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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Trp53tm1Brn
targeted mutation 1, Anton Berns
MGI:1931011
Summary 206 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Trp53tm1Brn/Trp53tm1Brn involves: 129P2/OlaHsd * FVB/N MGI:3831428
cn2
Trp53tm1Brn/Trp53tm1Brn involves: 129P2/OlaHsd MGI:3696698
cn3
Trp53tm1Brn/Trp53tm1Brn involves: 129P2/OlaHsd * FVB/N MGI:5544201
cn4
Trp53tm1Brn/Trp53tm1.1Brn involves: 129P2/OlaHsd MGI:4437464
cn5
Trp53tm1Brn/Trp53tm2Tyj involves: 129P2/OlaHsd * 129S4/SvJae MGI:5293783
cn6
Ptentm2.1Ppp/Ptentm2.1Ppp
Trp53tm1Brn/Trp53tm1Brn
Tg(TPO-cre)1Shk/0
129.Cg-Tg(TPO-cre)1Shk Trp53tm1Brn Ptentm2.1Ppp MGI:5897837
cn7
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Gfap-cre)2Brn/0
either: (involves: 129 * 129P2/OlaHsd * FVB/N) or (involves: 129 * 129P2/OlaHsd * C57BL/6 * FVB/N) MGI:5437517
cn8
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Tg(Tyr-NRAS*Q61K)1Bee/0
FVB.Cg-Tg(Tyr-cre/ERT2)13Bos Trp53tm1Brn Tg(Tyr-NRAS*Q61K)1Bee MGI:5645995
cn9
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)105Ayn/0
FVB.Cg-Trp53tm1Brn Rb1tm2Brn Tg(MMTV-cre)105Ayn MGI:4837145
cn10
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)105Ayn/0
FVB.Cg-Trp53tm1Brn Tg(MMTV-cre)105Ayn MGI:4837144
cn11
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Ren-cre)#Kwg/0
involves: 129 * 129P2/OlaHsd MGI:5662454
cn12
Prkar1atm1.2Lsk/Prkar1a+
Rb1tm2Brn/Rb1+
Tg(Col1a1-cre)1Kry/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N MGI:5796166
cn13
Prkar1atm1.2Lsk/Prkar1a+
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Col1a1-cre)1Kry/0
involves: 129 * 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N MGI:5796167
cn14
Calcatm1.1(cre/ERT2)Ptch/Calca+
Trp53tm1Brn/Trp53tm1Brn
Rb1tm2Brn/Rb1tm2Brn
Ptentm1Hwu/Ptentm1Hwu
involves: 129 * 129P2/OlaHsd * 129S4/SvJae * BALB/c * FVB/N MGI:5460854
cn15
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB/N MGI:5563244
cn16
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB/N MGI:5563247
cn17
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53+
involves: 129 * 129P2/OlaHsd * C57BL/6J * CD-1 * FVB/N MGI:5519100
cn18
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * 129P2/OlaHsd * C57BL/6J * CD-1 * FVB/N MGI:5519099
cn19
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Col1a1-cre)1Kry/0
involves: 129 * 129P2/OlaHsd * FVB/N MGI:5796161
cn20
Rb1tm2Brn/Rb1+
Trp53tm1Brn/Trp53tm1Brn
Tg(Col1a1-cre)1Kry/0
involves: 129 * 129P2/OlaHsd * FVB/N MGI:5796164
cn21
Calcatm1.1(cre/ERT2)Ptch/Calca+
Trp53tm1Brn/Trp53tm1Brn
Rb1tm2Brn/Rb1tm2Brn
involves: 129 * 129P2/OlaHsd * FVB/N MGI:5460840
cn22
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Gfap-cre)2Brn/0
involves: 129 * 129P2/OlaHsd * FVB/N MGI:5437518
cn23
Pgrtm2(cre)Lyd/Pgr+
Ptentm1Hwu/Ptentm1Hwu
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * C57BL/6 MGI:3813634
cn24
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308962
cn25
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308961
cn26
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308959
cn27
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308954
cn28
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308951
cn29
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308946
cn30
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Tg(Vil1-cre/ERT2)23Syr/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * C57BL/6 * CD-1 * DBA/2 MGI:5543693
cn31
Csnk1a1tm1.1Ybn/Csnk1a1+
Tg(Vil1-cre/ERT2)23Syr/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * C57BL/6 * CD-1 * DBA/2 MGI:5543694
cn32
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Vil1-cre)20Syr/0
involves: 129 * C57BL/6 * DBA/2 MGI:5634401
cn33
Ptentm1Rdp/Ptentm1Rdp
Smad4tm1Rdp/Smad4tm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129 * C57BL/6 * DBA/2 MGI:5431947
cn34
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)7Mul/0
involves: 129 * C57BL/6 * FVB/N MGI:5634403
cn35
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129 * C57BL/6 * FVB/N MGI:5634400
cn36
Cdh1tm2Kem/Cdh1tm2Kem
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129 * C57BL/6 * FVB/N MGI:5634407
cn37
Mettm1Sst/Mettm1Sst
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd MGI:5293779
cn38
Ptentm2Mak/Ptentm2Mak
Trp53tm1Brn/Trp53tm1Brn
Tg(Nes-cre/ERT2,-ALPP)1Sbk/0
involves: 129P2/OlaHsd MGI:5825466
cn39
Braftm1Mmcm/Braf+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd MGI:3712022
cn40
Brca1tm1Brn/Brca1tm1Brn
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd MGI:3696696
cn41
Rb1tm2Brn/Rb1+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd MGI:5704166
