JAX
Mouse Strain Datasheet - 012620
STOCK Trp53tm1Brd Brca1tm1Aash Tg(LGB-cre)74Acl/J
Also Known As: BLG-Cre; Brca1F22-24; p53 KO, BLG-Cre; Brca1F22-24/F22-24; p53+/-
These mice carry the beta-lactoglobulin Cre (BLG-Cre) transgene, are homozygous for floxed exons 22-24 of the breast cancer 1 (Brca1) allele, and are heterozygous for p53 tumor-suppressor gene (Trp53) deficiency. This strain may be useful for studying human basal-like cancer and breast cancer, as well as providing a useful tool for testing new therapeutics.
Donating Investigator
Afshan McCarthy, The Breakthrough Toby Robins Breast Canc
Genetic overview
| Genetic Background | Generation |
|---|---|
|
F?+F18
(06-FEB-17) |
Brca1tm1Aash
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Targeted (Conditional ready (e.g. floxed), No functional change) | Brca1 | breast cancer 1, early onset |
Tg(LGB-cre)74Acl
| Allele Type |
|---|
| Transgenic (Recombinase-expressing) |
Trp53tm1Brd
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Targeted (Null/Knockout) | Trp53 | transformation related protein 53 |
Research Applications
- Cancer Research
- Endocrine Deficiency Research
- Neurobiology Research
- Research Tools
Base Price
Starting at:
| $254.90 Domestic price for female |
| $493.00 Domestic price for breeder pair |
Important Note
To induce the tumor development in these mice, the donating investigator reports that BLG-Cre; Brca1tm1Aash; Trp53+/- mice should be allowed to go through two rounds of pregnancy and then set aside to allow Cre activation and the loss of Brca1 function.
Detailed Description
BLG-Cre; Brca1tm1Aash; Trp53+/- mice that carry the beta-lactoglobulin Cre (BLG-Cre) transgene are homozygous for floxed exons 22-24 of the breast cancer 1 (Brca1) allele, and are heterozygous for p53 tumor-suppressor gene (Trp53) deficiency. Mice of this genotype are viable, fertile, normal in size and do not display any behavioral abnormalities. BLG-Cre; Brca1tm1Aash; Trp53+/- females have expression of the BLG-Cre transgene during lactation; which leads to loss of Brca1 function in the mammary gland. This results in formation of mammary tumors exhibiting high grade central necrosis and metaplastic elements in the form of spindle cell and squamous cell differentiation; as seen in human basal-like breast cancers and BRCA1 mutation carriers. Heterozygosity for the mutant p53 allele accelerates the formation of mammary tumors. This strain may be useful for studying human basal-like cancer and breast cancer, as well as providing a useful tool for testing new therapeutics.
Development
This mouse colony harbors three mutations: a p53- mutation, the Brca1F22-24 mutation, and a BLG-Cre transgene. The description of each is below.
To generate the p53 mutant allele, a targeting vector was designed to replace part of exon 5 of the mouse p53 tumor-suppressor gene, p53, with a PolII-neomycin (neo) resistance cassette (Harvey et al, Nat Gen, 1993; 5; 225-29). This construct was electroporated into 129S7/SvEvBrd-Hprt1+-derived AB1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts and the resulting chimeric males were bred to C57BL/6 females. These mice were intercrossed to establish a colony of p53 transgenic mice.
To generate the Brca1F22-24 mutant allele, a targeting vector was designed by Dr. Alan Ashworth (Breakthrough Breast Cancer Research Centre, London) to replace exons 22-24 of the mouse breast cancer 1 gene (Brca1) with a loxP site, a cDNA sequence encoded by exons 22-24, a 3' myc epitope, bovine growth hormone polyA signal, a second loxP site, a splice acceptor sequence, and a PGK-neo cassette. This construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-Kitl+-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts and the resulting chimeric mice were bred to C57BL/6 mice. These mice were intercrossed to establish a colony of Brca1F22-24/F22-24 mice on a mixed background.
The BLG-Cre transgene was designed by Dr. Alan R. Clarke (while at University Medical School, Edinburgh, United Kingdom) to have Cre recombinase under the control of the sheep mammary gland specific promoter of the ovine beta-lactoglobulin (BLG) gene. The construct included exon 1 of sheep BLG, and a Cre recombinase with a modified initiation codon and a polyadenylation signal (polyA). The construct was microinjected into the pronuclei of (CBA x C57BL/6) fertilized oocytes, and mice from founder line 74 were identified and bred to C57BL/6 mice. These mice were intercrossed to establish a colony of BLG-cre mice on a mixed background.
