Search Criteria: Research Area is "Cancer Research: Increased Tumor Incidence (Other Tissues/Organs: osteosarcoma)"

New Strains Under Development

JAX^® Mice Strains

Stock Number	Strain Name   Strain Description	Standard Supply
008462	B6.129P2-Trp53tm1Brn/J	Repository- Live
	Exons 2-10 are flanked by loxP sites in this conditional targeted mutation. Mice homozygous for the floxed allele do not show any increase in disease incidence for at least a year. When bred to mice with a cre recombinase gene under the control of a promoter of interest, expression is deleted in the tissue of interest. For example, when crossed to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771), this mutant mouse strain may be useful in studies of medulloblastoma formation.
002101	B6.129S2-Trp53tm1Tyj/J	Repository- Live
	Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at three to six months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
007218	B6.129S6-Trp53tm2Xu/J	Repository- Live
	Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and also develop a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events, cancer development and apoptosis. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
008045	B6;129-Trp53tm2Holl/J	Repository- Live
	In this mutant strain, exons 4-9 of the endogenous mouse Trp53 gene have been replaced with the homologous human TRP53 region. Transcription of the human sequence is under the control of the endogenous mouse promoter. The inserted human sequence segment encodes the DNA binding domain and the TRP53 polyproline domain. This latter domain contains a polymorphism at codon 72 that encodes either arginine or proline in human populations. This mutant strain expresses the proline variant at codon 72 and the related strain, 129-Trp53tm1Holl/J (Stock No. 004301) expresses the arginine variant. Mice that are homozygous for this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immortalized cell lines derived from primary embryonic fibroblasts harvested from these mice frequently harbor a TRP53 (p53) mutation in the DNA binding domain t ..... For more information please see the full descriiption on the strain data sheet
006980	B6;129-Trp53tm2Xu/J	Repository- Live
	Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events in cancer development and apoptosis.
004301	129-Trp53tm1Holl/J	Repository-Cryopreserved
	In this mutant mouse strain, the endogenous murine sequence for exons 4-9 of the targeted gene, which encode the DNA binding domain of the tumor suppressor protein, have been replaced with the homologous normal human sequence. Transcription is under the control of the endogenous mouse promoter. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mutant mice exhibit normal expression and functional activity of the chimeric gene. Homozygous mutant mice have normal immunodetectable levels of p53 protein accumulation in nuclei in response to UV-induced DNA damage. Thymocytes from mutant mice are as susceptible to gamma-irradiation-induced and dexamethaxone-induced apoptosis as wildtype thymocytes. This mutant mouse strain may be useful in studies related to in vivo spontaneous and induced mutation of the human TRP53 gene sequence, and pharmacological agents for alt ..... For more information please see the full descriiption on the strain data sheet
002080	129-Trp53tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
008183	B6.129S4(Cg)-Trp53tm2.1Tyj/J	Repository-Cryopreserved
	Mice carrying this Trp53 (p53) R172H point mutation mimic human Li-Fraumeni Syndrome, both genotypically and phenotypically. Heterozygotes develop a broad spectrum of tumors with a mean survival time of 16 months. Prominent tumor types include osteosarcomas (often metastatic), hemangiosarcomas, B-cell lymphomas and a variety of carcinomas. Homozygous mice also develop a broad spectrum of tumors, particularly T-cell lymphomas, hemangiosarcomas, soft-tissue sarcomas, osteosarcomas, primitive tumors (particularly male teratocarcinomas), and a variety of epithelial carcinomas. Mutant protein is expressed at high levels in mouse embryonic fibroblasts, as determined by Western blotting.
008182	B6.129S4-Trp53tm3.1Tyj/J	Repository-Cryopreserved
	These targeted mutant mice carry a R270H missense mutation in exon 8 of the gene. Heterozygous mice develop a broad spectrum of tumors with a mean survival time of 16 months. Prominent tumor types include osteosarcomas (often metastatic), hemangiosarcomas, B-cell lymphomas and a variety of carcinomas. Homozygous mice also develop an array of tumor types including a variety of hematological tumors (particularly T-cell lymphomas), hemangiosarcomas, soft-tissue sarcomas, ostersarcomas, primitive tumors (particularly male teratocarcinomas), and a variety of epithelial carcinomas. Homozygotes have a mean survival time of 4.5 months. Mutant protein is expressed in all of the places that wildtype protein is expressed in normal tissues. Irradiation or DNA damage leads to substantially increased protein levels. Expression is also upregulated in some tumor types. This strain may be useful in studies of cancer and Li-Fraumeni Syndrome.
008191	B6;129S2-Trp53tm1Tyj Nf1tm1Tyj/J	Repository-Cryopreserved
	These mice carry Trp53 and Nf1 targeted mutations on the same chromosome (cis). Double homozygotes are embryonic lethal. Double heterozygotes survive an average of five months and exhibit a significant increase in the percentage of soft tissue sarcomas compared with mice of other genotypes (Nf1 +/-, 5%; p53, 57%; Nf1/Trp53 trans, 36%; Nf1/Trp53 cis, 81%). Furthermore, although Nf1/Trp53 trans mice exclusively develop osteo-, fibro-, rhabdomyo-, and hemangiosarcomas, about 30% of tumors from the Nf1/Trp53 cis animals stain positively for S100 (consistent with glial cell origin) and exhibit classic histological features of malignant peripheral nerve sheath tumors (MPNSTs). This strain may be useful in studies of astrocytomas/glioblastomas and tumor suppressor genes.
002103	B6;129S2-Trp53tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
008181	B6;129S4-Trp53tm4Tyj/J	Repository-Cryopreserved
	Mice homozygous for this S23A point mutation are viable and fertile. Cells from the mice, including thymocytes and neurons in the cerebellum, exhibit defective apoptosis in response to DNA damage and exhibit partially impaired TRP53 (p53) stabilization. Mice develop increased lymphomas (especially B-cell lineage) and other tumors between one and two years of age.
002526	C.129S2(B6)-Trp53tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
002547	C3Ou.129S2(B6)-Trp53tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
003446	C57BL/6J-Tg(Amy1TAg)501Knw/J	Repository-Cryopreserved
	C57BL/6-TgN(Amy1TAg)501Knw mice are viable and fertile. They express the SV40 tumor antigen under control of the liver promoter of the mouse alpha-amylase gene (Amy1a). This transgenic strain develops metastatic osteosarcomas at about 13 months of age. Note: This line, '501', contains the same trangene constuct as line '354' (Stock No. 003445). Divergent tumor development between these lines is reported to be a result of different transgene integration sites.
002899	FVB.129S2(B6)-Trp53tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors.
002659	FVB/N-Tg(Trp53R172H)8512Jmr/J	Repository-Cryopreserved
	The FVB/NTgN(Trp53R172H)8512Jmr express TRP53 with both dominant-negative and a gain-of function properties, i.e. this mutant is capable of inducing multiple drug resistance(MDR) promoter-driven reporter gene expression in transfection studies performed in p53 null cells. Transgene expression alone exerts no apparent effect on normal mammary gland development. Mice treated with the chemical carcinogen, dimethylbenz(a)anthracine (DMBA) or crossed with mice overexpressing erb-B2 develop tumors with significantly shorter latencies than controls. These tumors are characterized by large pleiomorphic nuclei and genomic instability. Spontaneous tumors are rarely observed in multiply bred animals in the first year of life.
002660	FVB/N-Tg(Trp53R172L)4491Jmr/J	Repository-Cryopreserved
	The FVB/N-TgN(Trp53R172L)4491Jmr express TRP53 with pseudo-wildtype properties capable of inducing p21 and mdm-2 expression. Lobuloalveolar development is altered and apoptosis is increased during late pregnancy. The few normal lobules observed during early lactation did not express the Trp53 transgene suggesting that they arose by clonal expansion of cells not expressing the transgene during mid-pregnancy. Transgenic mice fail to lactate. There is no apparent alteration in ductal development. Mice expressing a dominant negative 172Arg-His mutation do not exhibit any detectable alterations in mammary gland development and have a very low incidence of spontaneous mammary tumors. Mice bearing the 172Arg-Leu transgene and a pituitary isograft displayed a marked increase in apoptosis and a significant delay in DMBA-induced tumorigenesis, while those bearing the 172Arg-His dominant negative p53 transgene were more susceptible to DMBA-induced tumorigenesis.
003262	STOCK Tg(Trp53A135V)L3Ber/J	Repository-Cryopreserved
	Mice homozygous for the (Trp53A135V)2Ber transgene are viable and fertile, but show a high incidence of tumors, particularly lung adenocarcinomas, osteosarcomas, and lymphomas. This strain may serve as a model for Li-Fraumeni syndrome.