cn42
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd MGI:4437461
cn43
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd MGI:4437462
cn44
Trp53tm1Brn/Trp53+
Tg(MMTV-cre)#Tfln/0
involves: 129P2/OlaHsd MGI:5000480
cn45
Trp53tm1Brn/Trp53tm1Brn
Tg(Nes-cre/ERT2,-ALPP)1Sbk/0
involves: 129P2/OlaHsd MGI:5825464
cn46
Bcl11atm2.1Peli/Bcl11atm2.1Peli
Trp53tm1Brn/Trp53tm1Brn
Gt(ROSA)26Sortm2(cre/ERT2)Brn/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S1/Sv MGI:5475383
cn47
Cdkn2ctm1Bbd/Cdkn2ctm1Bbd
Trp53tm1Brn/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3710322
cn48
Pgrtm2(cre)Lyd/Pgr+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:3813635
cn49
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Trp53tm1Brn/Trp53tm1Brn
Tg(Vil1-cre/ERT2)23Syr/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:6448982
cn50
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5648533
cn51
Cdh1tm2Kem/Cdh1+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5634406
cn52
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5648534
cn53
Ptch1tm1Cklr/Ptch1+
Trp53tm1Brn/?
Pax7tm1(cre)Mrc/Pax7+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:4453164
cn54
Myf6tm1(cre)Mrc/Myf6+
Pax3tm1Mrc/Pax3tm1Mrc
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3844658
cn55
Myf6tm1(cre)Mrc/Myf6+
Pax3tm1Mrc/Pax3tm1Mrc
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3844657
cn56
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre/ERT)20Efu/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * CD-1 MGI:6246565
cn57
Prkar1atm1.2Lsk/Prkar1a+
Tg(Col1a1-cre)1Kry/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N MGI:5796169
cn58
Smarcb1tm2Sho/Smarcb1+
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)#Gtm/0
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA MGI:5771803
cn59
Smarcb1tm2Sho/Smarcb1+
Trp53tm1Brn/Trp53+
Tg(GFAP-cre)#Gtm/0
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA MGI:5771802
cn60
Smarcb1tm2Sho/Smarcb1tm2Sho
Trp53tm1Brn/Trp53+
Tg(GFAP-cre)#Gtm/0
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA MGI:5771804
cn61
Smarcb1tm2Sho/Smarcb1tm2Sho
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)#Gtm/0
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA MGI:5771805
cn62
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Slc1a3tm1(cre/ERT2)Mgoe/Slc1a3+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJaeSor MGI:5790976
cn63
Rb1tm1Tyj/Rb1tm2Brn
Rbl1tm1Tyj/Rbl1tm1Tyj
Trp53tm1Brn/Trp53tm1Brn
Tg(Chx10-EGFP/cre,-ALPP)2Clc/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3710238
cn64
Trp53tm1Brn/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3710323
cn65
Rb1tm1Tyj/Rb1tm2Brn
Rbl1tm1Tyj/Rbl1+
Trp53tm1Brn/Trp53tm1Brn
Tg(Chx10-EGFP/cre,-ALPP)2Clc/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3710240
cn66
Rb1tm1Tyj/Rb1tm2Brn
Rbl1tm1Tyj/Rbl1tm1Tyj
Trp53tm1Brn/Trp53tm1Tyj
Tg(Chx10-EGFP/cre,-ALPP)2Clc/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3710239
cn67
Mettm1Sst/Mettm1Sst
Trp53tm1Brn/Trp53tm2Tyj
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5293786
cn68
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716963
cn69
Rb1tm3Tyj/Rb1tm3Tyj
Rbl2tm2Tyj/Rbl2tm2Tyj
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae MGI:4459447
cn70
Rb1tm3Tyj/Rb1tm3Tyj
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae MGI:4459448
cn71
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716966
cn72
Trp53tm1Brn/Trp53tm1Brn
Tsc1tm1Djk/Tsc1tm1Djk
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5632129
cn73
Mettm1Sst/Mettm1Sst
Trp53tm1Brn/Trp53tm3Tyj
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5293785
cn74
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716968
cn75
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5510703
cn76
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Krt19tm1(cre/ERT)Ggu/Krt19+
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac MGI:5298083
cn77
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Shhtm2(cre/ERT2)Cjt/Shh+
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac MGI:5298088
cn78
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N MGI:6377665
cn79
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N MGI:6377664
cn80
Cd9tm1c(EUCOMM)Hmgu/Cd9tm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N MGI:6377669
cn81
Cd9tm1c(EUCOMM)Hmgu/Cd9tm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N MGI:6377668
cn82
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N MGI:6377672
cn83
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N MGI:6377671
cn84