Mutant mice were bred together to generate the triple mutant colony. Mice heterozygous for the p53 allele, homozygous for the floxed Brca1 allele (Brca1F22-24/F22-24), and hemizygous for the BLG-cre transgene (also called BLG-Cre; Brca1F22-24/F22-24; p53+/- mice) were maintained on a mixed genetic background prior to sending to The Jackson Laboratory Repository. Upon arrival, mice were bred to C57BL/6J inbred mice (Stock No. 000664) for at least one generation to establish the colony.
Expression Data
| Expressed Gene | cre, cre recombinase, bacteriophage P1 |
|---|---|
| Site of Expression | Cre recombinase is active in the mammary gland. |
| Site of Expression | Normal Trp53 expression is widespread. |
Control Suggestions
Selected References
- McCarthy A; Savage K; Gabriel A; Naceur C; Reis-Filho JS; Ashworth A. 2007. A mouse model of basal-like breast carcinoma with metaplastic elements. J Pathol 211(4):389-98. PubMed: 17212342MGI: J:119996
Brca1tm1Aash
Allele Symbol: Brca1tm1Aash
| Allele Name | targeted mutation 1, Alan Ashworth |
|---|---|
| Allele Type | Targeted (Conditional ready (e.g. floxed), No functional change) |
| Allele Synonym(s) | Brca1F22-24 |
| Gene Symbol and Name | Brca1, breast cancer 1, early onset |
| Gene Synonym(s) | BRCAI; BRCC1; BROVCA1; FANCS; IRIS; PNCA4; PPP1R53; PSCP; RNF53 |
| Site of Expression | mammary epithelial cells |
| Strain of Origin | (129X1/SvJ x 129S1/Sv)F1-Kitl<+> |
| Chromosome | 11 |
| Molecular Note | Exons 22-24 were replaced with a floxed sequence containing cDNA for exons 22-24 with an in frame myc epitope and a bovine growth hormone poly A sequence. This vector allows conditional excision of the second, terminal BRCT domain. Downstream of the floxed sequence, a splice acceptor and PGK-neo were inserted. |
| Mutations Made By | Alan Ashworth, The Breakthrough Toby Robins Breast canc |
Tg(LGB-cre)74Acl
Allele Symbol: Tg(LGB-cre)74Acl
| Allele Name | transgene insertion 74, Alan R Clarke |
|---|---|
| Allele Type | Transgenic (Recombinase-expressing) |
| Allele Synonym(s) | BLG-Cre; Blg-CreTg |
| Gene Symbol and Name | Tg(LGB-cre)74Acl, transgene insertion 74, Alan R Clarke |
| Gene Synonym(s) | BLG-Cre; Blg-CreTg |
| Promoter | LGB, beta-lactoglobulin, sheep |
| Expressed Gene | cre, cre recombinase, bacteriophage P1 |
| Site of Expression | Cre recombinase is active in the mammary gland. |
| Strain of Origin | (CBA x C57BL/6) |
| Chromosome | UN |
| Molecular Note | This transgene expresses Cre recombinase under the control of a sheep beta-lactoglobulin promoter (LGB), active in the mammary gland. |
| Mutations Made By | Alan Clarke, University Medical School, Edinburgh, Un |
Trp53tm1Brd
Allele Symbol: Trp53tm1Brd
| Allele Name | targeted mutation 1, Allan Bradley |
|---|---|
| Allele Type | Targeted (Null/Knockout) |
| Allele Synonym(s) | P-; TSG-p53; Trp53-; Trp53N; Trp53delta; p53-; p53N |
| Gene Symbol and Name | Trp53, transformation related protein 53 |
| Gene Synonym(s) | BCC7; LFS1; P53; TRP53; p44; p53 |
| Site of Expression | Normal Trp53 expression is widespread. |
| Strain of Origin | 129S7/SvEvBrd-Hprt<+> |
| Chromosome | 11 |
| Molecular Note | A PolII-neomycin resistance cassette which lacked a polyadenylation signal was inserted into exon 5 of the gene. The insertion was accompanied by a small deletion of a 450 bp fragment containing 106 nucleotides of exon 5 and 350 nucleotides of intron 4. |
Disease Terms
Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
- Adrenocortical Carcinoma, Hereditary; ADCC (TP53)
- Basal Cell Carcinoma, Susceptibility to, 7; BCC7 (TP53)
- Breast Cancer (BRCA1, TP53)
- Breast-Ovarian Cancer, Familial, Susceptibility to, 1; BROVCA1 (BRCA1)
- Colorectal Cancer; CRC (TP53)
- Glioma Susceptibility 1; GLM1 (TP53)
