Search Criteria: Research Area is "Reproductive Biology Research: Gonadal Tumors"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 002448 | 129S1/SvImJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains.(1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997.
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| 000691 | 129X1/SvJ | Level 2 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997.
In response to challenge, 129S1/SvImJ mice develop immune-mediated nephritis characterized by proteinuria, glome
..... | ||
| 100410 | WBB6F1/J-KitW/KitW-v/J | Level 2 |
| Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. KitW/KitW-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. KitW/KitW-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment. | ||
| 000690 | 129P3/J | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997. | ||
| 002065 | 129T2/SvEmsJ | Level 4 |
| Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson, et al., 1997. | ||
| 000049 | C57BL/6J-KitW-v/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 000692 | WB/ReJ KitW/J | Level 4 |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. The lack of germ cells in homozygous mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. | ||
| 001137 | 129P1/ReJ | Repository- Live |
| For a complete history of the numerous 129 substrains please refer to Simpson, et al., 1997. Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. Most recently 129 mice are widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of substrains into three major groups: parental substrains, steel substrains and "ter" substrains. Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. | ||
| 000160 | B6.D2-KitlSl-d/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu
..... For more information please see the full phenotype on the strain data sheet | ||
| 000693 | WC/ReJ KitlSl/J | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing
..... For more information please see the full phenotype on the strain data sheet | ||
| 100401 | WCB6F1/J KitlSl KitlSl-d | Repository- Live |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., KitlSl/KitlSl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall
..... For more information please see the full phenotype on the strain data sheet | ||
| 002357 | 129P3/JEmsJ | Repository-Cryopreserved |
| 001198 | 129P4/RrRkJ | Repository-Cryopreserved |
| For a complete history of the numerous 129 substrains please refer to Simpson, et al., 1997. Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. Most recently 129 mice are widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of substrains into three major groups: parental substrains, steel substrains and "ter" substrains. Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. | ||
| 000090 | 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J | Repository-Cryopreserved |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a
..... For more information please see the full phenotype on the strain data sheet | ||
| 002722 | 129S6/SvEv-Mostm1Ev/J | Repository-Cryopreserved |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 000091 | 129T1/Sv-Oca2+ Tyrc-ch Dnd1Ter/J | Repository-Cryopreserved |
| 002064 | 129T2/SvEms | Repository-Cryopreserved |
| 001263 | 129XAM/SvJ | Repository-Cryopreserved |
| Leroy Stevens reported that 96% (81 or 84) of 9XAM male genital ridges grafted to the testes of adults develop into testes with teratomas. Spontaneous teratomas were found in 1 of 187. | ||
| 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. | ||
| 000599 | B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J | Repository-Cryopreserved |
| 006564 | B6(C)-KitW-41J Gusbmps/BrkJ | Repository-Cryopreserved |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. In appearance, homozygous KitW-41J mice are mostly white with black eyes and brown or grey spots. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage disease
..... For more information please see the full phenotype on the strain data sheet | ||
| 002723 | B6.129S6-Mostm1Ev/J | Repository-Cryopreserved |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 002188 | B6.129S7-Amhtm1Bhr/J | Repository-Cryopreserved |
| Male mice homozygous for the Amhtm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia. Homozygous females are fertile. | ||
| 000122 | B6.C3-KitW-44J/J | Repository-Cryopreserved |
| KitW-44J heterozygotes have white-tipped feet and a white tail tip although the belly spot standardly found in KitW* mutations is very small in this mutant, sometimes restricted to only a few hairs. Homozygotes have a flecked pelt that is predominantly white, especially ventrally, with pigmented patches particularly at the lateral borders. The pigmentation fades with age yielding black-eyed white mice by approximately 9 months of age. While many KitW-44J homozygotes are viable, fertility is diminished. Homozygous females have greatly reduced fertility and gonads that are smaller in size with reduced activity. Homozygous males are sterile although spermatogenesis occurs. The KitW-44J allele does not produce anemia in either its heterozygous or homozygous state. The red blood cell count, white blood cell count, hematocrit, and mean cell volume are normal. However, bone marrow transplantation experiments reveal that t
..... For more information please see the full phenotype on the strain data sheet | ||
| 000164 | B6.Cg-KitW/J | Repository-Cryopreserved |
| 000124 | B6.Cg-KitlSl Krt71Ca/J | Repository-Cryopreserved |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva
..... For more information please see the full phenotype on the strain data sheet | ||
| 000194 | B6.Cg-Lx KitW-v/J | Repository-Cryopreserved |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Heterozygous lx mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hindfeet. Homozygotes show preaxial polydactyly or oligodactyly of the hindfeet, reduction of the tibia, loss of part of the femur and pubis, decrease in number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter.
