About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Trp53tm1Brd
targeted mutation 1, Allan Bradley
MGI:1857590
Summary 111 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Trp53tm1Brd/Trp53tm1Brd involves: 129S7/SvEvBrd MGI:2167491
hm2
Trp53tm1Brd/Trp53tm1Brd involves: 129S7/SvEvBrd * C57BL/6 MGI:2174779
hm3
Trp53tm1Brd/Trp53tm1Brd NIHOla.129S7-Trp53tm1Brd MGI:3774769
ht4
Trp53tm1Brd/Trp53+ involves: 129S7/SvEvBrd MGI:3689564
ht5
Trp53tm1Brd/Trp53+ involves: 129S7/SvEvBrd * C57BL/6 MGI:2174780
ht6
Trp53tm1Brd/Trp53tm8Xu involves: 129S7/SvEvBrd MGI:4946295
ht7
Trp53tm1Brd/Trp53tm1Ldo involves: 129S7/SvEvBrd * C57BL/6 MGI:3814538
cn8
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brd/Trp53+
Tg(Rbp3-cre)1Brn/0
involves: 129 * 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:2653661
cn9
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brd/Trp53tm1Brd
Tg(Gfap-cre)2Brn/0
involves: 129 * 129S7/SvEvBrd * FVB/N MGI:3804216
cn10
Smim3tm1Anjm/Smim3+
Cd74tm1Anjm/Cd74+
Lmo2tm2(cre)Thr/Lmo2+
Trp53tm1Brd/Trp53tm1Brd
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4421780
cn11
Smim3tm1Anjm/Smim3+
Cd74tm1Anjm/Cd74+
Lmo2tm2(cre)Thr/Lmo2+
Trp53tm1Brd/Trp53+
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4421779
cn12
Nbntm2Zqw/Nbntm2Zqw
Trp53tm1Brd/Trp53+
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA MGI:3579668
cn13
Nbntm2Zqw/Nbntm2Zqw
Trp53tm1Brd/Trp53tm1Brd
Tg(Nes-cre)1Wme/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA MGI:3579669
cn14
Brca2tm1Mak/Brca2tm2Mak
Trp53tm1Brd/Trp53tm1Brd
Tg(Lck-cre)548Jxm/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA MGI:3831545
cn15
Rev3ltm1Rwd/Rev3ltm2.1Rwd
Trp53tm1Brd/Trp53tm1Brd
Tg(MMTV-cre)1Mam/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:4441274
cn16
Rev3ltm1Rwd/Rev3ltm2.1Rwd
Trp53tm1Brd/Trp53+
Tg(MMTV-cre)1Mam/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:4441276
cn17
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brd/Trp53+
Tg(Mpz-cre)3Brn/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N MGI:3850409
cn18
Nf2tm2Gth/Nf2+
Trp53tm1Brd/Trp53+
Tg(Mpz-cre)3Brn/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N MGI:3850410
cn19
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brd/Trp53+
Tg(Mpz-cre)2Brn/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N MGI:3850407
cn20
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brd/Trp53tm1Brd
Tg(Mpz-cre)2Brn/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N MGI:3850408
cn21
Brca1tm2Mak/Brca1tm2Mak
Tg(Lck-cre)548Jxm/?
Trp53tm1Brd/Trp53tm1Brd
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3834730
cn22
Brca1tm2Mak/Brca1tm2Mak
Trp53tm1Brd/Trp53tm1Brd
Tg(Wap-cre)11738Mam/?
involves: 129P2/OlaHsd * C57BL/6 * CBA * SJL MGI:3834738
cn23
Brca1tm2Mak/Brca1tm2Mak
Trp53tm1Brd/Trp53+
Tg(Wap-cre)11738Mam/?
involves: 129P2/OlaHsd * C57BL/6 * CBA * SJL MGI:3834737
cn24
Brca1tm1Aash/Brca1tm1Aash
Trp53tm1Brd/Trp53+
Tg(LGB-cre)74Acl/0
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 * CBA MGI:3710354
cn25
Krastm1Bbd/Kras+
Trp53tm1Brd/Trp53+
Tg(Cela1-tTA)#Eps/?
Tg(tetO-cre)3Jig/?
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * FVB/N MGI:5502432
cn26
Brca1tm2Cxd/Brca1tm2Cxd
Pkmtm1.1Mgvh/Pkmtm1.1Mgvh
Trp53tm1Brd/Trp53+
Tg(MMTV-cre)4Mam/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * 129S7/SvEvBrd * FVB/N MGI:5547937
cn27
Brca1tm1Cxd/Brca1tm2Cxd
Trp53tm1Brd/Trp53+
Tg(MMTV-cre)4Mam/0
involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB MGI:2176786
cn28
Brca1tm2Cxd/Brca1tm2Cxd
Tg(MMTV-cre)4Mam/0
Tg(MMTV-rtTA)1Lach/0
Tg(tetO-Esr1)#Paf/0
Trp53tm1Brd/Trp53+
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB MGI:5297135
cn29
Brca1tm2Cxd/Brca1tm2Cxd
Trp53tm1Brd/Trp53+
Tg(MMTV-cre)4Mam/0
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB MGI:5297134
cn30
Trp53tm1Brd/Trp53+
Xrcc4tm2.1Fwa/Xrcc4tm2Fwa
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * SJL MGI:3652715
cn31
Trp53tm1Brd/Trp53tm1Brd
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * SJL MGI:3652719
cn32
Trp53tm1Brd/Trp53tm1Brd
Xrcc4tm2.1Fwa/Xrcc4tm2Fwa
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * SJL MGI:3652717
cn33
Trp53tm1Brd/Trp53tm1Brd
Tg(Lck-cre)1Cwi/0
involves: 129S7/SvEvBrd MGI:4430745
cn34
Dicer1tm1Snj/Dicer1tm1Snj
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6 MGI:3809304
cn35
Ptch1tm1Yy/Ptch1+
Trp53tm1Brd/Trp53+
Tg(BGLAP-cre)1Clem/0
involves: 129S7/SvEvBrd * C57BL/6 * FVB/NJ MGI:5781001
cn36
Tg(S100b-v-erbB)4496Waw/0
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6J * DBA/2J MGI:5762620
cx37
Nf1tm1Fcr/Nf1+
Trp53tm1Brd/Trp53+
B6.129-Trp53tm1Brd Nf1tm1Fcr MGI:5485355
cx38
Sirt1tm1.1Cxd/Sirt1+
Trp53tm1Brd/Trp53+
either: (involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB/N) or (involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N) MGI:3812172
cx39
Sirt1tm1.1Cxd/Sirt1tm1.1Cxd
Trp53tm1Brd/Trp53tm1Brd
either: (involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB/N) or (involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N) MGI:3812167
cx40
Sirt1tm1.1Cxd/Sirt1tm1.1Cxd
Trp53tm1Brd/Trp53+
either: (involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB/N) or (involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N) MGI:3812169
cx41
Trp53tm1Brd/Trp53tm1Brd
Wrntm1Led/Wrntm1Led
either: (involves: 129S/SvEv) or (involves: 129S/SvEv * NIH Black Swiss) MGI:2383960
cx42
Ing2tm1.1Ccha/Ing2tm1.1Ccha
Trp53tm1Brd/Trp53tm1Brd
involves: 129 * 129S7/SvEvBrd * C57BL/6J * FVB/N MGI:4879099
cx43
Tg(NES-TVA)J12Ech/0
Trp53tm1Brd/Trp53+
involves: 129 * C57BL/6 * FVB/N MGI:3835348
cx44
Ppm1dtm1Lad/Ppm1dtm1Lad
Tg(IghMyc)22Bri/0
Trp53tm1Brd/Trp53+
involves: 129 * C57BL * FVB/N * SJL MGI:3710184
cx45
Bbc3tm1Gpz/Bbc3tm1Gpz
Trp53tm1Brd/Trp53tm8Xu
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:4946296
cx46
Shmt1Gt(AD0236)Wtsi/Shmt1Gt(AD0236)Wtsi
Trp53tm1Brd/Trp53tm1Brd
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:5426852
cx47
Kmt2atm1.1Mlc/Kmt2atm1.1Mlc
Trp53tm1Brd/Trp53tm1Brd
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:5317824
cx48
Trp53tm1Brd/Trp53tm1Brd
Trp73tm2Mak/Trp73tm2Mak
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J MGI:4442800
cx49
Psmb9tm1Stl/Psmb9tm1Stl
Trp53tm1Brd/Trp53tm1Brd
involves: 129P2/OlaHsd * C57BL/6 MGI:3512781
cx50
Kat8tm2Thl/Kat8+
Trp53tm1Brd/Trp53tm1Brd
involves: 129S1/Sv * 129S7/SvEvBrd MGI:3769387
cx51
Rnf168Gt(156B6)Cmhd/Rnf168Gt(156B6)Cmhd
Trp53tm1Brd/Trp53tm1Brd
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 MGI:5505906
cx52
Trp53tm1Brd/Trp53+
Trp53bp2tm1Cdlo/Trp53bp2+
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 MGI:3839867
cx53
Rnf168Gt(405F11)Cmhd/Rnf168Gt(405F11)Cmhd
Trp53tm1Brd/Trp53tm1Brd
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 MGI:5505905
cx54
Npm1tm1Ppp/Npm1tm1Ppp
Trp53tm1Brd/Trp53tm1Brd
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 MGI:3606865
cx55
Npm1tm1Ppp/Npm1tm1Ppp
Trp53tm1Brd/Trp53+
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 MGI:3606866
cx56
Npm1tm1Ppp/Npm1+
Trp53tm1Brd/Trp53tm1Brd
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 MGI:3606864
cx57
E2f1tm1Njd/E2f1tm1Njd
Trp53tm1Brd/Trp53tm1Brd
involves: 129S2/SvPas * 129S7/SvEvBrd * SKH1 MGI:3840839
cx58
Cdkn1btm1Mlf/Cdkn1btm1Mlf
Trp53tm1Brd/Trp53tm1Brd
involves: 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6J MGI:3037841
cx59
Ing1Gt(OST206270)Lex/Ing1Gt(OST206270)Lex
Trp53tm1Brd/Trp53tm1Brd
involves: 129S5/SvEvBrd * 129S7/SvEvBrd * C57BL/6 MGI:3700393
cx60
Lig4tm1Fwa/Lig4tm1Fwa
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd MGI:3656003
cx61
Lig4tm1Fwa/Lig4tm1Fwa
Trp53tm1Brd/Trp53+
involves: 129S6/SvEvTac * 129S7/SvEvBrd MGI:3656004
cx62
Brca1tm2.1Cxd/Brca1tm2.1Cxd
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd MGI:4360340
cx63
Brca1tm2.1Cxd/Brca1tm2.1Cxd
Trp53tm1Brd/Trp53+
involves: 129S6/SvEvTac * 129S7/SvEvBrd MGI:4360339
cx64
Brca1tm1Cxd/Brca1tm1Cxd
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd MGI:3640093
cx65
Rbbp6tm1Xya/Rbbp6tm1Xya
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd MGI:3711895
cx66
Brca1tm2.1Cxd/Brca1tm2.1Cxd
Trp53tm1Brd/Trp53+
involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB MGI:4360341
cx67
H2axtm1Fwa/H2axtm1Fwa
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 MGI:2673482
cx68
H2axtm1Fwa/H2ax+
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 MGI:2673488
cx69
Ndor1Tg(UBC-cre/ERT2)1Ejb/Ndor1+
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:6403623
cx70
Nelfbtm1.2Roli/Nelfbtm1.2Roli
Trp53tm1Brd/Trp53+
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:3846184
cx71
Nelfbtm1.2Roli/Nelfbtm1.2Roli
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:3846186
cx72
Sirt6tm2.2Cxd/Sirt6tm2.2Cxd
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd * FVB/N * NIH Black Swiss MGI:4867474
cx73
Chek1tm1Sje/Chek1tm1Sje
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd MGI:3588912
cx74
Dp(4D4Mit190-D4Mit51)1Aam/0
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd MGI:3714608
cx75
Glipr1tm1Tt/Glipr1tm1Tt
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd MGI:3807671
cx76
Dp(4D4Mit190-D4Mit51)1Aam/0
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd MGI:3714609
cx77
Glipr1tm1Tt/Glipr1+
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd MGI:3807670
cx78
Mdm2tm1Bay/Mdm2tm1Bay
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd MGI:2183195
cx79
Stk11tm1Mmt/Stk11+
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd * 129X1/SvJ MGI:3851992
cx80
Atf4tm1Jml/Atf4tm1Jml
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * 129X1/SvJ MGI:3757692
cx81
Stk11tm1Mmt/Stk11+
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * 129X1/SvJ MGI:3851991
cx82
Cdkn2atm1Cjs/Cdkn2atm1Cjs
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 * NIH/OlaHsd MGI:3774770
cx83
Tg(Th-MYCN)41Waw/0
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd * BALB/c * C57BL/6J * FVB/N MGI:5009554
cx84
Tg(KRT14-Birc5)19Gros/0
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd * C3H * C57BL/6 MGI:3840587
cx85
Tg(KRT14-Birc5)19Gros/0
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd * C3H * C57BL/6 * C57BL/6NCr MGI:3794729
cx86
Rag1tm1Mom/Rag1tm1Mom
Trp53tm1Brd/Trp53tm1Brd
Xrcc5tm1Dbr/Xrcc5tm1Dbr
involves: 129S7/SvEvBrd * C57BL MGI:3818748
cx87
Rag1tm1Mom/Rag1tm1Mom
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL MGI:3818749
cx88
Trp53tm1Brd/Trp53tm1Brd
Xrcc5tm1Dbr/Xrcc5tm1Dbr
involves: 129S7/SvEvBrd * C57BL MGI:3818751
cx89
Dicer1tm1Snj/Dicer1tm1Snj
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6 MGI:3809302
cx90
Rad51tm1Hst/Rad51tm1Hst
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6 MGI:3795437
cx91
Trp53tm1Brd/Trp53tm1Brd
Twsg1tm1.1Mboc/Twsg1tm1.1Mboc
involves: 129S7/SvEvBrd * C57BL/6 MGI:5056121
cx92
Tg(Mdm2)1Snj/0
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6 MGI:5604449
cx93
Nabp2tm1Schg/Nabp2tm1Schg
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6 MGI:5770583
cx94
Trp53tm1Brd/Trp53tm1Brd
Tg(KRT14-rtTA)208Jek/Y
Tg(tetO-KLF4)32831Rup/0
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6NTac * SJL MGI:3717875
cx95
Trp53tm1Brd/Trp53+
Tg(KRT14-rtTA)208Jek/0
Tg(tetO-KLF4)32831Rup/0
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6NTac * SJL MGI:3717876
cx96
Cdca8tm1Tatn/Cdca8tm1Tatn
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:3798037
cx97
Pinx1tm1.1Kplu/Pinx1+
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:5013960
cx98
Pinx1tm1.1Kplu/Pinx1+
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:5013961
cx99
H2axtm1Nus/H2axtm1Nus
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6J MGI:3040401
cx100
Rb1tm1Brd/Rb1+
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd * C57BL/6J MGI:3834167
cx101
H2axtm1Nus/H2ax+
Trp53tm1Brd/Trp53tm1Brd
involves: 129S7/SvEvBrd * C57BL/6J MGI:3040402
cx102
Tg(S100b-v-erbB)4496Waw/0
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd * C57BL/6J * DBA/2J * FVB/N MGI:3822323
cx103
Tg(MMTV-KLF4)1Rup/0
Trp53tm1Brd/Trp53+
involves: 129S7/SvEvBrd * C57BL/6NTac * FVB/NJ * SJL MGI:3717873
cx104
Trp53tm1Brd/Trp53+
Tg(Cryaa-NCOA6*)AD5Cve/0
involves: 129S7/SvEvBrd * FVB/N MGI:4837884
cx105
Trp53tm1Brd/Trp53tm1Brd
Tg(Cryaa-NCOA6*)AD5Cve/0
involves: 129S7/SvEvBrd * FVB/N MGI:4837885
cx106
Egfrwa2/Egfr+
Nf1tm1Fcr/Nf1+
Trp53tm1Brd/Trp53+
involves: 129S/SvEv * 129S7/SvEvBrd * C57BL/6 * C57BL/6JEi * C3H/HeSnJ MGI:5485354
cx107
Dcntm1Ioz/Dcn+
Trp53tm1Brd/Trp53tm1Brd
involves: 129/Sv * Black Swiss * C57BL/6 MGI:3574393
cx108
Dcntm1Ioz/Dcntm1Ioz
Trp53tm1Brd/Trp53tm1Brd
involves: 129/Sv * Black Swiss * C57BL/6 MGI:3574392
cx109
Cdkn1btm1Mlf/Cdkn1btm1Mlf
Trp53tm1Brd/Trp53tm1Brd
involves: C3H * C57BL/6J * NIH MGI:3037835
cx110
Pole4tm1(KOMP)Vlcg/Pole4tm1(KOMP)Vlcg
Trp53tm1Brd/Trp53+
involves: C57BL/6J * C57BL/6NTac MGI:6163836
cx111
Pole4tm1(KOMP)Vlcg/Pole4tm1(KOMP)Vlcg
Trp53tm1Brd/Trp53tm1Brd
involves: C57BL/6J * C57BL/6NTac MGI:6163840