Col1a1tm4(CAG-FGFR2_iIIIb*K660N)Kkw/Col1a1+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/c * C57BL/6 MGI:5661330
cn85
Col1a1tm5(CAG-FGFR2_iIIIb*W290C)Kkw/Col1a1+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/c * C57BL/6 MGI:5661331
cn86
Trp53tm1Brn/Trp53+
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:6695307
cn87
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5528686
cn88
Trp53tm1Brn/Trp53tm1Brn
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:6695306
cn89
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5559052
cn90
Krastm5Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sortm1(cre/ERT2)Tyj
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5007795
cn91
Krastm4Tyj/Kras+
Myod1tm1.1(cre/ERT,TVA)Gcg/Myod1+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5547939
cn92
Setd4tm1c(KOMP)Wtsi/Setd4tm1c(KOMP)Wtsi
Trp53tm1Brn/Trp53tm1Brn
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6N MGI:6695303
cn93
Setd4tm1c(KOMP)Wtsi/Setd4tm1c(KOMP)Wtsi
Trp53tm1Brn/Trp53+
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6N MGI:6695305
cn94
Braftm1Mmcm/Braf+
Trp53tm1Brn/Trp53tm3.1Tyj
Tg(TPO-cre/ERT2)1139Tyj/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac MGI:5897858
cn95
Braftm1Mmcm/Braf+
Tg(TPO-cre/ERT2)1139Tyj/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac MGI:5897859
cn96
Rb1tm3Tyj/Rb1tm3Tyj
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CD-1 MGI:5521545
cn97
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428898
cn98
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428907
cn99
Brca1tm1Brn/Brca1tm1Brn
Tg(Krt18-EGFP,-TAg121)36Ysng/0
Trp53tm1Brn/Trp53tm2Tyj
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N MGI:5617496
cn100
Brca2tm1Brn/Brca2tm1Brn
Tg(Krt18-EGFP,-TAg121)36Ysng/0
Trp53tm1Brn/Trp53tm2Tyj
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N MGI:5617497
cn101
Tg(Krt18-EGFP,-TAg121)36Ysng/0
Trp53tm1Brn/Trp53tm2Tyj
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N MGI:5617494
cn102
Ptentm1Hwu/Ptentm1Hwu
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:3844324
cn103
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:5486065
cn104
Cdkn2atm2.1Nesh/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835045
cn105
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835042
cn106
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835041
cn107
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5659893
cn108
Rb1tm3Tyj/Rb1tm3Tyj
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * CD-1 * FVB/N MGI:5519096
cn109
Rb1tm3Tyj/Rb1+
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * CD-1 * FVB/N MGI:5519095
cn110
Rb1tm3Tyj/Rb1tm3Tyj
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * CD-1 * FVB/N MGI:5519094
cn111
Rb1tm3Tyj/Rb1+
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * CD-1 * FVB/N MGI:5519097
cn112
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6N * FVB/N MGI:6377667
cn113
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre/ERT)20Efu/0
involves: 129P2/OlaHsd * 129S4/SvJae * CD-1 MGI:5298084
cn114
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:4835046
cn115
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJaeSor MGI:5790977
cn116
Palb2tm1.1Dli/Palb2tm1.1Dli
Trp53tm1Brn/Trp53+
Tg(KRT14-cre)1Amc/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * CBA MGI:5495973
cn117
Palb2tm1.1Dli/Palb2tm1.1Dli
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)1Amc/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * CBA MGI:5495972
cn118
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB MGI:5563238
cn119
Knl1tm1c(EUCOMM)Hmgu/Knl1tm1c(EUCOMM)Hmgu
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6N * FVB/N MGI:6358254
cn120
Gt(ROSA)26Sortm1(Pik3ca*H1047R)Egan/Gt(ROSA)26Sor+
Tg(MMTV-cre)#Tfln/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:5000479
cn121
Gt(ROSA)26Sortm1(Pik3ca*H1047R)Egan/Gt(ROSA)26Sor+
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)#Tfln/0
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:5000478
cn122
Hrastm1Jaf/Hrastm1Jaf
Trp53tm1Brn/Trp53tm1Brn
Tg(TPO-cre)1Shk/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6 * FVB/NCr MGI:5784771
cn123
Ptentm1Rdp/Ptentm1Rdp
Terttm1Rdp/Terttm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5431943
cn124
Ptentm1Rdp/Ptentm1Rdp
Terttm3Rdp/Terttm3Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5431978
cn125
Ptentm1Rdp/Ptentm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5431945
cn126
Ptentm1Rdp/Ptentm1Rdp
Terttm1Rdp/Tert+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5431944
cn127
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5634402