- Hepatocellular Carcinoma (TP53)
- Li-Fraumeni Syndrome 1; LFS1 (TP53)
- Nasopharyngeal Carcinoma (TP53)
- Osteogenic Sarcoma (TP53)
- Pancreatic Cancer (TP53)
- Pancreatic Cancer, Susceptibility to, 4; PNCA4 (BRCA1)
- Papilloma of Choroid Plexus; CPP (TP53)
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Cancer Research
- Increased Tumor Incidence
- Mammary Gland Tumors
- Mammary Gland Tumors: females only
- Other
- tumor metastasis
- Increased Tumor Incidence
- Endocrine Deficiency Research
- Mammary Gland Defects
- Neurobiology Research
- Cre-lox System
- loxP-flanked Sequences
- Cre-lox System
- Research Tools
- Cre-lox System
- Cre Recombinase Expression
- Developmental Biology Research
- Cre-lox System
- Genetics Research
- Mutagenesis and Transgenesis
- Mutagenesis and Transgenesis: Cre-lox System
- Reproductive Biology Research
- Cre-lox System
- Cre-lox System
Genotype: cre related
- Research Tools
- Cre-lox System
- Genetics Research
- Mutagenesis and Transgenesis
- Mutagenesis and Transgenesis: Cre-lox System
Mammalian Phenotype Terms by Genotype
Genotype: Brca1tm1Aash/Brca1tm1Aash Trp53tm1Brd/Trp53+ Tg(LGB-cre)74Acl/0
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 * CBA
digestive/alimentary phenotype
- increased salivary adenocarcinoma incidence
- some (2/59) develop salivary gland malignant myoepithelial tumors (MGI Ref ID J:119996)
neoplasm
- increased mammary gland ductal carcinoma incidence
- high grade ductal carcinoma in situ (DCIS) is observed admixed with, or adjacent to, the invasive tumor in some cases, and occasionally columnar cell lesions with cytological atypia are seen with those tumors; columnar cell changes are found in adjacent tissue in a few tumorsissue in a few tumors (MGI Ref ID J:119996)
- increased mammary gland tumor incidence
- majority of tumors (30/33) show marked nuclear pleomorphism; central necrosis is seen in about 67% of tumors (23/32) (MGI Ref ID J:119996)
- mice develop mammary gland tumors with higher frequency (64%; 25/39 animals) and shorter latency of 6-46 weeks (all but one tumor had developed by 31 weeks) relative to control mice; 6/39 mice had multiple tumors in the same and in adjacent glands (MGI Ref ID J:119996)
- most (29/33) neoplasms show mixed pushing and infiltrative borders, while only 4/33 showed a prominent inflammatory infiltrate (MGI Ref ID J:119996)
- most (29/33) tumors show homologous metaplastic elements in form of squamous or spindly differentiation (MGI Ref ID J:119996)
- tumors develop in the inguinal and thoracic glands with equal frequency, and on both sides of the body (MGI Ref ID J:119996)
- increased salivary adenocarcinoma incidence
- some (2/59) develop salivary gland malignant myoepithelial tumors (MGI Ref ID J:119996)
endocrine/exocrine gland phenotype
- abnormal mammary gland development
- only 2/33 tumors show beta-catenin upregulation that was restricted to areas of squamous differentiation and basaloid cells (MGI Ref ID J:119996)
- increased mammary gland ductal carcinoma incidence
- high grade ductal carcinoma in situ (DCIS) is observed admixed with, or adjacent to, the invasive tumor in some cases, and occasionally columnar cell lesions with cytological atypia are seen with those tumors; columnar cell changes are found in adjacent tissue in a few tumorsissue in a few tumors (MGI Ref ID J:119996)
- increased mammary gland tumor incidence
- majority of tumors (30/33) show marked nuclear pleomorphism; central necrosis is seen in about 67% of tumors (23/32) (MGI Ref ID J:119996)
- mice develop mammary gland tumors with higher frequency (64%; 25/39 animals) and shorter latency of 6-46 weeks (all but one tumor had developed by 31 weeks) relative to control mice; 6/39 mice had multiple tumors in the same and in adjacent glands (MGI Ref ID J:119996)