Genotype
MGI:2167491
hm1
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• 1 of 42 tumors is a rhabdomyosarcoma

mortality/aging
• by day 7 after myocardial infarction, homozygotes have significantly better survival rate than wild-type
• 50% of mice are dead by 21-22 weeks
• associated with tumor formation

neoplasm
• develop fatal spontaneous tumors by 10 months of age (J:108183)
• about 80% of mice succumb to malignant lymphomas, chiefly thymic in origin
• 3 of 42 tumors are carcinomas
• 9% of all tumors seen in mice are sarcomas
• 1 of 42 tumors is an undifferentiated sarcoma
• 1 of 42 tumors is a rhabdomyosarcoma
• 2 of 42 tumors are osteosarcomas

skeleton
• 2 of 42 tumors are osteosarcomas

cellular
• after 14 weeks of selection with L-aspartic acid, N-(phosphonoacetyl) (PALA, an assay for gene amplification) homozygous MEFs develop resistance to up to 500uM PALA unlike wild-type cells which do not develop resistance
• retroviral transfection of homozygous MEFs with an activated ras allele produces obvious transformed cells that are able to form colonies in soft agar, unlike wild-type MEFs where the introduction of 2 activated oncogenes is needed for transformation (J:57882)
• the number of colonies produced in the soft agar assay is greater than in transfected homozygous Gadd45a null MEFs (J:57882)
• confluent 2nd passage renal medullary cells show reduced viability 16 hours after osmolality is increased above 640 mosmol/kg water by addition of urea of NaCl (J:110650)
• survival is less than wild-type when NaCl is added at 1040 or 1240 mosmol/kg water (J:110650)
• survival is less than wild-type when urea is added at 840 mosmol/kg water or above (J:110650)
• enhanced glycolysis in mouse embryonic fibroblasts (J:186159)
• MEFs fail to arrest after exposure to 6 Gy or 12 Gy irradiation (J:118244)
• more mouse embryonic fibroblasts are in the S-phase compared with wild-type cells (J:175018)
• mouse embryonic cells (MEFs) fail to arrest at G1 upon exposure to gamma radiation and the G1/S-phase checkpoint is defective in gamma-irradiated thymic cells (J:78491)
• mouse embryonic fibroblast cells fail to arrest in G1 following exposure to ionizing radiation as do wild-type cells (J:126186)
• following ionizing radiation no apoptosis is seen in homozygous MEFs unlike wild-type cells (J:57882)
• adriamycin-induced apoptosis is significantly reduced or absent at both low and high concentrations of adriamycin compared to wild-type cells (J:118244)
• mouse embryonic fibroblast cells fail to undergo apoptosis following exposure to ionizing radiation as do wild-type cells (J:126186)
• after exposure to 10-Gy ionizing radiation, 78.5% of CD4/CD8 double positive T cells survive compared to 45.5% in wild-type (J:118602)
• irradiated mouse embryonic fibroblasts exhibit fail to exhibit a reduction in S-phase populations compared with similarly treated wild-type cells (J:175018)
• unlike wild-type epidermal cells that show a reduction in proliferation 24 hours post ionizing radiation, mutant epidermal cells exhibit no reduction in proliferation (J:78491)
• mouse embryonic fibroblast cells fail to arrest in G1 or undergo apoptosis following exposure to ionizing radiation as do wild-type cells (J:126186)
• MEFs transfected with retrovirus encoding a puromycin resistance gene are resistant to adriamycin-induced apoptosis compared to transfected wild-type cells
• gamma-irradiation-induced apoptosis is virtually abrogated
• proliferation in the outer medullas of triple knockouts (J:110650)
• primary fibroblasts proliferated faster than wild-type or Ing1-null cells in culture (J:118602)
• low passage MEFs have a plating efficiency of about 1.6% compared to 0.005% in wild-type cells, 0.025% in Gadd45a null cells, 1.2% in Cdkn1a null cells, and up to 1.4% in Gadd45a Cdkn1a double null cells (J:57882)
• in mouse embryonic fibroblasts (J:175018)
• in mouse embryonic fibroblasts (J:186159)
• in mouse embryonic fibroblasts
• Ras-transfected mouse embryonic fibroblasts fail to exhibit senescence unlike similarly treated wild-type cells (J:175018)
• in mouse embryonic fibroblasts (J:186159)
• increased reactive oxygen species in mouse embryonic fibroblasts

cardiovascular system
• homozygotes exhibit a better survival rate than wild-type and have a lower incidence of left ventricular rupture despite comparable infarct size, heart rate, and mean arterial blood pressure
• exhibit a thicker infarct wall and show fewer numbers of apoptotic cells in the infarct area than in wild-type after myocardial infarction

homeostasis/metabolism
• homozygotes exhibit a better survival rate than wild-type and have a lower incidence of left ventricular rupture despite comparable infarct size, heart rate, and mean arterial blood pressure
• exhibit a thicker infarct wall and show fewer numbers of apoptotic cells in the infarct area than in wild-type after myocardial infarction

hematopoietic system
• CD4+/CD8+ thymocytes are resistant to Trp53-mediated death unlike wild-type cells
• gamma-irradiation-induced apoptosis is virtually abrogated

immune system
• CD4+/CD8+ thymocytes are resistant to Trp53-mediated death unlike wild-type cells
• gamma-irradiation-induced apoptosis is virtually abrogated

endocrine/exocrine glands
• CD4+/CD8+ thymocytes are resistant to Trp53-mediated death unlike wild-type cells
• gamma-irradiation-induced apoptosis is virtually abrogated




Genotype
MGI:2174779
hm2
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 6 of 35 die from unknown causes, with no tumors (J:1999)
• mice succumb to tumorigenesis by 8 months of age (J:126497)

neoplasm
• 26 of 35 (76%) develop a variety of neoplasms by 6 months of age (J:1999)
• tumor occurrence increases rapidly between 15 and 25 weeks of age (J:1999)
• spontaneously develop fatal tumors by 10 months of age (J:108183)
• most frequent tumors observed are malignant lymphomas that involve the thymus and other major visceral organs
• sarcomas are also frequently observed and include hemangiosarcoma, undifferentiated sarcomas and osteosarcoma (J:1999)
• in 8 of 26 mice (J:126497)

cellular
• the G2 to M check point is impaired after irradiation of mouse embryonic fibroblasts
• MEFs sensitized to apoptosis by E1A overexpression show very low levels of apoptosis induced by irradiation or chemical treatment compared to wild-type or Trp53tm1Wahl MEFs (J:108183)
• p53-dependent apoptosis following exposure to radiation is abolished (J:126497)
• E12.5 primary telencephalic cultures show resistance to AraC induced caspase 3 activation and neuronal cell death

nervous system
• E12.5 primary telencephalic cultures show resistance to AraC induced caspase 3 activation and neuronal cell death

skeleton

endocrine/exocrine glands




Genotype
MGI:3774769
hm3
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
NIHOla.129S7-Trp53tm1Brd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Tumor multiplicity and proliferation index in Cdkn2atm1Cjs/Cdkn2atm1Cjs, Trp53tm1Brd/Trp53tm1Brd and Cdkn2atm1Cjs/Cdkn2atm1Cjs Trp53tm1Brd/Trp53tm1Brd mice

neoplasm
• mutants develop fewer and smaller induced tumors than wild-type or Cdkn2atm1Cjsmice, averaging 4 fewer papillomas 10-16 weeks after DMBA/TPA administration than wild-type
• mutants develop smaller induced tumors than wild-type after DMBA/TPA administration

homeostasis/metabolism
• mutants develop fewer and smaller induced tumors than wild-type or Cdkn2atm1Cjsmice, averaging 4 fewer papillomas 10-16 weeks after DMBA/TPA administration than wild-type