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New Strains Under Development

(See informational text following listing of strains)

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.

	Stock Number	Strain Name   Strain Description	Standard Supply
	007962	B6.FVB-Tg(MMTV-neu/OT-I/OT-II)CBnel Tg(Trp53R172H)8512Jmr/J	Under Development for Production
	These compound transgenic mice carry a rat Erbb2/HER-2/neu oncogene tagged with ovalbumin epitopes OT-I and OT-II, which are recognized by T cell receptors, under the control of the MMTV promoter (termed fusion protein neuOT-I/OT-II). In addition, this strain carries a mouse Trp53 mini-gene, harboring a G to A point mutation in codon 172 (changing Arg to His; R172H) driven by the rat whey acidic protein promoter. Approximately 85% of compound mutant females develop focal mammary tumors at 6-10 months of age. Both virgin and breeder mice develop tumors. Approximately 37% of tumor-bearing mice develop metastatic disease to the lung. High expression of neu is detected in tumor tissue while very low levels are found in lung and ovary. Female mice carrying only the neuOT-I/OT-II mutation develop focal mammary tumors at approximately 18 months of age. This strain may be useful in studies of cancer immunotherapy.
	008190	B6;129S2-Nf2tm1Tyj/J	Under Development for Production
	Most embryos that are homozygous for this targeted mutation fail between embryonic days 6.5 and 7.0, exhibiting a collapsed extraembryonic region and the absence of organized extraembryonic ectoderm. The embryo proper continues to develop, but fails to initiate gastrulation. Heterozygotes develop a variety of malignant tumors over the course of 10-30 months, including osteosarcoma (63%), lymphoma (15%), lung adenocarcinoma (10%), hepatocellular carcinoma (9%), and fibrosarcoma (9%). A high rate of metastasis to distant sites such as the lung and liver was found. Schwannomas, meningiomas and ependymomas were not detected. RT-PCR analysis and sequencing of the product have shown that a mutant form of mRNA is transcribed and spliced. Immunoblotting fails to detect any full-length or shortened protein products, however. This strain may be useful in studies of embryonic development and cancer.

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New Strains Under Development

• Receive periodic updates on the status of the colony UNDER DEVELOPMENT
• Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
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The 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.

1. Strains that will be made available from a live distribution colony at The Jackson Laboratory.
   These strains are designated as: "Under Development for Distribution Colony"
2. Strains that will be made available through the Cryopreservation Repository.
   These strains are designated as: "Under Development for Cryopreservation Repository"

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.

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