Homozygotes exhibit skin disorders (abnormal collagen fiber patterns, reduced tensile strength, increased fragility) and skin fibroblasts have attachment defects. Mice also exhibit an increase in total density/cortical thickness of the long bones, abnormally long bleeding times, and a significant increase in blood vessel density. Homozygous mice exhibit accelerated wound healing after biopsy and accelerated/increased tumor formation following chemically-induced skin carcinogenesis. Mutant mice may be useful in studies of collagen fibrillogenesis in skin and tendons, angiogenesis and vascular pathophysiology, wound healing, chemically-induced tumor progression, and as a potential model for Ehlers Danlos syndrome. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are fre
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| 001737 | B6.A-H2-T18a.HRS-Hrhr/J | Repository-Cryopreserved |
| Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. In an attempt to offer alleles on
..... For more information please see the full descriiption on the strain data sheet | ||
| 004853 | B6.C3-Tg(KRT14-Birc5)19Gros/J | Repository-Cryopreserved |
| These transgenic mice express the mouse baculoviral IAP repeat-containing 5, Birc5 (survivin), gene under the direction of the human keratin 14 promoter. Transgene expression is specific to epidermal and follicular keratinocytes. Mice hemizygous for the transgenic insert are resistant to chemical (DMBA)- and UVB-induced keratinocyte apoptosis in vivo. Although hemizygotes were less susceptible to DMBA-induced papilloma formation, spontaneous papilloma regression was not observed and there was enhanced conversion of papillomas to carcinomas. This mutant mouse strain represents a model that may be useful in studies of keratinocyte apoptosis and skin cancer development. | ||
| 005514 | B6;129X1-Mmp8tm1Lotn/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of peripheral blood cells. Male mice homozygous for the mutation are more susceptible to experimentally induced invasive papillomas and fibrosarcomas. Latency of papilloma tumor formation is shorter. Female homozygotes exhibit increased skin cancer incidence when treated with tamoxifen or ovarectomy. Carcinogen administration causes persistent inflammatory response with neutrophil accumulation at the site of injection. Lipopolysaccharide (LPS) challenge causes a two-fold increase in polymorphonuclear cell accumulation in affected lung tissue of male homozygotes. This mutant mouse strain may be useful in studies of carcinogenesis, metastasis, and inflammation. | ||
| 002922 | D2.HRS-Hrhr/J | Repository-Cryopreserved |
| 005705 | FVB-Tg(KRT14-Vegfa)3Dtm/J | Repository-Cryopreserved |
| Mice hemizygous for the transgene are viable and fertile. Transgene expression is demonstrated in the basal keratinocyte layer of the epidermis and outer root sheath keratinocytes of hair follicles. Homozygous mice spontaneously develop severe psoriasis-like lesions between 3-6 months of age, where hemizygous mice do not. Transgenic mice have increased density of tortuous cutaneous blood capillaries with elevated expression of select VEGF receptors, most prominently in neonates. Dermal mast cell localization and capillary hyperpermeability are also increased. Postcapillary venules exhibit significantly enhanced leukocyte rolling and adhesion. Transgenic expression promotes lymphangiogenesis associated not only with delayed-type hypersensitivity induced psoriasis-like skin inflammation but also with cutaneous tissue repair after wounding. Further, transgenic mice have accelerated chemically induced skin carcinogenesis with tumor associated lymphangiogenesis and angiogenesis. Elevated me
..... For more information please see the full descriiption on the strain data sheet | ||
| 000673 | HRS/J | Repository-Cryopreserved |
| Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. HRS/J mice, fed an ather
..... For more information please see the full descriiption on the strain data sheet | ||
| 001103 | HRS/J-Hrhr Esdb/+ Esdb/J | Repository-Cryopreserved |
| Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. | ||
| 002746 | SENCARA/PtJ | Repository-Cryopreserved |
| The acronym SENCAR is derived from SENsitivity to CARcinogenesis. SENCAR mice are commonly used for studies of susceptibility and resistance to the induction of skin tumors. Dr. Michael Potter of the National Cancer Institute developed three inbred lines, designated A, B, and C, from random breeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three inbred strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Promotion by mezerein as well as carcinogenesis by repeated treatment with DMBA or MNNG produced papillomas with a high frequency of conversion to squamous cell carcinomas (SCCs). Compared with outbred SENCAR mice, development of both squamous papillomas and carcinomas was increased at least two-fold by all protocols tested. | ||
| 002747 | SENCARB/PtJ | Repository-Cryopreserved |
| The acronym SENCAR is derived from SENsitivity to CARcinogenesis. SENCAR mice are commonly used for studies of susceptibility and resistance to the induction of skin tumors. Dr. Michael Potter of the National Cancer Institute developed three inbred lines, designated A, B, and C, from random breeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three inbred strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Promotion by mezerein as well as carcinogenesis by repeated treatment with DMBA or MNNG produced papillomas with a high frequency of conversion to squamous cell carcinomas (SCCs). Compared with outbred SENCAR mice, development of both squamous papillomas and carcinomas was increased at least two-fold by all protocols tested. | ||
| 002748 | SENCARC/PtJ | Repository-Cryopreserved |
| The acronym SENCAR is derived from SENsitivity to CARcinogenesis. SENCAR mice are commonly used for studies of susceptibility and resistance to the induction of skin tumors. Dr. Michael Potter of the National Cancer Institute developed three inbred lines, designated A, B, and C, from random breeding of outbred SENCAR mice. Characterization of these mice for sensitivity to skin tumor development indicated that mice of all three inbred strains displayed increased sensitivity to initiation by 7,12-dimethylbenz[a]anthracene (DMBA), urethane, or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Promotion by mezerein as well as carcinogenesis by repeated treatment with DMBA or MNNG produced papillomas with a high frequency of conversion to squamous cell carcinomas (SCCs). Compared with outbred SENCAR mice, development of both squamous papillomas and carcinomas was increased at least two-fold by all protocols tested. | ||
| 002335 | SKH2/J | Repository-Cryopreserved |
| Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. Black juvenile hair coa
..... For more information please see the full descriiption on the strain data sheet | ||
| 000147 | WLHR/LeJ | Repository-Cryopreserved |
| WLHR/Le is a balanced stock with wabbler-lethal (wl) and hairless (hr) spontaneous mutations maintained in repulsion on Chromosome 14. Homozygous wabbler-lethal mutant mice are first recognizable at 12 days of age and usually die at about four weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. In an extensive study of behavioral development of this mutant, homozygous wabbler-lethal mice were shown to be deficient in nearly all behaviors tested. Histological examination showed myelin degeneration widely distributed throughout the CNS, particularly in the vestibulocerebellar and spinocerebellar systems. Electron microscopy showed widespread axonal (Wallerian) degeneration in the medulla with secondary myelin dissolution. Similar abnormalities were present to a lesser extent in the basal ganglia, spinal cord, and cerebellum and in the optic nerve. Homozygous hairless mutant mice have a higher incidence and earlier onset of leukemia, reducible by v
..... For more information please see the full descriiption on the strain data sheet | ||
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