Genotype
MGI:3689564
ht4
Allelic
Composition
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by day 7 after myocardial infarction, heterozygotes have significantly better survival rate (80% vs. 69% in wild-type) than wild-type

cardiovascular system
• heterozygotes exhibit a better survival rate than wild-type and have a lower incidence of left ventricular rupture despite comparable infarct size, heart rate, and mean arterial blood pressure
• exhibit a thicker infarct wall and show fewer numbers of apoptotic cells in the infarct area than in wild-type after myocardial infarction

homeostasis/metabolism
• heterozygotes exhibit a better survival rate than wild-type and have a lower incidence of left ventricular rupture despite comparable infarct size, heart rate, and mean arterial blood pressure
• exhibit a thicker infarct wall and show fewer numbers of apoptotic cells in the infarct area than in wild-type after myocardial infarction




Genotype
MGI:2174780
ht5
Allelic
Composition
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• very mild increase in tumor incidence with 2 of 96 heterozygotes developing either embryonal carcinoma or malignant lymphoma (none seen in wild-type) (J:1999)
• 80% of mice develop life-threatening tumors compared to 45% of wild-type mice over their lifespan (J:73757)
• mice develop lymphomas, osterosarcomas, soft tissue sarcomas and carcinomas (J:73757)

nervous system
• E12.5 primary telencephalic cultures show a small resistance to AraC induced neuronal cell death relative to wild-type

cellular
• E12.5 primary telencephalic cultures show a small resistance to AraC induced neuronal cell death relative to wild-type

skeleton




Genotype
MGI:4946295
ht6
Allelic
Composition
Trp53tm1Brd/Trp53tm8Xu
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Trp53tm8Xu mutation (0 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by 6 weeks of age
• mice exhibit aging-related phenotypes including acute spine curvature, bone marrow hypoplasia, lymphopenia, and anemia unlike wild-type mice

reproductive system
• progressive
• the number of spermatogonial stem cells is depleted compared to in wild-type mice

hematopoietic system
• progressive
• by 2 weeks of age
• in the fetal liver and bone marrow

growth/size/body
• by 2 weeks of age
• by 4 weeks of age

nervous system

skeleton

digestive/alimentary system

endocrine/exocrine glands
• progressive

immune system
• by 2 weeks of age

cellular




Genotype
MGI:3814538
ht7
Allelic
Composition
Trp53tm1Brd/Trp53tm1Ldo
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Trp53tm1Ldo mutation (1 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive 9 to 10 months

neoplasm
• tumorigenesis is slightly delayed compared to in Trp53tm1Brd homozygotes but mice still exhibit an increase in the numbers of T-cell lymphomas and soft tissue sarcomas compared to in wild-type mice

endocrine/exocrine glands




Genotype
MGI:2653661
cn8
Allelic
Composition
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brd/Trp53+
Tg(Rbp3-cre)1Brn/0
Genetic
Background
involves: 129 * 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (106 available)
Tg(Rbp3-cre)1Brn mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• loss of heterozygosity of Trp53 in the neuroendocrine tumors
• develop pituitary gland and pineal gland tumors
• pinealoblastomas locally invade the brain




Genotype
MGI:3804216
cn9
Allelic
Composition
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brd/Trp53tm1Brd
Tg(Gfap-cre)2Brn/0
Genetic
Background
involves: 129 * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (106 available)
Tg(Gfap-cre)2Brn mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop highly aggressive embryonal tumors of the cerebellum with typical features of medulloblastoma
• tumors are identified as early as 7 weeks of age on the outer surface of the molecular layer, corresponding to the location of the cerebellar external granular layer cells during development

behavior/neurological
• loss of balance
• mutants hold their heads to one side
• gait is disturbed with ataxia

nervous system
• mutants develop highly aggressive embryonal tumors of the cerebellum with typical features of medulloblastoma
• tumors are identified as early as 7 weeks of age on the outer surface of the molecular layer, corresponding to the location of the cerebellar external granular layer cells during development

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:61961




Genotype
MGI:4421780
cn10
Allelic
Composition
Smim3tm1Anjm/Smim3+
Cd74tm1Anjm/Cd74+
Lmo2tm2(cre)Thr/Lmo2+
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd74tm1Anjm mutation (0 available); any Cd74 mutation (33 available)
Lmo2tm2(cre)Thr mutation (0 available); any Lmo2 mutation (31 available)
Smim3tm1Anjm mutation (0 available); any Smim3 mutation (9 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• absence of Trp53 expression completely rescues hematopoetic defects seen in mutant mice wild-type for Trp53

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
chromosome 5q deletion syndrome DOID:0090016 OMIM:153550
J:155870




Genotype
MGI:4421779
cn11
Allelic
Composition
Smim3tm1Anjm/Smim3+
Cd74tm1Anjm/Cd74+
Lmo2tm2(cre)Thr/Lmo2+
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd74tm1Anjm mutation (0 available); any Cd74 mutation (33 available)
Lmo2tm2(cre)Thr mutation (0 available); any Lmo2 mutation (31 available)
Smim3tm1Anjm mutation (0 available); any Smim3 mutation (9 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• a decrease in granulocyte/macrophage colony-forming units in bone marrow
• by flow cytometry, there is a reduction in granulocyte-monocyte progenitors in the bone marrow
• as measured by erythroid colony-forming units in bone marrow
• a reduced number of circulating red blood cells
• in bone marrow and spleen
• by flow cytometry, there is a reduction in megakaryocytic-erythroid progenitors in the bone marrow




Genotype
MGI:3579668
cn12
Allelic
Composition
Nbntm2Zqw/Nbntm2Zqw
Trp53tm1Brd/Trp53+
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nbntm2Zqw mutation (0 available); any Nbn mutation (59 available)
Tg(Nes-cre)1Wme mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• foliation structure is improved compared to mutants wild-type for Trp53
• a marginal increase in granule cell numbers is seen compared to mutants wild-type for Trp53

behavior/neurological
• performance on the balance beam test is improved compared to mutants wild-type for Trp53 but is impaired compared to controls and mutants that are homozygous null for Trp53




Genotype
MGI:3579669
cn13
Allelic
Composition
Nbntm2Zqw/Nbntm2Zqw
Trp53tm1Brd/Trp53tm1Brd
Tg(Nes-cre)1Wme/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nbntm2Zqw mutation (0 available); any Nbn mutation (59 available)
Tg(Nes-cre)1Wme mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• brain weight and cerebellar morphology are normal unlike in mutants with wild-type Trp53

behavior/neurological
N
• motor coordination defects seen in mutants with wild-type Trp53 are not seen in mutants that are homozygous null for Trp53

neoplasm
• similar to other Trp53 null mutations sarcomas and lymphomas are seen; however no cerebellar tumors have been detected




Genotype
MGI:3831545
cn14
Allelic
Composition
Brca2tm1Mak/Brca2tm2Mak
Trp53tm1Brd/Trp53tm1Brd
Tg(Lck-cre)548Jxm/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Mak mutation (0 available); any Brca2 mutation (132 available)
Brca2tm2Mak mutation (1 available); any Brca2 mutation (132 available)
Tg(Lck-cre)548Jxm mutation (2 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• proliferating T cells fail to exhibit the same increase in spontaneous apoptosis observed in Brca2tm1Mak/Brca2tm2Mak Tg(Lck-cre)548Jxm mice
• likely due to decreased apoptosis

neoplasm
• tumorigenesis is accelerated compared to in wild-type and Trp53tm1Brd/Trp53tm1Brd Tg(Lck-cre)548Jxm mice but not compared to in Trp53tm1Brd homozygotes
• 90% of mice succumb to T-cell lymphomas compared to 70% of Trp53tm1Brd/Trp53tm1Brd Tg(Lck-cre)548Jxm mice
• mice develop high grade malignancies

cellular
• T cells exhibit increased frequencies of chromatid or chromosomal breaks, tri-radial structures, and chromosomal fragments compared to in Brca2tm1Mak/Brca2tm2Mak Tg(Lck-cre)548Jxm mice or wild-type cells
• thymocytes are resistant to ionizing radiation-induced cell death unlike wild-type cells
• however, response to UV- or methyl methane sulfonate-induced cell death is normal

hematopoietic system
• likely due to decreased apoptosis

skeleton




Genotype
MGI:4441274
cn15
Allelic
Composition
Rev3ltm1Rwd/Rev3ltm2.1Rwd
Trp53tm1Brd/Trp53tm1Brd
Tg(MMTV-cre)1Mam/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rev3ltm1Rwd mutation (0 available); any Rev3l mutation (118 available)
Rev3ltm2.1Rwd mutation (2 available); any Rev3l mutation (118 available)
Tg(MMTV-cre)1Mam mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival is 91 days compared with 134 to 117 days for Trp53tm1Brd homozygous control mice

neoplasm
• in all mice develop thymic lymphomas compared with 70% to 77% of Trp53tm1Brd homozygous control mice
• tumors are frequently oligoclonal
• incidence of thymic lymphomas is increased while latency to development of tumors is decreased compared with Trp53tm1Brd homozygous control mice

endocrine/exocrine glands
• in all mice develop thymic lymphomas compared with 70% to 77% of Trp53tm1Brd homozygous control mice
• tumors are frequently oligoclonal
• incidence of thymic lymphomas is increased while latency to development of tumors is decreased compared with Trp53tm1Brd homozygous control mice




Genotype
MGI:4441276
cn16
Allelic
Composition
Rev3ltm1Rwd/Rev3ltm2.1Rwd
Trp53tm1Brd/Trp53+
Tg(MMTV-cre)1Mam/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rev3ltm1Rwd mutation (0 available); any Rev3l mutation (118 available)
Rev3ltm2.1Rwd mutation (2 available); any Rev3l mutation (118 available)
Tg(MMTV-cre)1Mam mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 11 of 36 mice develop mammary tumors consisting of solid carcinoma, carcinosarcoma, adenosquamous carcinoma, and osteosarcoma
• incidence of mammary tumors is increased while latency to development of tumors is decreased compared with Trp53tm1Brd heterozygotes
• in the mammary tissue of some mice
• in the mammary tissue of one mouse

integument
• 11 of 36 mice develop mammary tumors consisting of solid carcinoma, carcinosarcoma, adenosquamous carcinoma, and osteosarcoma
• incidence of mammary tumors is increased while latency to development of tumors is decreased compared with Trp53tm1Brd heterozygotes

skeleton
• in the mammary tissue of one mouse

endocrine/exocrine glands
• 11 of 36 mice develop mammary tumors consisting of solid carcinoma, carcinosarcoma, adenosquamous carcinoma, and osteosarcoma
• incidence of mammary tumors is increased while latency to development of tumors is decreased compared with Trp53tm1Brd heterozygotes




Genotype
MGI:3850409
cn17
Allelic
Composition
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brd/Trp53+
Tg(Mpz-cre)3Brn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf2tm2Gth mutation (3 available); any Nf2 mutation (65 available)
Tg(Mpz-cre)3Brn mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 4 of 12 mice die prematurely due to malignant peripheral nerve sheath tumors, 3 of which are 5 months old

neoplasm

nervous system




Genotype
MGI:3850410
cn18
Allelic
Composition
Nf2tm2Gth/Nf2+
Trp53tm1Brd/Trp53+
Tg(Mpz-cre)3Brn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf2tm2Gth mutation (3 available); any Nf2 mutation (65 available)
Tg(Mpz-cre)3Brn mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice exhibit a decrease in survival rate when the Nf2 and Trp53 alleles are carried in cis as opposed to trans, but live longer than conditional mutants carrying Tg(P0-Cre)2Gth

neoplasm
• between 3.5 and 13.5 months,19% of mice develop malignant peripheral nerve sheath tumors when the Nf2 and Trp53 alleles are carried in cis
• however, no tumors form in mice when the Nf2 and Trp53 alleles are carried in trans
• when the Nf2 and Trp53 alleles are carried in trans mice develop osteogenic tumors not restricted to neural crest-derived bone
• 81% of mice develop osteogenic (osteomas and osteosarcomas) tumors when the Nf2 and Trp53 alleles are carried in cis
• 81% of mice develop osteogenic (osteomas and osteosarcomas) tumors when the Nf2 and Trp53 alleles are carried in cis

skeleton
• when the Nf2 and Trp53 alleles are carried in trans mice develop osteogenic tumors not restricted to neural crest-derived bone
• 81% of mice develop osteogenic (osteomas and osteosarcomas) tumors when the Nf2 and Trp53 alleles are carried in cis
• 81% of mice develop osteogenic (osteomas and osteosarcomas) tumors when the Nf2 and Trp53 alleles are carried in cis

nervous system
• between 3.5 and 13.5 months,19% of mice develop malignant peripheral nerve sheath tumors when the Nf2 and Trp53 alleles are carried in cis
• however, no tumors form in mice when the Nf2 and Trp53 alleles are carried in trans