Although homozygous KitW-v/
..... | ||
| 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 phenotype on the strain data sheet | ||
| 002187 | B6;129S7-Amhtm1Bhr/J | Repository-Cryopreserved |
| Male mice homozygous for the Amhtm1Bhr mutation have testes that are fully descended and produce functional sperm. They also develop a uterus which interferes with sperm transfer rendering most infertile. The testes develop Leydig cell hyperplasia. | ||
| 002404 | B6;CBA-Mostm1Ev/J | Repository-Cryopreserved |
| Mice homozygous for the Mostm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings. | ||
| 000350 | B6By.Cg-KitW-v MitfMi-wh T/J | Repository-Cryopreserved |
| Kit mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. KitW-v homozygotes resemble KitW homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (MitfMi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes show slight microphthalmia but a normal skeleton. Heterozygotes (MitfMi-wh/+) have a dilut
..... For more information please see the full phenotype on the strain data sheet | ||
| 000291 | C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J | Repository-Cryopreserved |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva
..... For more information please see the full phenotype on the strain data sheet | ||
| 000627 | C3H/HeJ-KitW-x/J | Repository-Cryopreserved |
| 000847 | C3Sn.B6-KitW-39J/J | Repository-Cryopreserved |
| 001380 | C3Sn.Cg-KitlSl-con/J | Repository-Cryopreserved |
| Both homozygous and heterozygous mice with the contrasted induced mutation (KitlSl-con) are viable. Male homozygous mutant mice are fertile but females are usually sterile. Mice heterozygous for the contrasted mutation are recognizable soon after birth by dark pigmentation of the genital papilla with the adult coat being slightly lighter than normal. Homozygous mutant mice also have dark genitalia and a markedly diluted coat and mild macrocytic anemia. | ||
| 000134 | C57BL/6J-KitW-37J/J | Repository-Cryopreserved |
| 000062 | C57BL/6J-KitW-39J/J | Repository-Cryopreserved |
| 000121 | C57BL/6J-KitW-40J/J | Repository-Cryopreserved |
| 000119 | C57BL/6J-KitW-41J/J | Repository-Cryopreserved |
| 000127 | C57BL/6J-KitW-42J/J | Repository-Cryopreserved |
| 003252 | C57BL/6J-KitlSl-20J/J | Repository-Cryopreserved |
| KitlSl-20J is a dominant allele. On the C57BL/6J background heterozyggotes have a light black coat color with lighter tail and feet and a steel colored belly with a belly spot. Heterozygotes of both sexes are viable and fertile. See also Mouse Genome Database entry | ||
| 000965 | CBACa.C3-KitW-x/J | Repository-Cryopreserved |
| 000092 | FL/1Re-KitW/J | Repository-Cryopreserved |
| 002971 | FVB-Tg(BCL2OVARY)1Ah/J | Repository-Cryopreserved |
| The human BCL2 gene in this strain is under the control of the mouse Inha(inhibin alpha) promoter, restricting expression to ovary, testis and adrenal cortex. This strain exhibits a suppression of follicular cell apotosis, enhancement of folliculogenesis, larger litter sizes and an increased occurrence of benign ovarian teratomas. | ||
| 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. | ||
| 000979 | STOCK KitlSl-16J/J | Repository-Cryopreserved |
| The steel mutations cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations. Most steel homozygous mice are severely anemic in utero and die usually at 15 to 16 days of gestation. However, compounds of two MgfSl mutants (e.g. MgfSl/MgfSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable MgfSl/ MgfSl homozygotes and deficient in the MgfSl/+ heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age. | ||
| 003911 | SWR.SJL-(DXMit210-DXMit38)/BmJ | Repository-Cryopreserved |
| 000161 | WB.D2-KitlSl-d/J | Repository-Cryopreserved |
| The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (KitlSl-d/KitlSl-d) and compounds of steel and steel Dickie (KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu
..... For more information please see the full phenotype on the strain data sheet | ||
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IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 001079 | SWXJ9/BmJ | Research Strain |
| SWXJ-9 female mice develop ovarian granulosa cell carcinomas with an incidence of approximately 12% and a latency of 4-6 weeks. Tumor incidence can be increased to approximately 40% by treatment with dehydroepiandrosterone (DHEA) or testosterone immediately after weaning. Treatment with estradiol during this period completely suppresses tumorigenesis. Neoplasias are first observed as hemorrhagic follicles in which the antrum is blood-filled and lined with irregular masses of proliferating granulosa cells. By 6-10 weeks of age, the primary tumor encompasses the entire ovary. Metastases to lung, renal node, and liver are common by 6 to 9 months of age, with other sites occasionally affected. Susceptibility to granulosa cell carcinomas is controlled by a small number of genes, including a major susceptibility locus on Chromosome 4 and a major modifier locus on the X chromosome. | ||
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How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
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These strains are designated as: "Under Development for Cryopreservation Repository"
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