cn128
Ptentm1Rdp/Pten+
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:3831280
cn129
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5634408
cn130
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659885
cn131
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)7Mul/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * FVB/N MGI:5634404
cn132
Cdkn2atm1.1Brn/Cdkn2a+
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:3850449
cn133
Cdkn2atm1.1Brn/Cdkn2atm1.1Brn
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:3850451
cn134
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:3850443
cn135
Cdkn2atm1.1Brn/Cdkn2atm1.1Brn
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:3850439
cn136
Nf2tm2Gth/Nf2+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:3850446
cn137
Nf2tm2Gth/Nf2tm2Gth
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:3850447
cn138
Amhr2tm3(cre)Bhr/Amhr2+
KitW-v/KitW-v
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J * FVB/N MGI:5811264
cn139
Dicer1tm1Snj/Dicer1tm1Snj
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT5-cre/PGR)1Der/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6N * FVB/N * ICR MGI:5618123
cn140
Dicer1tm1Snj/Dicer1tm1Snj
Trp53tm1Brn/Trp53+
Tg(KRT5-cre/PGR)1Der/0
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6N * FVB/N * ICR MGI:5618124
cn141
Mdm4tm2Glo/Mdm4tm2.1Glo
Tg(Myh6-cre)2182Mds/0
Trp53tm1Tyj/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S/Sv * C57BL/6J * FVB/N MGI:5907135
cn142
Ctnnb1tm1Mmt/Ctnnb1+
Trp53tm1Brn/Trp53+
Tg(Fabp7-cre,-lacZ)3Gtm/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * CBA MGI:5438218
cn143
Ctnnb1tm1Mmt/Ctnnb1+
Pik3catm1Gilb/Pik3ca+
Trp53tm1Brn/Trp53+
Tg(Fabp7-cre,-lacZ)3Gtm/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * CBA MGI:5438217
cn144
Atmintm1.2Jhh/Atmintm1.2Jhh
Trp53tm1Brn/Trp53tm1Brn
Cd79atm1(cre)Reth/Cd79a+
involves: 129P2/OlaHsd * BALB/c * C57BL/6 MGI:5463974
cn145
Brca1tm1Brn/Brca1tm1Brn
Trp53tm1Brn/Trp53+
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * BALB/cJ * FVB/N MGI:3762187
cn146
Brca1tm1Brn/Brca1+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * BALB/cJ * FVB/N MGI:3762186
cn147
Brca1tm1Brn/Brca1tm1Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * BALB/cJ * FVB/N MGI:3762188
cn148
Noc2ltm1.1Arte/Noc2ltm1.1Arte
Trp53tm1Brn/Trp53tm1Brn
Tg(CD2-icre)4Kio/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/10 * CBA/Ca MGI:5662110
cn149
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * CD-1 MGI:5521544
cn150
Gt(ROSA)26Sortm18(Zeb2)Jhai/Gt(ROSA)26Sortm18(Zeb2)Jhai
Tg(Tek-cre)1Ywa/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL MGI:6195747
cn151
Tg(Tek-cre)1Ywa/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL MGI:6195749
cn152
Gt(ROSA)26Sortm18(Zeb2)Jhai/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL MGI:6195748
cn153
Gt(ROSA)26Sortm1(Gck)Ydor/Gt(ROSA)26Sor+
Trp53tm1Brn/Trp53tm1Brn
Tg(Ins2-cre)25Mgn/0
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:5581817
cn154
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:4819193
cn155
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Brn/Trp53+
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:4819194
cn156
Tg(KRT14-cre)8Brn/0
Tg(KRT5-Akt1*)Jmpa/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * DBA/2J * FVB/N MGI:3842833
cn157
Ptentm1Mro/Ptentm1Mro
Tg(KRT14-cre)8Brn/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * DBA/2J * FVB/N MGI:3842835
cn158
Tg(Krt18-EGFP,-TAg121)36Ysng/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * FVB/N MGI:5617495
cn159
Brca1tm1Brn/Brca1tm1Brn
Tg(Krt18-EGFP,-TAg121)36Ysng/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * FVB/N MGI:5617499
cn160
Trp53tm1Brn/Trp53tm1Brn
Tg(Upk2-cre)1Rkl/0
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:5014309
cn161
Ptentm2Mak/Ptentm2Mak
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)#Tfln/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:5752193
cn162
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)#Tfln/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:5752199
cn163
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)25Mes/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3831281
cn164
Ptentm2Mak/Ptentm2Mak
Trp53tm1Brn/Trp53tm1Brn
Tg(Wap-cre)11738Mam/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL MGI:5752196
cn165
Brca1tm1Brn/Brca1tm1.1Jjon
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * C57BL/6J * FVB/N MGI:5307256
cn166
KitW-v/KitW-v
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6J * FVB/N MGI:5811262
cn167