Genotype
MGI:3850407
cn19
Allelic
Composition
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brd/Trp53+
Tg(Mpz-cre)2Brn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf2tm2Gth mutation (3 available); any Nf2 mutation (65 available)
Tg(Mpz-cre)2Brn mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median age of death is 4.5 months

neoplasm
• 23% of mice develop osseous metaplasia
• one mouse developed lymphosarcoma
• in 8% of mice with metastasis to the liver
• 85% of mice develop peripheral nerve tumors
• 8% of mice develop neurofibroma
• 77% of mice develop peripheral nerve tumors from peripheral nerves of the limbs and from the dorsal root ganglia
• 11% of mice develop schwannoma

skeleton
• 35% of mice exhibit odontoblastic hyperplasia
• 15% of mice develop osteogenic hyperplasia

nervous system
• 85% of mice develop peripheral nerve tumors
• 8% of mice develop neurofibroma
• 77% of mice develop peripheral nerve tumors from peripheral nerves of the limbs and from the dorsal root ganglia
• 11% of mice develop schwannoma
• 81% of mice exhibit Schwann cell hyperplasia with increased incidence of diffuse Schwann cell hyperplasia in major peripheral nerve trunks

renal/urinary system
• 73% of mice exhibit renal tubular cell hyperplasia

vision/eye
• 85% of mice

craniofacial
• 35% of mice exhibit odontoblastic hyperplasia

growth/size/body
• 35% of mice exhibit odontoblastic hyperplasia

muscle
• in 8% of mice with metastasis to the liver




Genotype
MGI:3850408
cn20
Allelic
Composition
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brd/Trp53tm1Brd
Tg(Mpz-cre)2Brn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf2tm2Gth mutation (3 available); any Nf2 mutation (65 available)
Tg(Mpz-cre)2Brn mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die a few months of birth

neoplasm
• 38% of mice develop osseous metaplasia
• at 2 to 3.5 months, 25% of mice develop 4 sarcoma mainly in the ganglia
• at 2 to 3.5 months, 50% of mice develop 4 malignant peripheral nerve sheath tumors
• one mouse developed osteomas

skeleton
• one mouse developed osteomas
• 25% of mice develop osteogenic hyperplasia

nervous system
• at 2 to 3.5 months, 50% of mice develop 4 malignant peripheral nerve sheath tumors
• 38% of mice exhibit Schwann cell hyperplasia

renal/urinary system
• 63% of mice exhibit renal tubular cell hyperplasia

vision/eye
• 75% of mice

muscle




Genotype
MGI:3834730
cn21
Allelic
Composition
Brca1tm2Mak/Brca1tm2Mak
Tg(Lck-cre)548Jxm/?
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm2Mak mutation (1 available); any Brca1 mutation (113 available)
Tg(Lck-cre)548Jxm mutation (2 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• increased incidence
• reduced latency

mortality/aging
• most mice with thymic lymphomas are moribund or die by 3 months of age

cellular
• increased frequency of aberrations such as polyploidy, quadriradial chromosomes, and telomeric translocations

immune system
N
• thymus cellularity restored
• T cell numbers in lymph nodes are improved

neoplasm
• increased incidence
• reduced latency




Genotype
MGI:3834738
cn22
Allelic
Composition
Brca1tm2Mak/Brca1tm2Mak
Trp53tm1Brd/Trp53tm1Brd
Tg(Wap-cre)11738Mam/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm2Mak mutation (1 available); any Brca1 mutation (113 available)
Tg(Wap-cre)11738Mam mutation (3 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• usually succumb early to other tumors before developing mammary tumors




Genotype
MGI:3834737
cn23
Allelic
Composition
Brca1tm2Mak/Brca1tm2Mak
Trp53tm1Brd/Trp53+
Tg(Wap-cre)11738Mam/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm2Mak mutation (1 available); any Brca1 mutation (113 available)
Tg(Wap-cre)11738Mam mutation (3 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• about 80% develop acinar adenocarcenomas

integument
• about 80% develop acinar adenocarcenomas

endocrine/exocrine glands
• about 80% develop acinar adenocarcenomas




Genotype
MGI:3710354
cn24
Allelic
Composition
Brca1tm1Aash/Brca1tm1Aash
Trp53tm1Brd/Trp53+
Tg(LGB-cre)74Acl/0
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Aash mutation (3 available); any Brca1 mutation (113 available)
Tg(LGB-cre)74Acl mutation (2 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• some (2/59) develop salivary gland malignant myoepithelial tumors
• 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
• tumors develop in the inguinal and thoracic glands with equal frequency, and on both sides of the body
• majority of tumors (30/33) show marked nuclear pleomorphism; central necrosis is seen in about 67% of tumors (23/32)
• most (29/33) neoplasms show mixed pushing and infiltrative borders, while only 4/33 showed a prominent inflammatory infiltrate
• most (29/33) tumors show homologous metaplastic elements in form of squamous or spindly differentiation
• 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 tumors

endocrine/exocrine glands
• some (2/59) develop salivary gland malignant myoepithelial tumors
• only 2/33 tumors show beta-catenin upregulation that was restricted to areas of squamous differentiation and basaloid cells
• 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
• tumors develop in the inguinal and thoracic glands with equal frequency, and on both sides of the body
• majority of tumors (30/33) show marked nuclear pleomorphism; central necrosis is seen in about 67% of tumors (23/32)
• most (29/33) neoplasms show mixed pushing and infiltrative borders, while only 4/33 showed a prominent inflammatory infiltrate
• most (29/33) tumors show homologous metaplastic elements in form of squamous or spindly differentiation
• 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 tumors

integument
• only 2/33 tumors show beta-catenin upregulation that was restricted to areas of squamous differentiation and basaloid cells
• 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
• tumors develop in the inguinal and thoracic glands with equal frequency, and on both sides of the body
• majority of tumors (30/33) show marked nuclear pleomorphism; central necrosis is seen in about 67% of tumors (23/32)
• most (29/33) neoplasms show mixed pushing and infiltrative borders, while only 4/33 showed a prominent inflammatory infiltrate
• most (29/33) tumors show homologous metaplastic elements in form of squamous or spindly differentiation
• 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 tumors

digestive/alimentary system
• some (2/59) develop salivary gland malignant myoepithelial tumors




Genotype
MGI:5502432
cn25
Allelic
Composition
Krastm1Bbd/Kras+
Trp53tm1Brd/Trp53+
Tg(Cela1-tTA)#Eps/?
Tg(tetO-cre)3Jig/?
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm1Bbd mutation (2 available); any Kras mutation (76 available)
Tg(Cela1-tTA)#Eps mutation (0 available)
Tg(tetO-cre)3Jig mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% mortality by 6 months of age
• 100% mortality by 1 year of age

neoplasm
• all mice develop moderately to poorly differentiated pancreatic ductal adenocarcinomas, peritoneal explants, and perineural extensions
• metastases develop affecting liver, diaphragm, lungs, lymph nodes, and spleen

endocrine/exocrine glands
• all mice develop moderately to poorly differentiated pancreatic ductal adenocarcinomas, peritoneal explants, and perineural extensions

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:119988




Genotype
MGI:5547937
cn26
Allelic
Composition
Brca1tm2Cxd/Brca1tm2Cxd
Pkmtm1.1Mgvh/Pkmtm1.1Mgvh
Trp53tm1Brd/Trp53+
Tg(MMTV-cre)4Mam/0
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm2Cxd mutation (3 available); any Brca1 mutation (113 available)
Pkmtm1.1Mgvh mutation (2 available); any Pkm mutation (75 available)
Tg(MMTV-cre)4Mam mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• accelerated tumor associated mortality relative to control mice

neoplasm
• mice develop breast tumors similar to control mice
• liver metastases observed in 3/5 mice as compared to 0/7 relative to control mice
• liver metastases observed in 3/5 mice as compared to 0/7 relative to control mice

endocrine/exocrine glands
• mice develop breast tumors similar to control mice

integument
• mice develop breast tumors similar to control mice

liver/biliary system
• liver metastases observed in 3/5 mice as compared to 0/7 relative to control mice




Genotype
MGI:2176786
cn27
Allelic
Composition
Brca1tm1Cxd/Brca1tm2Cxd
Trp53tm1Brd/Trp53+
Tg(MMTV-cre)4Mam/0
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Cxd mutation (1 available); any Brca1 mutation (113 available)
Brca1tm2Cxd mutation (3 available); any Brca1 mutation (113 available)
Tg(MMTV-cre)4Mam mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• by 6-8 months of age, 8 of 11 females developed mammary gland tumors that exhibited several distinct histopathologies

endocrine/exocrine glands
• by 6-8 months of age, 8 of 11 females developed mammary gland tumors that exhibited several distinct histopathologies

integument
• by 6-8 months of age, 8 of 11 females developed mammary gland tumors that exhibited several distinct histopathologies




Genotype
MGI:5297135
cn28
Allelic
Composition
Brca1tm2Cxd/Brca1tm2Cxd
Tg(MMTV-cre)4Mam/0
Tg(MMTV-rtTA)1Lach/0
Tg(tetO-Esr1)#Paf/0
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm2Cxd mutation (3 available); any Brca1 mutation (113 available)
Tg(MMTV-cre)4Mam mutation (1 available)
Tg(MMTV-rtTA)1Lach mutation (0 available)
Tg(tetO-Esr1)#Paf mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop hyperplastic alveolar nodules
• 100% of mutants develop invasive mammary cancer
• some cancers are Esr1-negative while others are Esr1-positive

neoplasm
• 100% of mutants develop invasive mammary cancer
• some cancers are Esr1-negative while others are Esr1-positive
• mutants develop mammary gland preneoplasia
• some preneoplasia are Esr1-negative while others are Esr1-positive

integument
• mutants develop hyperplastic alveolar nodules
• 100% of mutants develop invasive mammary cancer
• some cancers are Esr1-negative while others are Esr1-positive

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
hereditary breast ovarian cancer syndrome DOID:5683 J:132088




Genotype
MGI:5297134
cn29
Allelic
Composition
Brca1tm2Cxd/Brca1tm2Cxd
Trp53tm1Brd/Trp53+
Tg(MMTV-cre)4Mam/0
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm2Cxd mutation (3 available); any Brca1 mutation (113 available)
Tg(MMTV-cre)4Mam mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants exhibit increased mammary epithelial cellular proliferation compared to controls when treated with exogenous estrogen
• mutants exposed to estrogen exhibit an increase in the number of hyperplastic alveolar nodules per mammary gland compared to mutants with wild-type Trp53 and also an increase in the percentage of mice with hyperplastic alveolar nodules
• 25% of mutants develop invasive mammary cancer when exposed to exogenous estrogen
• cancers are Esr1-negative

neoplasm
• 25% of mutants develop invasive mammary cancer when exposed to exogenous estrogen
• cancers are Esr1-negative
• mutants develop mammary gland preneoplasia that are Esr1-negative

renal/urinary system
• 25% of mutants develop ureteral obstruction 1-3 months after estrogen pellet placement

integument
• mutants exhibit increased mammary epithelial cellular proliferation compared to controls when treated with exogenous estrogen
• mutants exposed to estrogen exhibit an increase in the number of hyperplastic alveolar nodules per mammary gland compared to mutants with wild-type Trp53 and also an increase in the percentage of mice with hyperplastic alveolar nodules
• 25% of mutants develop invasive mammary cancer when exposed to exogenous estrogen
• cancers are Esr1-negative

cellular
• mutants exhibit increased mammary epithelial cellular proliferation compared to controls when treated with exogenous estrogen

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
hereditary breast ovarian cancer syndrome DOID:5683 J:132088




Genotype
MGI:3652715
cn30
Allelic
Composition
Trp53tm1Brd/Trp53+
Xrcc4tm2.1Fwa/Xrcc4tm2Fwa
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Xrcc4tm2.1Fwa mutation (0 available); any Xrcc4 mutation (25 available)
Xrcc4tm2Fwa mutation (0 available); any Xrcc4 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice survive beyond 16 months




Genotype
MGI:3652719
cn31
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% of mice are dead by 21-22 weeks

neoplasm
• solid tumors are common

endocrine/exocrine glands




Genotype
MGI:3652717
cn32
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Xrcc4tm2.1Fwa/Xrcc4tm2Fwa
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Xrcc4tm2.1Fwa mutation (0 available); any Xrcc4 mutation (25 available)
Xrcc4tm2Fwa mutation (0 available); any Xrcc4 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice become moribund between 12 and 14 weeks of age with 20/23 mice dead by 25 weeks

nervous system
• mice develop medulloblastomas
• mice at 4 and 8.5 weeks of age show multifocal tumor masses expanding from the granular layer
• at 12-14 weeks mice have aggressive medulloblastomas in the vermis or hemisphere

craniofacial
• at 12-14 weeks skulls of mice show rapid morphological enlargement

skeleton
• at 12-14 weeks skulls of mice show rapid morphological enlargement

neoplasm
• mice develop medulloblastomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:109585