- most (29/33) neoplasms show mixed pushing and infiltrative borders, while only 4/33 showed a prominent inflammatory infiltrate (MGI Ref ID J:119996)
- most (29/33) tumors show homologous metaplastic elements in form of squamous or spindly differentiation (MGI Ref ID J:119996)
- tumors develop in the inguinal and thoracic glands with equal frequency, and on both sides of the body (MGI Ref ID J:119996)
- increased salivary adenocarcinoma incidence
- some (2/59) develop salivary gland malignant myoepithelial tumors (MGI Ref ID J:119996)
integument phenotype
- abnormal mammary gland development
- only 2/33 tumors show beta-catenin upregulation that was restricted to areas of squamous differentiation and basaloid cells (MGI Ref ID J:119996)
- increased mammary gland ductal carcinoma incidence
- high grade ductal carcinoma in situ (DCIS) is observed admixed with, or adjacent to, the invasive tumor in some cases, and occasionally columnar cell lesions with cytological atypia are seen with those tumors; columnar cell changes are found in adjacent tissue in a few tumorsissue in a few tumors (MGI Ref ID J:119996)
- increased mammary gland tumor incidence
- majority of tumors (30/33) show marked nuclear pleomorphism; central necrosis is seen in about 67% of tumors (23/32) (MGI Ref ID J:119996)
- mice develop mammary gland tumors with higher frequency (64%; 25/39 animals) and shorter latency of 6-46 weeks (all but one tumor had developed by 31 weeks) relative to control mice; 6/39 mice had multiple tumors in the same and in adjacent glands (MGI Ref ID J:119996)
- most (29/33) neoplasms show mixed pushing and infiltrative borders, while only 4/33 showed a prominent inflammatory infiltrate (MGI Ref ID J:119996)
- most (29/33) tumors show homologous metaplastic elements in form of squamous or spindly differentiation (MGI Ref ID J:119996)
- tumors develop in the inguinal and thoracic glands with equal frequency, and on both sides of the body (MGI Ref ID J:119996)
References
- McCarthy A; Savage K; Gabriel A; Naceur C; Reis-Filho JS; Ashworth A. 2007. A mouse model of basal-like breast carcinoma with metaplastic elements. J Pathol 211(4):389-98. PubMed: 17212342MGI: J:119996
Additional - Brca1tm1Aash related
- Huang HS; Chu SC; Hsu CF; Chen PC; Ding DC; Chang MY; Chu TY. 2015. Mutagenic, surviving and tumorigenic effects of follicular fluid in the context of p53 loss: initiation of fimbria carcinogenesis. Carcinogenesis 36(11):1419-28. PubMed: 26363031MGI: J:226629
- Mgbemena VE; Signer RA; Wijayatunge R; Laxson T; Morrison SJ; Ross TS. 2017. Distinct Brca1 Mutations Differentially Reduce Hematopoietic Stem Cell Function. Cell Rep 18(4):947-960. PubMed: 28122244MGI: J:240315
- Molyneux G; Geyer FC; Magnay FA; McCarthy A; Kendrick H; Natrajan R; Mackay A; Grigoriadis A; Tutt A; Ashworth A; Reis-Filho JS; Smalley MJ. 2010. BRCA1 basal-like breast cancers originate from luminal epithelial progenitors and not from basal stem cells. Cell Stem Cell 7(3):403-17. PubMed: 20804975MGI: J:164435
- Vasanthakumar A; Arnovitz S; Marquez R; Lepore J; Rafidi G; Asom A; Weatherly M; Davis EM; Neistadt B; Duszynski R; Vardiman JW; Le Beau MM; Godley LA; Churpek JE. 2016. Brca1 deficiency causes bone marrow failure and spontaneous hematologic malignancies in mice. Blood 127(3):310-3. PubMed: 26644450MGI: J:231547
- Zhang Z; Christin JR; Wang C; Ge K; Oktay MH; Guo W. 2016. Mammary-Stem-Cell-Based Somatic Mouse Models Reveal Breast Cancer Drivers Causing Cell Fate Dysregulation. Cell Rep 16(12):3146-56. PubMed: 27653681MGI: J:239126
Additional - Trp53tm1Brd related
- Adam J; Deans B; Thacker J. 2007. A role for Xrcc2 in the early stages of mouse development. DNA Repair (Amst) 6(2):224-34. PubMed: 17116431MGI: J:120961