Brca1tm1Brn/Brca1tm1Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * C57BL/6J * FVB/N MGI:5307257
cn168
Trp53tm1Brn/Trp53tm1Brn
Tg(Cdh16-cre)91Igr/0
involves: 129P2/OlaHsd * C57BL/6J * FVB/N * ICR MGI:5604728
cn169
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT5-cre/PGR)1Der/0
involves: 129P2/OlaHsd * C57BL/6N * FVB/N * ICR MGI:5618126
cn170
Coro1ctm1c(KOMP)Wtsi/Coro1ctm1c(KOMP)Wtsi
Ptentm2Mak/Ptentm2Mak
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre/Esr1*,-lacZ)ASbk/0
involves: 129P2/OlaHsd * C57BL/6N * FVB/NJ MGI:6444814
cn171
Atriptm1.1Pof/Atriptm1.1Pof
Tg(Nes-cre)1Kln/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:6501211
cn172
Trp53tm1Brn/Trp53tm1Brn
Tubb5tm2.1Dak/Tubb5+
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:6119482
cn173
Cd79atm1(cre)Reth/Cd79a+
Huwe1tm1.1Mak/Y
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5314906
cn174
Krt14tm1.1(cre)Wbm/Krt14+
Tg(KRT14-Snai1)1Efu/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * CD-1 MGI:6196149
cn175
Rb1tm2Brn/Rb1tm2Brn
Rbl1tm1Htr/Rbl1+
Trp53tm1Brn/Trp53tm1Brn
Tg(En2-cre)22Alj/0
involves: 129P2/OlaHsd * CD-1 MGI:3707502
cn176
Chek1tm2.1Sje/Chek1tm2.1Sje
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)#Mam/0
involves: 129P2/OlaHsd * FVB MGI:4818615
cn177
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)#Mam/0
involves: 129P2/OlaHsd * FVB MGI:4818620
cn178
Chek1tm2.1Sje/Chek1+
Trp53tm1Brn/Trp53+
Tg(MMTV-cre)#Mam/0
involves: 129P2/OlaHsd * FVB MGI:4818619
cn179
Chek1tm2.1Sje/Chek1tm2.1Sje
Trp53tm1Brn/Trp53+
Tg(MMTV-cre)#Mam/0
involves: 129P2/OlaHsd * FVB MGI:4818618
cn180
Chek1tm2.1Sje/Chek1+
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)#Mam/0
involves: 129P2/OlaHsd * FVB MGI:4818610
cn181
Trp53tm1Brn/Trp53tm1Brn
Tg(Wap-cre)51Nki/0
involves: 129P2/OlaHsd * FVB/N MGI:6296607
cn182
Cdh1tm1Jjon/Cdh1+
Trp53tm1Brn/Trp53tm1Brn
Tg(Wap-cre)51Nki/0
involves: 129P2/OlaHsd * FVB/N MGI:6296608
cn183
Cdh1tm1Jjon/Cdh1tm1Jjon
Trp53tm1Brn/Trp53+
Tg(Wap-cre)51Nki/0
involves: 129P2/OlaHsd * FVB/N MGI:6296609
cn184
Dcctm1Nki/Dcctm1Nki
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/?
involves: 129P2/OlaHsd * FVB/N MGI:5308805
cn185
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * FVB/N MGI:3831430
cn186
Trp53tm1Brn/Trp53tm1Brn
Tg(Gfap-cre)2Brn/0
involves: 129P2/OlaHsd * FVB/N MGI:3804219
cn187
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Gfap-cre)2Brn/0
involves: 129P2/OlaHsd * FVB/N MGI:3804217
cn188
Tg(Amh-SMAD2*)#Jebu/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * FVB/N MGI:5543911
cn189
Cdh1tm1Jjon/Cdh1tm1Jjon
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * FVB/N MGI:3695271
cn190
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * FVB/N MGI:3695270
cn191
Cdh1tm1Jjon/Cdh1tm1Jjon
Trp53tm1Brn/Trp53+
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * FVB/N MGI:3695272
cn192
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Brn/Trp53+
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * FVB/N MGI:3831432
cn193
Cdh1tm1Jjon/Cdh1+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * FVB/N MGI:3695273
cn194
Brca2tm1Brn/Brca2+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre)8Brn/0
involves: 129P2/OlaHsd * FVB/N MGI:3831431
cn195
Cdh1tm1Jjon/Cdh1tm1Jjon
Trp53tm1Brn/Trp53tm1Brn
Tg(Wap-cre)51Nki/0
involves: 129P2/OlaHsd * FVB/N MGI:6296606
cn196
Nf2tm2Gth/Nf2tm2Gth
Ptgdstm1.1(cre)Gvn/Ptgds+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * FVB/N MGI:5051644
cn197
Ptentm2Mak/Ptentm2Mak
Tg(GFAP-cre/Esr1*,-lacZ)ASbk/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * FVB/NJ MGI:6444813
cn198
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Scgb1a1-rtTA)1Jaw/0
involves: 129S4/SvJae MGI:4368025
cn199
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182tm1.1Dgk
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704424
cn200
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182+
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704427
cn201
Gt(ROSA)26Sortm1(CAG-Mir182)Dgk/Gt(ROSA)26Sortm1(CAG-Mir182)Dgk
Krastm4Tyj/Krastm4Tyj
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704425
cn202
Krastm4Tyj/Kras+
Pax7tm2.1(cre/ERT2)Fan/Pax7+
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129X1/SvJ * C57BL/6 MGI:5547938
cn203
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm3Glo
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722604
cn204
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722603
cn205
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722605
cn206
Apctm2Rak/Apc+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * FVB/N * SJL MGI:5898453