Genotype
MGI:4430745
cn33
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Tg(Lck-cre)1Cwi/0
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Lck-cre)1Cwi mutation (3 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all die of thymic lymphomas by 50 weeks of age

neoplasm
• in all mice by 50 weeks of age

endocrine/exocrine glands
• in all mice by 50 weeks of age




Genotype
MGI:3809304
cn34
Allelic
Composition
Dicer1tm1Snj/Dicer1tm1Snj
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dicer1tm1Snj mutation (0 available); any Dicer1 mutation (94 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
N
• mouse embryonic fibroblasts treated with an adenovirus cre exhibit normal cellular senescence




Genotype
MGI:5781001
cn35
Allelic
Composition
Ptch1tm1Yy/Ptch1+
Trp53tm1Brd/Trp53+
Tg(BGLAP-cre)1Clem/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * FVB/NJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptch1tm1Yy mutation (0 available); any Ptch1 mutation (115 available)
Tg(BGLAP-cre)1Clem mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• lower body paralysis due to spine tumors

neoplasm
• occasionally, pulmonary metastasis is seen in the lungs
• mice develop bone tumors as early as 7 months of age, with incidence significantly increased at 11 months onwards with about 70% penetrance
• bone tumors are located mostly in the forelimbs and hindlimbs and frequently in the spine and are found less frequently in the ribs and skull
• primary tumors are composed of highly mineralized tissues and abundant osteoids with multinucleated cells resembling human osteoblastic osteosarcoma
• the majority of mutants develop only bone tumors

skeleton
• mice develop bone tumors as early as 7 months of age, with incidence significantly increased at 11 months onwards with about 70% penetrance
• bone tumors are located mostly in the forelimbs and hindlimbs and frequently in the spine and are found less frequently in the ribs and skull
• primary tumors are composed of highly mineralized tissues and abundant osteoids with multinucleated cells resembling human osteoblastic osteosarcoma
• the majority of mutants develop only bone tumors

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
osteosarcoma DOID:3347 OMIM:259500
J:214349




Genotype
MGI:5762620
cn36
Allelic
Composition
Tg(S100b-v-erbB)4496Waw/0
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J * DBA/2J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(S100b-v-erbB)4496Waw mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• marker analysis indicates that oligodendroglial progenitor cell-derived high grade glioma has proneural character
• in vivo radiation of the high grade glioma induces proneural-to-mesenchymal transition, increasing invasiveness and malignancy
• irradiated proneural high grade glioma cells undergoing proneural-to-mesenchymal transition show increased invasiveness and resistance to temozolomide treatment

nervous system
• marker analysis indicates that oligodendroglial progenitor cell-derived high grade glioma has proneural character
• in vivo radiation of the high grade glioma induces proneural-to-mesenchymal transition, increasing invasiveness and malignancy
• irradiated proneural high grade glioma cells undergoing proneural-to-mesenchymal transition show increased invasiveness and resistance to temozolomide treatment

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
high grade glioma DOID:3070 OMIM:PS137800
J:137800




Genotype
MGI:5485355
cx37
Allelic
Composition
Nf1tm1Fcr/Nf1+
Trp53tm1Brd/Trp53+
Genetic
Background
B6.129-Trp53tm1Brd Nf1tm1Fcr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Fcr mutation (3 available); any Nf1 mutation (157 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• develop sarcomas and brain tumors as early as 15 weeks of age

mortality/aging
• mice that develop malignant tumors die by 26 weeks of age

neoplasm
• 11 of 19 (57.9%) mice develop malignant tumors and die by 26 weeks of age
• develop sarcomas and brain tumors as early as 15 weeks of age
• develop sarcomas and brain tumors as early as 15 weeks of age




Genotype
MGI:3812172
cx38
Allelic
Composition
Sirt1tm1.1Cxd/Sirt1+
Trp53tm1Brd/Trp53+
Genetic
Background
either: (involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB/N) or (involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sirt1tm1.1Cxd mutation (0 available); any Sirt1 mutation (78 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tumors exhibit extensive aneuploidy and chromosomal aberrations, notably translocations, chromosome breaks, deletions and dicentric chromosomes
• mice begin to develop tumors at 5 months of age with tumor incidence reaching 76% by 20 months of age compared to only 2 of 21 Sirt1tm1.1Cxd heterozygotes and 3 of 23 Trp53tm1Brd heterozygotes
• however, treatment of mice with resveratrol decreases the incidence of tumors and delays onset
• 35% of tumors are lymphomas
• 16% of tumors are carcinomas
• 46% of tumors are sarcomas
• 22% of tumors are teratomas




Genotype
MGI:3812167
cx39
Allelic
Composition
Sirt1tm1.1Cxd/Sirt1tm1.1Cxd
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
either: (involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB/N) or (involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sirt1tm1.1Cxd mutation (0 available); any Sirt1 mutation (78 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• only one mouse survives birth
• no mice are alive at weaning
• fewer than expected mice are alive at E15.5




Genotype
MGI:3812169
cx40
Allelic
Composition
Sirt1tm1.1Cxd/Sirt1tm1.1Cxd
Trp53tm1Brd/Trp53+
Genetic
Background
either: (involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB/N) or (involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sirt1tm1.1Cxd mutation (0 available); any Sirt1 mutation (78 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 5 mice are alive at weaning
• fewer than expected mice survive to birth
• fewer than expected mice are alive at E15.5




Genotype
MGI:2383960
cx41
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Wrntm1Led/Wrntm1Led
Genetic
Background
either: (involves: 129S/SvEv) or (involves: 129S/SvEv * NIH Black Swiss)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Wrntm1Led mutation (0 available); any Wrn mutation (91 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 50% of mice by the age of 3 months developed tumors
• an acceleration of tumorigenesis, in comparison to Wrntm1Led homozygous mice




Genotype
MGI:4879099
cx42
Allelic
Composition
Ing2tm1.1Ccha/Ing2tm1.1Ccha
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129 * 129S7/SvEvBrd * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ing2tm1.1Ccha mutation (0 available); any Ing2 mutation (16 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Ing2tm1.1Ccha/Ing2tm1.1Ccha and Trp53tm1Brd/Trp53tm1Brd Ing2tm1.1Ccha/Ing2tm1.1Ccha mice exhibit increased testicular apoptosis and decreased testis weight

reproductive system
• hypospermia in epididymides
• reduced numbers of normal spermatozoa in semen
• degenerated large, round cells were accumulated in epididymis and semen
• less severe than those in Ing2tm1.1Ccha homozygous males
• degeneration of seminiferous tubules
• enhanced apoptosis
• reduced testis weight
• less severe than those in Ing2tm1.1Ccha homozygous males
• infertile in males

cellular
• hypospermia in epididymides
• reduced numbers of normal spermatozoa in semen
• degenerated large, round cells were accumulated in epididymis and semen
• less severe than those in Ing2tm1.1Ccha homozygous males
• increased numbers of TUNEL positive tubules and TUNEL-positive cells per tubule
• less severe than those in Ing2tm1.1Ccha homozygous males

endocrine/exocrine glands
• degeneration of seminiferous tubules
• enhanced apoptosis
• reduced testis weight
• less severe than those in Ing2tm1.1Ccha homozygous males




Genotype
MGI:3835348
cx43
Allelic
Composition
Tg(NES-TVA)J12Ech/0
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(NES-TVA)J12Ech mutation (2 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 3 of 8 mice transfected with replication-competent ALV splice acceptor viral vector expressing a constitutively active EGFR and Cdk4 develop gliomas compared to 1 of 8 similarly treated wild-type mice
• 17 of 39 mice transfected with replication-competent ALV splice acceptor viral vector expressing a constitutively active EGFR, Cdk4, and bFGF develop gliomas compared to 3 of 29 similarly treated wild-type mice
• however, mice transfected with replication-competent ALV splice acceptor viral vector expressing a constitutively active EGFR do not develop gliomas
• in mice transfected with replication-competent ALV splice acceptor viral vector expressing a constitutively active EGFR, Cdk4, and bFGF

neoplasm
• 3 of 8 mice transfected with replication-competent ALV splice acceptor viral vector expressing a constitutively active EGFR and Cdk4 develop gliomas compared to 1 of 8 similarly treated wild-type mice
• 17 of 39 mice transfected with replication-competent ALV splice acceptor viral vector expressing a constitutively active EGFR, Cdk4, and bFGF develop gliomas compared to 3 of 29 similarly treated wild-type mice
• however, mice transfected with replication-competent ALV splice acceptor viral vector expressing a constitutively active EGFR do not develop gliomas




Genotype
MGI:3710184
cx44
Allelic
Composition
Ppm1dtm1Lad/Ppm1dtm1Lad
Tg(IghMyc)22Bri/0
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129 * C57BL * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppm1dtm1Lad mutation (1 available); any Ppm1d mutation (28 available)
Tg(IghMyc)22Bri mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• the median lifespan of 31 days

neoplasm
• based on median survival time, mice carrying single Trp53tm1Brd allele were no more resistant to tumor formation induced by myc than mice with homozygous wild-type Ppm1d+ allele




Genotype
MGI:4946296
cx45
Allelic
Composition
Bbc3tm1Gpz/Bbc3tm1Gpz
Trp53tm1Brd/Trp53tm8Xu
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bbc3tm1Gpz mutation (0 available); any Bbc3 mutation (18 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Trp53tm8Xu mutation (0 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• the segmental progeria phenotypes observed in Trp53tm1Brd/Trp53tm8Xu mice are rescued
• mice survive longer than Trp53tm1Brd/Trp53tm8Xu mice

reproductive system
N
• testes atrophy observed in Trp53tm1Brd/Trp53tm8Xu mice is rescued
• depletion of adult stem cells in the testes observed in Trp53tm1Brd/Trp53tm8Xu mice is rescued

immune system
• not as severe as in Trp53tm1Brd/Trp53tm8Xu mice

nervous system
N
• depletion of adult stem cells in the brain observed in Trp53tm1Brd/Trp53tm8Xu mice is rescued

digestive/alimentary system
N
• apoptosis in the crypt of small intestine observed in Trp53tm1Brd/Trp53tm8Xu mice is rescued

hematopoietic system
N
• depletion of adult stem cells in the bone marrow observed in Trp53tm1Brd/Trp53tm8Xu mice is rescued
• not as severe as in Trp53tm1Brd/Trp53tm8Xu mice

endocrine/exocrine glands
• not as severe as in Trp53tm1Brd/Trp53tm8Xu mice




Genotype
MGI:5426852
cx46
Allelic
Composition
Shmt1Gt(AD0236)Wtsi/Shmt1Gt(AD0236)Wtsi
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Shmt1Gt(AD0236)Wtsi mutation (0 available); any Shmt1 mutation (43 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mice exhibit the same tumorigenesis as Trp53tm1Brd




Genotype
MGI:5317824
cx47
Allelic
Composition
Kmt2atm1.1Mlc/Kmt2atm1.1Mlc
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kmt2atm1.1Mlc mutation (0 available); any Kmt2a mutation (135 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
N
• early cellular replicative senescence observed in mouse embryonic fibroblasts is rescued




Genotype
MGI:4442800
cx48
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Trp73tm2Mak/Trp73tm2Mak
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Trp73tm2Mak mutation (2 available); any Trp73 mutation (42 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• the increased apoptosis in response to DNA damaging agents is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels

immune system
• the increased apoptosis in response to DNA damaging agents is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels

cellular
• the increased apoptosis in response to gamma-irradiation is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels
• the increased apoptosis in response to DNA damaging agents is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels

endocrine/exocrine glands
• the increased apoptosis in response to DNA damaging agents is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels




Genotype
MGI:3512781
cx49
Allelic
Composition
Psmb9tm1Stl/Psmb9tm1Stl
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Psmb9tm1Stl mutation (2 available); any Psmb9 mutation (22 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 89% of mice develop tumors
• somewhat decreased survival compared to singly homozygous Trp53tm1Brd
• with lesser frequency than lymphomas




Genotype
MGI:3769387
cx50
Allelic
Composition
Kat8tm2Thl/Kat8+
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kat8tm2Thl mutation (0 available); any Kat8 mutation (36 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die earlier than Trp53tm1Brdhomozygotes




Genotype
MGI:5505906
cx51
Allelic
Composition
Rnf168Gt(156B6)Cmhd/Rnf168Gt(156B6)Cmhd
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rnf168Gt(156B6)Cmhd mutation (0 available); any Rnf168 mutation (73 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice exhibit decreased tumor free survival compared with Trp53tm1Brd homozygotes