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- Akhtar RS; Geng Y; Klocke BJ; Roth KA. 2006. Neural precursor cells possess multiple p53-dependent apoptotic pathways. Cell Death Differ 13(10):1727-39. PubMed: 16514420MGI: J:126291
- Akli S; Van Pelt CS; Bui T; Meijer L; Keyomarsi K. 2011. Cdk2 is Required for Breast Cancer Mediated by the Low-Molecular-Weight Isoform of Cyclin E. Cancer Res 71(9):3377-86. PubMed: 21385896MGI: J:171726
- Akli S; Van Pelt CS; Bui T; Multani AS; Chang S; Johnson D; Tucker S; Keyomarsi K. 2007. Overexpression of the low molecular weight cyclin E in transgenic mice induces metastatic mammary carcinomas through the disruption of the ARF-p53 pathway. Cancer Res 67(15):7212-22. PubMed: 17671189MGI: J:123914
- Alexander BM; Van Kirk EA; Naughton LM; Murdoch WJ. 2007. Ovarian morphometrics in TP53-deficient mice. Anat Rec (Hoboken) 290(1):59-64. PubMed: 17441198MGI: J:174177
- Allen SM; Florell SR; Hanks AN; Alexander A; Diedrich MJ; Altieri DC; Grossman D. 2003. Survivin expression in mouse skin prevents papilloma regression and promotes chemical-induced tumor progression. Cancer Res 63(3):567-72. PubMed: 12566297MGI: J:81530
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- An JY; Kim EA; Jiang Y; Zakrzewska A; Kim DE; Lee MJ; Mook-Jung I; Zhang Y; Kwon YT. 2010. UBR2 mediates transcriptional silencing during spermatogenesis via histone ubiquitination. Proc Natl Acad Sci U S A 107(5):1912-7. PubMed: 20080676MGI: J:157596
- Antonini D; Russo MT; De Rosa L; Gorrese M; Del Vecchio L; Missero C. 2010. Transcriptional repression of miR-34 family contributes to p63-mediated cell cycle progression in epidermal cells. J Invest Dermatol 130(5):1249-57. PubMed: 20090763MGI: J:159929
- Armata HL; Garlick DS; Sluss HK. 2007. The ataxia telangiectasia-mutated target site Ser18 is required for p53-mediated tumor suppression. Cancer Res 67(24):11696-703. PubMed: 18089799MGI: J:130855
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- Balboni AL; Hutchinson JA; DeCastro AJ; Cherukuri P; Liby K; Sporn MB; Schwartz GN; Wells WA; Sempere LF; Yu PB; DiRenzo J. 2013. DeltaNp63alpha-mediated activation of bone morphogenetic protein signaling governs stem cell activity and plasticity in normal and malignant mammary epithelial cells. Cancer Res 73(2):1020-30. PubMed: 23243027MGI: J:194364
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- Baxter EW; Blyth K; Donehower LA; Cameron ER; Onions DE; Neil JC. 1996. Moloney murine leukemia virus-induced lymphomas in p53-deficient mice: overlapping pathways in tumor development? J Virol 70(4):2095-100. PubMed: 8642629MGI: J:93778
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- Behesti H; Bhagat H; Dubuc AM; Taylor MD; Marino S. 2013. Bmi1 overexpression in the cerebellar granule cell lineage of mice affects cell proliferation and survival without initiating medulloblastoma formation. Dis Model Mech 6(1):49-63. PubMed: 23065639MGI: J:193730
- Berton TR; Mitchell DL; Guo R; Johnson DG. 2005. Regulation of epidermal apoptosis and DNA repair by E2F1 in response to ultraviolet B radiation. Oncogene 24(15):2449-60. PubMed: 15735727MGI: J:97525
- Bhandoola A; Dolnick B; Fayad N; Nussenzweig A; Singer A. 2000. Immature thymocytes undergoing receptor rearrangements are resistant to an Atm-dependent death pathway activated in mature T cells by double-stranded DNA breaks. J Exp Med 192(6):891-7. PubMed: 10993919MGI: J:112013
- Bianchetta MJ; Lam TT; Jones SN; Morabito MA. 2011. Cyclin-dependent kinase 5 regulates PSD-95 ubiquitination in neurons. J Neurosci 31(33):12029-35. PubMed: 21849563MGI: J:176050
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