Genotype
MGI:3831428
hm1
Allelic
Composition
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are normal




Genotype
MGI:3696698
cn2
Allelic
Composition
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• in 6 of 7 mice treated with a cre-expressing adenovirus (J:86077)
• in 6 of 7 mice following treatment with cre-expressing adenovirus (J:157319)

cellular
N
• ovarian surface epithelium (OSE) cells do not show any enhancement of proliferation after adenoviral cre treatment
• ovarian surface epithelium cells transfected with a cre-expressing adenovirus exhibit increased cell motility and invasion compared with cells transfected with a lacZ-expressing adenovirus
• after adenoviral cre infection, OSE cells in culture show significantly higher sensitivity to cisplatin treatment compared to control cells (31% remain ater 48 hours compared to 40% of control cells remaining)
• ovarian surface epithelium cells transfected with a cre-expressing adenovirus exhibit increased cell motility compared with cells transfected with a lacZ-expressing adenovirus

neoplasm
N
• mice do not develop mesothelioma following injection of adenovirus expressing Cre into the bladder or intraperitoneally at 2-3 months of age
• in 6 of 7 mice treated with a cre-expressing adenovirus (J:86077)
• in 6 of 7 mice following treatment with cre-expressing adenovirus (J:157319)

homeostasis/metabolism
• ovarian surface epithelium cells with a cre-expressing adenovirus exhibit enhanced wound closure compared with cells transfected with a lacZ-expressing adenovirus




Genotype
MGI:5544201
cn3
Allelic
Composition
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa develop bursal cysts 6 months after injection
• however, mice injected with an adenovirus expressing cre recombinase into the oviduct exhibit no change in phenotype 3 months after injection

endocrine/exocrine glands
• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa develop bursal cysts 6 months after injection
• however, mice injected with an adenovirus expressing cre recombinase into the oviduct exhibit no change in phenotype 3 months after injection
• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa exhibit ovary degeneration 6 months after injection

reproductive system
• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa develop bursal cysts 6 months after injection
• however, mice injected with an adenovirus expressing cre recombinase into the oviduct exhibit no change in phenotype 3 months after injection
• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa exhibit ovary degeneration 6 months after injection