Genotype
MGI:3839867
cx52
Allelic
Composition
Trp53tm1Brd/Trp53+
Trp53bp2tm1Cdlo/Trp53bp2+
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53bp2tm1Cdlo mutation (0 available); any Trp53bp2 mutation (52 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• increased tumor incidence compared to wild-type controls but not compared to mice heterozygous for the Trp53 allele alone




Genotype
MGI:5505905
cx53
Allelic
Composition
Rnf168Gt(405F11)Cmhd/Rnf168Gt(405F11)Cmhd
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rnf168Gt(405F11)Cmhd mutation (0 available); any Rnf168 mutation (73 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice exhibit decreased tumor free survival compared with Trp53tm1Brd homozygotes




Genotype
MGI:3606865
cx54
Allelic
Composition
Npm1tm1Ppp/Npm1tm1Ppp
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Npm1tm1Ppp mutation (1 available); any Npm1 mutation (33 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:3606866
cx55
Allelic
Composition
Npm1tm1Ppp/Npm1tm1Ppp
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Npm1tm1Ppp mutation (1 available); any Npm1 mutation (33 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryonic lethality by E13.5




Genotype
MGI:3606864
cx56
Allelic
Composition
Npm1tm1Ppp/Npm1+
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Npm1tm1Ppp mutation (1 available); any Npm1 mutation (33 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• MEFs are fully rescued in the growth defect at early passage (P3-P5) that is seen in heterozygous Npm1tm1Ppp mice and grow faster than wildtype controls




Genotype
MGI:3840839
cx57
Allelic
Composition
E2f1tm1Njd/E2f1tm1Njd
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd * SKH1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
E2f1tm1Njd mutation (1 available); any E2f1 mutation (25 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• increased apoptosis response to UVB




Genotype
MGI:3037841
cx58
Allelic
Composition
Cdkn1btm1Mlf/Cdkn1btm1Mlf
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn1btm1Mlf mutation (2 available); any Cdkn1b mutation (25 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• the median latency to morbidity from tumor burden is significantly decreased in the double mutant compared to mice homozygous for Trp53tm1Brd alone
• this effect is synergistic

neoplasm
• the most common types of tumors are similar to mice homozygous for Trp53tm1Brd alone, however additional tumor types are found in the double homozygous mice
• the most common type of tumor is T-cell lymphoma
• the second most common types of tumor are sarcomas including; rhabdomyosarcoma, osteosarcoma, hemangiosarcoma, and poorly differentiated

endocrine/exocrine glands
• the most common type of tumor is T-cell lymphoma




Genotype
MGI:3700393
cx59
Allelic
Composition
Ing1Gt(OST206270)Lex/Ing1Gt(OST206270)Lex
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S5/SvEvBrd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ing1Gt(OST206270)Lex mutation (0 available); any Ing1 mutation (25 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• after exposure to 10-Gy ionizing radiation, only 56.3% of CD4/CD8 double positive T cells survive compared to 78.5% in Trp53-null mice
• rate of growth is higher than in Trp53-single null cells




Genotype
MGI:3656003
cx60
Allelic
Composition
Lig4tm1Fwa/Lig4tm1Fwa
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lig4tm1Fwa mutation (1 available); any Lig4 mutation (44 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice appear normal until 6 weeks of age, when survival drops precipitously
• embryonic lethality is dramatically abrogated in double mutants (34/369 double null offspring) compared to nearly total lethality with Lig4-deficiency alone (8/369 observed)
• numbers of double heterozygotes observed are similar to expected numbers

growth/size/body
• postnatally, mice are smaller (only 50% of control littermate weight) than wild-type or doubly-heterozygous littermates

cellular
• cells are markedly sensitive to radiation
• low levels of pyknotic nuclei are observed between E12.5 and E14.5, indicating significant rescue of neuronal apoptosis which is seen in Lig4-deficient embryos
• cultured MEFs show significantly high rates of doubling compared to Lig4-deficient mice and are close to wild-type levels

immune system
• little rescue of thymocyte number is observed compared to Lig4-deficient mice
• moderately increased B220+ CD43+ cell numbers are seen in bone marrow compared to Lig4-null, Trp53-heterozygous mice

hematopoietic system
• little rescue of thymocyte number is observed compared to Lig4-deficient mice
• moderately increased B220+ CD43+ cell numbers are seen in bone marrow compared to Lig4-null, Trp53-heterozygous mice

nervous system
• low levels of pyknotic nuclei are observed between E12.5 and E14.5, indicating significant rescue of neuronal apoptosis which is seen in Lig4-deficient embryos

neoplasm
• almost all (15/16) mice develop aggressive widely disseminated lymphoma which infiltrates the spleen, bone marrow, lymph nodes and thymus

endocrine/exocrine glands
• little rescue of thymocyte number is observed compared to Lig4-deficient mice




Genotype
MGI:3656004
cx61
Allelic
Composition
Lig4tm1Fwa/Lig4tm1Fwa
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lig4tm1Fwa mutation (1 available); any Lig4 mutation (44 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• majority of mice die at less than 8 weeks of age, with a significant drop in survival at ~3 weeks of age
• embryonic lethality is dramatically abrogated in double mutants (20/369 double null offspring) compared to nearly total lethality with Lig4-deficiency alone (8/369 observed)
• numbers of double heterozygotes observed are similar to expected numbers

growth/size/body
• postnatally, mice are much smaller (only 25% of control littermate weight) than wild-type or doubly-heterozygous littermates

nervous system
• neuronal apoptosis is significantly rescued with Trp53 haploinsufficiency

cellular
• neuronal apoptosis is significantly rescued with Trp53 haploinsufficiency




Genotype
MGI:4360340
cx62
Allelic
Composition
Brca1tm2.1Cxd/Brca1tm2.1Cxd
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm2.1Cxd mutation (1 available); any Brca1 mutation (113 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• lymphoma cells display polyploidy

endocrine/exocrine glands
• lymphoma cells display polyploidy




Genotype
MGI:4360339
cx63
Allelic
Composition
Brca1tm2.1Cxd/Brca1tm2.1Cxd
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm2.1Cxd mutation (1 available); any Brca1 mutation (113 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• survival to birth is normal
• increased sensitivity to paraquat induced lethality
• die shortly after developing respiratory difficulty

endocrine/exocrine glands
N
• normal mammary gland development
• seen on autopsy of mice that die prematurely
• enlarged thymus takes up most of the free space in the thorax
• develop mammary gland tumors by 6-10 months of age
• develop in many mice
• lymphomas display a loss of heterozygocity at the Trp53 locus
• lymphoma cells display aneuploidy
• various chromosomal aberrations such as double minute chromosomes are greatly increased in frequency

neoplasm
• develop mammary gland tumors by 6-10 months of age
• develop in many mice
• lymphomas display a loss of heterozygocity at the Trp53 locus
• lymphoma cells display aneuploidy
• various chromosomal aberrations such as double minute chromosomes are greatly increased in frequency
• increased incidence of esophageal tumors when treated with methyl N-amylnitrosamine
• stomach and esophageal dysplasia and carcinomas at 8 month
• invasive carcinomas at 8-12 months

cellular
• partial or complete loss of G1 to S checkpoint control
• in E14.5 embryos but still less than when both Trp53 alleles are normal
• embryonic fibroblasts (MEFs) grow better in culture than when both Trp53 alleles are normal

immune system
• seen on autopsy of mice that die prematurely
• enlarged thymus takes up most of the free space in the thorax

respiratory system
• develop breathing difficulties and become sick

digestive/alimentary system
• hyperkeratosis at 6 months
• increased cell proliferation in the basal layers
• hyperplasia and metaplasia at 6 months
• dysplasia and carcinomas at 8 months
• hyperkeratosis of the forestomach at 6 months
• increased cell proliferation in the basal layers
• hyperplasia and metaplasia at 6 months
• dysplasia and carcinomas at 8 months

homeostasis/metabolism
• increased sensitivity to paraquat induced lethality
• increased incidence of esophageal tumors when treated with methyl N-amylnitrosamine

hematopoietic system
• seen on autopsy of mice that die prematurely
• enlarged thymus takes up most of the free space in the thorax

embryo
• in E14.5 embryos but still less than when both Trp53 alleles are normal

integument
• develop mammary gland tumors by 6-10 months of age




Genotype
MGI:3640093
cx64
Allelic
Composition
Brca1tm1Cxd/Brca1tm1Cxd
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Cxd mutation (1 available); any Brca1 mutation (113 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• double mutant embryos survive on average of 2 days longer than Brca1tm1Cxd single homozygous embryos
• at E10.5, all double homozygous embryos are dead or dying

embryo
• morphologically abnormal compared to controls

cellular
• 29% of cells contained more than 40 chromosomes and 43% of cells contained less than 40 chromosomes
• many cells show chromosomal rearrangements such as translocations and dicentric chromosomes

growth/size/body




Genotype
MGI:3711895
cx65
Allelic
Composition
Rbbp6tm1Xya/Rbbp6tm1Xya
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rbbp6tm1Xya mutation (0 available); any Rbbp6 mutation (55 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• just over half of embryos survive past E11.5

embryo
N
• unlike Rbbp6tm1Xya homozygotes, mice form anterior-posterior with a head, trunk and tail region




Genotype
MGI:4360341
cx66
Allelic
Composition
Brca1tm2.1Cxd/Brca1tm2.1Cxd
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * Black Swiss * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm2.1Cxd mutation (1 available); any Brca1 mutation (113 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 30% of males die of lymphoma by 7 months of age
• most males are dead by 12 months of age
• 8 month and older males develop aging phenotypes
• aging phenotypes also seen in female mice

growth/size/body
• greatly reduced body weight

skeleton
• loss of trabecular bone

homeostasis/metabolism
• reduced anaesthetic stress tolerance
• reduced re-epithelialization at wound edges

adipose tissue
• reduced subcutaneous adipose tissue
• adipose tissue generally reduced

muscle

neoplasm
• increased tumorigenesis in females

reproductive system
• apoptotic spermatocytes in seminiferous tubules increased at 16 and 21 days of age relative to controls
• significantly smaller than controls at 16 days of age
• homologous chromosomes synapse but fail to separate
• males over six weeks of age lack spermatozoa in the testes
• testes histologically normal at 10 days
• no spermatids present at 21 days of age
• no diplotene stage spermatocytes detected at 16 days of age
• spermatogenesis does not progress beyond meiosis I
• spermatocytes do not pass through pachytene stage

endocrine/exocrine glands
• significantly smaller than controls at 16 days of age

cellular
• males over six weeks of age lack spermatozoa in the testes
• testes histologically normal at 10 days
• no spermatids present at 21 days of age
• apoptotic spermatocytes in seminiferous tubules increased at 16 and 21 days of age relative to controls

integument
• reduced subcutaneous adipose tissue
• reduced hair regeneration




Genotype
MGI:2673482
cx67
Allelic
Composition
H2axtm1Fwa/H2axtm1Fwa
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2axtm1Fwa mutation (0 available); any H2ax mutation (7 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die with lymphomas as early as 6 weeks of age, with 50% mortality by 10 weeks and most dead by 13 weeks

neoplasm
• some mutants develop multiple cancers
• seen in some mutants with multiple cancers
• aggressive thymic lymphomas
• B220+/IgM- B lineage lymphomas and pro-B cell lymphomas; often harboring translocations involving chromosomes 12 (Igh) and 15 (Myc)
• seen in some mutants with multiple cancers

digestive/alimentary system
• seen in some mutants with multiple cancers

endocrine/exocrine glands
• aggressive thymic lymphomas




Genotype
MGI:2673488
cx68
Allelic
Composition
H2axtm1Fwa/H2ax+
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2axtm1Fwa mutation (0 available); any H2ax mutation (7 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% mortality by 17 weeks of age

neoplasm
• develop lymphomas very early
• B lineage lymphomas, including Igmu+/IgL- pre-B cell lymphoma and IgM- B lineage lymphoma
• often harboring translocations involving chromosomes 12 (Igh) and 15 (Myc)
• develop teratomas very early

endocrine/exocrine glands




Genotype
MGI:6403623
cx69
Allelic
Composition
Ndor1Tg(UBC-cre/ERT2)1Ejb/Ndor1+
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ndor1Tg(UBC-cre/ERT2)1Ejb mutation (6 available); any Ndor1 mutation (32 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• in tamoxifen treated mice compared with untreated mice due to increased apoptosis in tumor cells




Genotype
MGI:3846184
cx70
Allelic
Composition
Nelfbtm1.2Roli/Nelfbtm1.2Roli
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nelfbtm1.2Roli mutation (0 available); any Nelfb mutation (24 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no viable mice are produced