Genotype
MGI:4437464
cn4
Allelic
Composition
Trp53tm1Brn/Trp53tm1.1Brn
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1.1Brn mutation (0 available); any Trp53 mutation (210 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• in all mice treated with a cre-expressing adenovirus (J:86077)
• in 6 of 7 mice following treatment with cre-expressing adenovirus (J:157319)

neoplasm
• in all mice treated with a cre-expressing adenovirus (J:86077)
• in 6 of 7 mice following treatment with cre-expressing adenovirus (J:157319)




Genotype
MGI:5293783
cn5
Allelic
Composition
Trp53tm1Brn/Trp53tm2Tyj
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• ovarian surface epithelium cells transfected with a cre-expressing adenovirus exhibit increased invasion compared with control cells that is not as severe as in similarly treated cells from Trp53tm1Brn homozygotes




Genotype
MGI:5897837
cn6
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Trp53tm1Brn/Trp53tm1Brn
Tg(TPO-cre)1Shk/0
Genetic
Background
129.Cg-Tg(TPO-cre)1Shk Trp53tm1Brn Ptentm2.1Ppp
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (78 available)
Tg(TPO-cre)1Shk mutation (1 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival is 38.4 weeks

neoplasm
• 4-8 week old mice only show areas of well differentiated follicular carcinomas but go on to develop well-differentiated follicular carcinomas by 8-10 months of age exhibiting spindle cell morphology, giant, osteoclast-like, multinucleated cells and areas of osseous metaplasia resembling human thyroid anaplastic carcinomas
• anaplastic thyroid carcinomas undergo dedifferentiation, genomic instability and epithelial-to-mesenchymal transition and exhibit a shift from an oxidative to a glycolytic pathway
• aggressive tumors invade locally into the muscle and trachea and metastasize to the lungs in 28% of mice, or less often, to the liver

endocrine/exocrine glands
• all 8-10 month old mice exhibit enlarged thyroid gland causing severe tracheal compression
• 4-8 week old mice only show areas of well differentiated follicular carcinomas but go on to develop well-differentiated follicular carcinomas by 8-10 months of age exhibiting spindle cell morphology, giant, osteoclast-like, multinucleated cells and areas of osseous metaplasia resembling human thyroid anaplastic carcinomas
• anaplastic thyroid carcinomas undergo dedifferentiation, genomic instability and epithelial-to-mesenchymal transition and exhibit a shift from an oxidative to a glycolytic pathway

homeostasis/metabolism
• reduction in TSH serum levels
• however, T4 levels are normal

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
thyroid gland carcinoma DOID:3963 J:211100




Genotype
MGI:5437517
cn7
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Gfap-cre)2Brn/0
Genetic
Background
either: (involves: 129 * 129P2/OlaHsd * FVB/N) or (involves: 129 * 129P2/OlaHsd * C57BL/6 * FVB/N)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki mutation (0 available); any Gt(ROSA)26Sor mutation (765 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Tg(Gfap-cre)2Brn mutation (1 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands

nervous system
• as in Rb1tm2Brn/Rb1tm2Brn Trp53tm1Brn/Trp53tm1Brn Tg(Gfap-cre)2Brn mice

neoplasm
• as in Rb1tm2Brn/Rb1tm2Brn Trp53tm1Brn/Trp53tm1Brn Tg(Gfap-cre)2Brn mice
• large cell carcinoma




Genotype
MGI:5645995
cn8
Allelic
Composition
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Tg(Tyr-NRAS*Q61K)1Bee/0
Genetic
Background
FVB.Cg-Tg(Tyr-cre/ERT2)13Bos Trp53tm1Brn Tg(Tyr-NRAS*Q61K)1Bee
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
Tg(Tyr-NRAS*Q61K)1Bee mutation (1 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• spontaneous development of malignant melanoma by 200 days of age in all mice treated with tamoxifen
• tumors of tamoxifen-treated mice are relatively small, with regular ovoid shape and high levels of Ki-67 staining
• naevi are not seen above dermal malignant melanomas in tamoxifen treated mice, although small nests of melanocytes in a subepidermal location are occasionally seen
• early lesions of tamoxifen treated mice do not show evidence of tumor derivation from the upper dermis and appear to be derived from follicular or other deep dermal precursors
• majority of tumors of tamoxifen treated mice are located on the back
• all mice treated with tamoxifen develop malignant melanoma before 150 days of age after a single neonatal UVB dose
• tamoxifen-treated mice show a diminished response of melanocyte emigration from the upper regions of hair follicles to the epidermal basal layer 3-5 days after neonatal UV radiation compared to controls