Genotype
MGI:3846186
cx71
Allelic
Composition
Nelfbtm1.2Roli/Nelfbtm1.2Roli
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nelfbtm1.2Roli mutation (0 available); any Nelfb mutation (24 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no viable mice are produced




Genotype
MGI:4867474
cx72
Allelic
Composition
Sirt6tm2.2Cxd/Sirt6tm2.2Cxd
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * FVB/N * NIH Black Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sirt6tm2.2Cxd mutation (0 available); any Sirt6 mutation (39 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die within the first year after birth

growth/size/body

homeostasis/metabolism




Genotype
MGI:3588912
cx73
Allelic
Composition
Chek1tm1Sje/Chek1tm1Sje
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chek1tm1Sje mutation (0 available); any Chek1 mutation (41 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die by E2.5-3.5
• the presence of the p53 mutant allele does not rescue or delay the lethality phenotype of the single Chek1tm1Sje mutation

cellular
• TUNEL-positive cells are observed in double mutant blastocysts to a similar degree as the singly Chek1tm1Sje mutant blastocysts, but not in control blastocysts




Genotype
MGI:3714608
cx74
Allelic
Composition
Dp(4D4Mit190-D4Mit51)1Aam/0
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dp(4D4Mit190-D4Mit51)1Aam mutation (0 available); any Dp(4D4Mit190-D4Mit51)1Aam mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• some mice die prior to weaning

embryo
• defects in development are less severe than in Dp(4D4Mit190-D4Mit51)1AAM heterozygotes

growth/size/body
• some mice are runted

behavior/neurological
• some mice develop ataxia




Genotype
MGI:3807671
cx75
Allelic
Composition
Glipr1tm1Tt/Glipr1tm1Tt
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Glipr1tm1Tt mutation (0 available); any Glipr1 mutation (17 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 45 out of 74 mice develop tumors compared to 31 out of 63 mice in littermate controls
• tumors differ in their type and location, and include lymphomas, sarcomas, plasmacytomas and others




Genotype
MGI:3714609
cx76
Allelic
Composition
Dp(4D4Mit190-D4Mit51)1Aam/0
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dp(4D4Mit190-D4Mit51)1Aam mutation (0 available); any Dp(4D4Mit190-D4Mit51)1Aam mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are viable




Genotype
MGI:3807670
cx77
Allelic
Composition
Glipr1tm1Tt/Glipr1+
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Glipr1tm1Tt mutation (0 available); any Glipr1 mutation (17 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 59 out of 104 mice develop tumors compared to 31 out of 63 mice in littermate controls
• tumors differ in their type and location, and include lymphomas, sarcomas, plasmacytomas and others




Genotype
MGI:2183195
cx78
Allelic
Composition
Mdm2tm1Bay/Mdm2tm1Bay
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mdm2tm1Bay mutation (1 available); any Mdm2 mutation (54 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are normal, fertile and indistinguishable from controls, suggesting that the absence of Trp53 resuces the embryonic lethal phenotype of the Mdm2tm1Bay homozygous mice




Genotype
MGI:3851992
cx79
Allelic
Composition
Stk11tm1Mmt/Stk11+
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stk11tm1Mmt mutation (0 available); any Stk11 mutation (34 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• after 20 weeks, mice develop gastric hamartomas unlike wild-type mice
• at 24 weeks, all mice develop gastric hamartomas unlike wild-type mice
• hamartomas are composed of glandular and cystic epithelial layers without dysplastic signs




Genotype
MGI:3757692
cx80
Allelic
Composition
Atf4tm1Jml/Atf4tm1Jml
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atf4tm1Jml mutation (0 available); any Atf4 mutation (21 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
N
• eye and eyelid morphology are normal and there is a marked suppression in the microphthalmia that is seen in single Atf4 homozygotes
• lenses are present, however they show an increased number of cells in the bow region
• decrease in numbers of lens fiber cells




Genotype
MGI:3851991
cx81
Allelic
Composition
Stk11tm1Mmt/Stk11+
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stk11tm1Mmt mutation (0 available); any Stk11 mutation (34 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice by at 7 months

neoplasm
• at 25 weeks, one mouse develops bladder tumor unlike wild-type mice
• in two mice at 30 weeks
• 12 mice develop hepatic nodular foci unlike in wild-type mice
• between 25 and 30 weeks in one mouse
• after 12 weeks, all mice develop gastric hamartomas unlike wild-type mice

liver/biliary system
• enlarged and dysplastic in nodules
• 12 mice develop hepatic nodular foci unlike in wild-type mice
• between 25 and 30 weeks in one mouse

reproductive system
• in two mice at 30 weeks

endocrine/exocrine glands
• in two mice at 30 weeks




Genotype
MGI:3774770
cx82
Allelic
Composition
Cdkn2atm1Cjs/Cdkn2atm1Cjs
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 * NIH/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Cjs mutation (6 available); any Cdkn2a mutation (62 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Tumor multiplicity and proliferation index in Cdkn2atm1Cjs/Cdkn2atm1Cjs, Trp53tm1Brd/Trp53tm1Brd and Cdkn2atm1Cjs/Cdkn2atm1Cjs Trp53tm1Brd/Trp53tm1Brd mice

neoplasm
• mutants show a papilloma multiplicity similar to wild-type after DMBA/TPA treatment, however tumors that develop are larger than in wild-type
• tumor development is similar to wild-type after DMBA/TPA treatment although tumors are flatter and grow in an endophytic pattern compared to a highly exophytic pattern
• however, tumor progression is accelerated compared to single Trp53 homozygotes
• carcinoma latency and multiplicity after DMBA/TPA is similar to that seen in single homozygous Cdkn2a mutants, however size of carcinomas is larger than in wild-type or in single Trp53 mutants




Genotype
MGI:5009554
cx83
Allelic
Composition
Tg(Th-MYCN)41Waw/0
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd * BALB/c * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Th-MYCN)41Waw mutation (2 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants exhibit a tumor incidence similar to that of single hemizygous Tg(Th-MYCN)41Waw mice

nervous system
• mutants exhibit a tumor incidence similar to that of single hemizygous Tg(Th-MYCN)41Waw mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
neuroblastoma DOID:769 J:41126




Genotype
MGI:3840587
cx84
Allelic
Composition
Tg(KRT14-Birc5)19Gros/0
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd * C3H * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-Birc5)19Gros mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• fewer transgenic mice develop skin tumors after topical application of DMBA and PMA than Trp53 heterozygote controls
• median time to tumor formation is 25 weeks versus 16 weeks for the Trp53 heterozygote controls
• a lower percentage of mice (71% versus 89%) have tumors 32-weeks after DMBA application compared with controls
• mean tumor burden is 2.29 tumors per mouse compared to 3.0 tumors in controls
• tumor regression is not observed in transgenic mice whereas 10% of tumors in non-transgenic mice regress
• transgenic mice have an increased incidence of atypical papillomas that progress to squamous cell carcinoma

homeostasis/metabolism
• fewer transgenic mice develop skin tumors after topical application of DMBA and PMA than Trp53 heterozygote controls
• median time to tumor formation is 25 weeks versus 16 weeks for the Trp53 heterozygote controls
• a lower percentage of mice (71% versus 89%) have tumors 32-weeks after DMBA application compared with controls
• mean tumor burden is 2.29 tumors per mouse compared to 3.0 tumors in controls
• tumor regression is not observed in transgenic mice whereas 10% of tumors in non-transgenic mice regress
• transgenic mice have an increased incidence of atypical papillomas that progress to squamous cell carcinoma




Genotype
MGI:3794729
cx85
Allelic
Composition
Tg(KRT14-Birc5)19Gros/0
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd * C3H * C57BL/6 * C57BL/6NCr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-Birc5)19Gros mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• mice exhibit a reduction in sunburn cells associated with UVB-irradiation compared to wild-type mice and Trp53 heterozygotes but do not exhibit as much of a reduction as in Trp53 homozygotes
• mice exhibit a reduction in skin cell apoptosis associated with UVB-irradiation compared to wild-type mice or Trp53 null mice




Genotype
MGI:3818748
cx86
Allelic
Composition
Rag1tm1Mom/Rag1tm1Mom
Trp53tm1Brd/Trp53tm1Brd
Xrcc5tm1Dbr/Xrcc5tm1Dbr
Genetic
Background
involves: 129S7/SvEvBrd * C57BL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rag1tm1Mom mutation (49 available); any Rag1 mutation (120 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Xrcc5tm1Dbr mutation (0 available); any Xrcc5 mutation (70 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median lifespan is 14 weeks compared to 7 weeks in Trp53tm1Brd Xrcc5tm1Dbr
• maximum lifespan is 20 weeks compared to 16 weeks in Trp53tm1Brd Xrcc5tm1Dbr

neoplasm
• one mouse developed a stomach neoplasm
• 55% mice develop T cell lymphomas in the liver, spleen, lymph nodes, bone marrow, kidney, heart, lungs and ovaries
• mice that exhibit vertigo develop medulloblastoma
• 66.7% of mice exhibit medulloblastoma at the time of morbidity

respiratory system
• one-fifth of mice exhibit labored breathing prior to death compared to two-thirds of Rag1tm1Mom Trp53tm1Brd

behavior/neurological
• two-thirds of mice exhibit an acute onset of vertigo that leads to disabled mobility and severe dehydration as a result of inability to reach the water source

homeostasis/metabolism
• two-thirds of mice exhibit an acute onset of vertigo that leads to disabled mobility and severe dehydration as a result of inability to reach the water source

endocrine/exocrine glands
• 55% mice develop T cell lymphomas in the liver, spleen, lymph nodes, bone marrow, kidney, heart, lungs and ovaries

nervous system
• mice that exhibit vertigo develop medulloblastoma
• 66.7% of mice exhibit medulloblastoma at the time of morbidity

digestive/alimentary system
• one mouse developed a stomach neoplasm

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:141515




Genotype
MGI:3818749
cx87
Allelic
Composition
Rag1tm1Mom/Rag1tm1Mom
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rag1tm1Mom mutation (49 available); any Rag1 mutation (120 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die by 45 weeks of age

neoplasm
• 53% mice develop T cell lymphomas
• mice that exhibit vertigo develop medulloblastoma
• 8.1% of mice exhibit medulloblastoma at the time of morbidity

respiratory system
• in two-thirds of mice

behavior/neurological
• one mouse exhibited an acute onset of vertigo that led to disabled mobility and severe dehydration as a result of inability to reach the water source

homeostasis/metabolism
• one mouse exhibited an acute onset of vertigo that led to disabled mobility and severe dehydration as a result of inability to reach the water source

nervous system
• mice that exhibit vertigo develop medulloblastoma
• 8.1% of mice exhibit medulloblastoma at the time of morbidity

endocrine/exocrine glands
• 53% mice develop T cell lymphomas

liver/biliary system




Genotype
MGI:3818751
cx88
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Xrcc5tm1Dbr/Xrcc5tm1Dbr
Genetic
Background
involves: 129S7/SvEvBrd * C57BL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Xrcc5tm1Dbr mutation (0 available); any Xrcc5 mutation (70 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median lifespan is 7 weeks
• maximum lifespan is 16 weeks

neoplasm
• in 8 of 13 mice

nervous system




Genotype
MGI:3809302
cx89
Allelic
Composition
Dicer1tm1Snj/Dicer1tm1Snj
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dicer1tm1Snj mutation (0 available); any Dicer1 mutation (94 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular




Genotype
MGI:3795437
cx90
Allelic
Composition
Rad51tm1Hst/Rad51tm1Hst
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rad51tm1Hst mutation (0 available); any Rad51 mutation (31 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• double mutant embryos survive longer than Rad51tm1Hst homozygous mice; embryos appear grossly normal at E7.5, but are smaller at E8.5 and do not develop further

cellular
• MEFs derived from double-homozygous mice do not proliferate in culture and exhibit characteristics of cells entering premature senescence




Genotype
MGI:5056121
cx91
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Twsg1tm1.1Mboc/Twsg1tm1.1Mboc
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
Twsg1tm1.1Mboc mutation (0 available); any Twsg1 mutation (20 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• up to 66% of neonates exhibit perinatal death

craniofacial
• mice exhibit reduced craniofacial defects compared with Twsg1tm1.1Mboc homozygotes

nervous system




Genotype
MGI:5604449
cx92
Allelic
Composition
Tg(Mdm2)1Snj/0
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Mdm2)1Snj mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 67% of mice develop lymphoma
• 14 of 26 tumors are malignant lymphoma
• 1 of 16 tumors is a medulloblastoma
• 1 of 16 tumors is a squamous cell carcinoma
• 8 of 26 tumors are hemangiosarcomas
• 2 of 16 tumors are osteosarcomas

skeleton
• 2 of 16 tumors are osteosarcomas

nervous system
• 1 of 16 tumors is a medulloblastoma




Genotype
MGI:5770583
cx93
Allelic
Composition
Nabp2tm1Schg/Nabp2tm1Schg
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nabp2tm1Schg mutation (0 available); any Nabp2 mutation (16 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• disseminated lymphoma in the kidney and liver unlike in Trp53tm1Brd mice
• however, total cancer incidents are not elevated




Genotype
MGI:3717875
cx94
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Tg(KRT14-rtTA)208Jek/Y
Tg(tetO-KLF4)32831Rup/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6NTac * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-rtTA)208Jek mutation (1 available)
Tg(tetO-KLF4)32831Rup mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• male animals exhibit epithelial dysplasia associated with infiltration of the dermis by well-vascularized, cellular or fibrotic stroma, or a fibrovascular response upon induction by doxycycline




Genotype
MGI:3717876
cx95
Allelic
Composition
Trp53tm1Brd/Trp53+
Tg(KRT14-rtTA)208Jek/0
Tg(tetO-KLF4)32831Rup/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6NTac * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT14-rtTA)208Jek mutation (1 available)
Tg(tetO-KLF4)32831Rup mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• females display focal changes including cystic follicles and mild changes in the adjacent interfollicular epithelium




Genotype
MGI:3798037
cx96
Allelic
Composition
Cdca8tm1Tatn/Cdca8tm1Tatn
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdca8tm1Tatn mutation (1 available); any Cdca8 mutation (23 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no embryos are found at E7.5




Genotype
MGI:5013960
cx97
Allelic
Composition
Pinx1tm1.1Kplu/Pinx1+
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pinx1tm1.1Kplu mutation (0 available); any Pinx1 mutation (17 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die between 9 and 12 months

neoplasm
• mice develop epithelial carcinomas such as lung, liver, breast, and gastrointestinal cancers
• mice develop epithelial carcinomas such as lung, liver, breast, and gastrointestinal cancers

liver/biliary system

respiratory system

reproductive system

integument

endocrine/exocrine glands




Genotype
MGI:5013961
cx98
Allelic
Composition
Pinx1tm1.1Kplu/Pinx1+
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pinx1tm1.1Kplu mutation (0 available); any Pinx1 mutation (17 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die between 6 and 9 months

neoplasm
• mice develop epithelial carcinomas such as lung, liver, breast, and gastrointestinal cancers

liver/biliary system

digestive/alimentary system

endocrine/exocrine glands

integument

respiratory system




Genotype
MGI:3040401
cx99
Allelic
Composition
H2axtm1Nus/H2axtm1Nus
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2axtm1Nus mutation (1 available); any H2ax mutation (7 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• onset of death is 8 weeks for double homozygotes significantly earlier than for mice with only Trp53tm1Brd

neoplasm
• in double homozygotes T and B cell lymphomas predominate




Genotype
MGI:3834167
cx100
Allelic
Composition
Rb1tm1Brd/Rb1+
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm1Brd mutation (0 available); any Rb1 mutation (106 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• life span is shorter compared to littermates with only a single gene defect




Genotype
MGI:3040402
cx101
Allelic
Composition
H2axtm1Nus/H2ax+
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2axtm1Nus mutation (1 available); any H2ax mutation (7 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• onset of death is 10 weeks for double homozygotes significantly earlier than for mice with only Trp53tm1Brd

neoplasm
• these mice have a broader tumor spectrum than the double homozygotes that includes thymic lymphomas. sarcomas, leukemia, and brain tumors




Genotype
MGI:3822323
cx102
Allelic
Composition
Tg(S100b-v-erbB)4496Waw/0
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J * DBA/2J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(S100b-v-erbB)4496Waw mutation (1 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 80% of mice die within 6 months of high grade oligodendroglioma

neoplasm
• mice develop gliomas as in Cdkn2atm1Rdp/Cdkn2atm1Rdp Tg(S100b-v-erbB)4496Waw mice with loss of function of the wild-type Trp53 allele
• 80% of mice die within 6 months of high grade oligodendroglioma

nervous system
• mice develop gliomas as in Cdkn2atm1Rdp/Cdkn2atm1Rdp Tg(S100b-v-erbB)4496Waw mice with loss of function of the wild-type Trp53 allele
• 80% of mice die within 6 months of high grade oligodendroglioma

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
oligodendroglioma DOID:3181 J:82649




Genotype
MGI:3717873
cx103
Allelic
Composition
Tg(MMTV-KLF4)1Rup/0
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6NTac * FVB/NJ * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(MMTV-KLF4)1Rup mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• lifespan is ~8 months due to sarcomas

neoplasm
• all mice develop sarcoma outgrowth within the fibrovascular response
• tumors 1-1.5 cm in diameter and are composed of spindled, anaplastic cells and scattered giant cells

integument
• vascular, fibrotic dermis
• between 6 and 8 months of age, dorsal skin lesions similar to those in the inducible models develop in all animals




Genotype
MGI:4837884
cx104
Allelic
Composition
Trp53tm1Brd/Trp53+
Tg(Cryaa-NCOA6*)AD5Cve/0
Genetic
Background
involves: 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Cryaa-NCOA6*)AD5Cve mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• eye size is increased compared to in Tg(Cryaa-NCOA6*)AD5Cve mice




Genotype
MGI:4837885
cx105
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Tg(Cryaa-NCOA6*)AD5Cve/0
Genetic
Background
involves: 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Cryaa-NCOA6*)AD5Cve mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• the number of double strand break positive nuclei in the lenses is reduced 60% compared to in Tg(Cryaa-NCOA6*)AD5Cve mice
• 1.35- to 1.65-fold compared with wild-type mice




Genotype
MGI:5485354
cx106
Allelic
Composition
Egfrwa2/Egfr+
Nf1tm1Fcr/Nf1+
Trp53tm1Brd/Trp53+
Genetic
Background
involves: 129S/SvEv * 129S7/SvEvBrd * C57BL/6 * C57BL/6JEi * C3H/HeSnJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Egfrwa2 mutation (3 available); any Egfr mutation (85 available)
Nf1tm1Fcr mutation (3 available); any Nf1 mutation (157 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• only 1 of 17 (5.9%) mice develop a tumor, a spindle cell tumor compared to 57.9% of double heterozygous Nf1 and Trp53 mutants; this mouse was sacrificed at 21 weeks of age




Genotype
MGI:3574393
cx107
Allelic
Composition
Dcntm1Ioz/Dcn+
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129/Sv * Black Swiss * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dcntm1Ioz mutation (0 available); any Dcn mutation (27 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• these mutants survive longer than double homozygotes with a 50% mean survival rate of ~6 months, similar to that observed in Trp53tm1Brd mice; surprisingly, no increased incidence of infections is observed

neoplasm
• similar to double homozygotes, these mutants are predisposed to an accelerated mortality due to increased tumorigenesis, with no differences between male and female occurrence
• the majority of tumors are high-grade lymphomas arising from the transformation of immature thymocytes
• tumor cells are highly invasive and infiltrate the soft tissues of mediastinum, the salivary glands, the periaortic spaces, the pericardium, and the bronchial wall

respiratory system
• mutants with thymic lymphomas die of pericardial compression or respiratory distress

endocrine/exocrine glands
• the majority of tumors are high-grade lymphomas arising from the transformation of immature thymocytes
• tumor cells are highly invasive and infiltrate the soft tissues of mediastinum, the salivary glands, the periaortic spaces, the pericardium, and the bronchial wall




Genotype
MGI:3574392
cx108
Allelic
Composition
Dcntm1Ioz/Dcntm1Ioz
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: 129/Sv * Black Swiss * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dcntm1Ioz mutation (0 available); any Dcn mutation (27 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by ~4 months of age, ~50% of double homozygotes die or need to be sacrificed because of ill health
• by 5 months, ~90% of double homozygotes succumb to tumor growth

neoplasm
• double homozygotes are predisposed to an accelerated mortality due to increased tumorigenesis, with no differences between male and female occurrence
• double mutants show a significant homogeneity in tumor spectrum and do not exhibit multiple tumors
• the majority of tumors are high-grade lymphomas arising from the transformation of immature thymocytes
• tumor cells are highly invasive and infiltrate the soft tissues of mediastinum, the salivary glands, the periaortic spaces, the pericardium, and the bronchial wall
• only one double homozygote developed a high-grade hemangiosarcoma in the submandibular region

immune system
• ~5% of double homozygotes have a significantly enlarged thymus, in the absence of overt tumors
• ~5% of double homozygotes display no overt neoplasms but show thymic hyperplasia with foci of atypical lymphocytes infiltrating the mediastinal soft tissues and signs of early-invading malignant lymphomas

respiratory system
• double homozygotes with thymic lymphomas die of pericardial compression or respiratory distress

hematopoietic system
• ~5% of double homozygotes have a significantly enlarged thymus, in the absence of overt tumors
• ~5% of double homozygotes display no overt neoplasms but show thymic hyperplasia with foci of atypical lymphocytes infiltrating the mediastinal soft tissues and signs of early-invading malignant lymphomas

endocrine/exocrine glands
• ~5% of double homozygotes have a significantly enlarged thymus, in the absence of overt tumors
• ~5% of double homozygotes display no overt neoplasms but show thymic hyperplasia with foci of atypical lymphocytes infiltrating the mediastinal soft tissues and signs of early-invading malignant lymphomas
• the majority of tumors are high-grade lymphomas arising from the transformation of immature thymocytes
• tumor cells are highly invasive and infiltrate the soft tissues of mediastinum, the salivary glands, the periaortic spaces, the pericardium, and the bronchial wall




Genotype
MGI:3037835
cx109
Allelic
Composition
Cdkn1btm1Mlf/Cdkn1btm1Mlf
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: C3H * C57BL/6J * NIH
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn1btm1Mlf mutation (2 available); any Cdkn1b mutation (25 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• the most common type of tumor is T-cell lymphoma

mortality/aging
• the median latency to morbidity from tumor burden is significantly decreased in the double mutant compared to mice homozygous for Trp53tm1Brd alone
• this effect is synergistic

neoplasm
• the most common types of tumors are similar to mice homozygous for Trp53tm1Brd alone, however additional tumor types are found in the double homozygous mice
• the most common type of tumor is T-cell lymphoma
• the second most common types of tumor are sarcomas including; rhabdomyosarcoma, osteosarcoma, hemangiosarcoma, and poorly differentiated




Genotype
MGI:6163836
cx110
Allelic
Composition
Pole4tm1(KOMP)Vlcg/Pole4tm1(KOMP)Vlcg
Trp53tm1Brd/Trp53+
Genetic
Background
involves: C57BL/6J * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pole4tm1(KOMP)Vlcg mutation (0 available); any Pole4 mutation (7 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• unlike single Pole4tm1(KOMP)Vlcg homozygotes, which are essentially embryonic lethal in the inbred C57BL/6 background, mice are born at slightly sub-Mendelian ratios (10.1% born versus 12.5% expected)

behavior/neurological
• loss of rotarod coordination, observed in single Pole4tm1(KOMP)Vlcg homozygotes, is not rescued by deleting a single Trp53 allele

immune system

hematopoietic system

neoplasm
• ~90% of mice present with lymphomas
• lymphoma-free survival is significantly reduced to 226 days relative to 480 days in Trp53tm1Brd heterozygotes, indicating accelerated tumorigenesis

endocrine/exocrine glands
• ~90% of mice present with lymphomas




Genotype
MGI:6163840
cx111
Allelic
Composition
Pole4tm1(KOMP)Vlcg/Pole4tm1(KOMP)Vlcg
Trp53tm1Brd/Trp53tm1Brd
Genetic
Background
involves: C57BL/6J * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pole4tm1(KOMP)Vlcg mutation (0 available); any Pole4 mutation (7 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• unlike single Pole4tm1(KOMP)Vlcg homozygotes, which are essentially embryonic lethal in the inbred C57BL/6 background, double-mutant mice are born at sub-Mendelian ratios (3.7% born versus 6.25% expected)

behavior/neurological
• loss of rotarod coordination, observed in single Pole4tm1(KOMP)Vlcg homozygotes, is only partially rescued by deleting both Trp53 alleles

growth/size/body
N
• double-mutant mice lack gross abnormalities and exhibit a size similar to that of single Trp53tm1Brd homozygotes

immune system
N
• double-mutant mice exhibit rescue of the absolute number and proportion of white blood cells; the numbers of T cells (CD4+ and CD8+) and B cells are restored to levels comparable to those in single Trp53tm1Brd homozygotes





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
04/16/2024
MGI 6.23
The Jackson Laboratory