integument
• spontaneous development of malignant melanoma by 200 days of age in all mice treated with tamoxifen
• tumors of tamoxifen-treated mice are relatively small, with regular ovoid shape and high levels of Ki-67 staining
• naevi are not seen above dermal malignant melanomas in tamoxifen treated mice, although small nests of melanocytes in a subepidermal location are occasionally seen
• early lesions of tamoxifen treated mice do not show evidence of tumor derivation from the upper dermis and appear to be derived from follicular or other deep dermal precursors
• majority of tumors of tamoxifen treated mice are located on the back




Genotype
MGI:4837145
cn9
Allelic
Composition
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)105Ayn/0
Genetic
Background
FVB.Cg-Trp53tm1Brn Rb1tm2Brn Tg(MMTV-cre)105Ayn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Tg(MMTV-cre)105Ayn mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• 4 of 40 mice develop lung metastasis

endocrine/exocrine glands
• 15 of 17 mice develop mammary neoplasms
• mammary tumor cells exhibit increased genomic instability compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice

integument
• 15 of 17 mice develop mammary neoplasms
• mammary tumor cells exhibit increased genomic instability compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice

neoplasm
• 15 of 17 mice develop mammary neoplasms
• mammary tumor cells exhibit increased genomic instability compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice
• cell proliferation in mammary carcinomas is increased compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice
• 10 of 43 neoplasms are well-differentiated carcinomas
• while one tumor is an adenosquamous carcinoma the remaining tumors are poorly differentiated carcinomas with spindle or polygonal, frequently pleomorphic cells
• 1 adenosquamous carcinoma
• 4 of 40 mice develop lung metastasis

cellular
• mammary tumor cells exhibit increased genomic instability compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice




Genotype
MGI:4837144
cn10
Allelic
Composition
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)105Ayn/0
Genetic
Background
FVB.Cg-Trp53tm1Brn Tg(MMTV-cre)105Ayn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(MMTV-cre)105Ayn mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• 3 of 27 mice develop lung metastasis

endocrine/exocrine glands
• by 700 days, 8 of 16 mice develop mammary neoplasms
• however, mice do not exhibit lymphomas or other non-mammary neoplasms

integument
• by 700 days, 8 of 16 mice develop mammary neoplasms
• however, mice do not exhibit lymphomas or other non-mammary neoplasms

neoplasm
• by 700 days, 8 of 16 mice develop mammary neoplasms
• however, mice do not exhibit lymphomas or other non-mammary neoplasms
• 8 of 27 neoplasms are well-differentiated carcinomas
• while one tumor is an adenosquamous carcinoma the remaining tumors are poorly differentiated carcinomas with spindle or polygonal, frequently pleomorphic cells
• 1 adenosquamous carcinoma
• 3 of 27 mice develop lung metastasis




Genotype
MGI:5662454
cn11
Allelic
Composition
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Ren-cre)#Kwg/0
Genetic
Background
involves: 129 * 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Tg(Ren-cre)#Kwg mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• pancreatic tumors and liver metastasis express high levels of glucagon and mice exhibit increased circulating glucagon levels indicating that tumors are glucagonoma
• mice develop pancreatic neuroendocrine tumors that are classified as metastatic islet cell carcinoma; tumors are nodular and highly vascularized
• marker analysis indicates that both the primary pancreatic tumor and the liver metastases are pancreatic neuroendocrine in origin

neoplasm
• pancreatic tumors and liver metastasis express high levels of glucagon and mice exhibit increased circulating glucagon levels indicating that tumors are glucagonoma
• mice develop pancreatic neuroendocrine tumors that are classified as metastatic islet cell carcinoma; tumors are nodular and highly vascularized
• marker analysis indicates that both the primary pancreatic tumor and the liver metastases are pancreatic neuroendocrine in origin
• metastasis to the liver and lymph node is seen; liver metastases are nodular and highly vascularized
• liver also contains many separate metastatic foci
• mice develop subcutaneous tumors infrequently at around 3-4 months of age; these tumors have a solid growth pattern and are consistent with high-grade vascular sarcoma

mortality/aging
• primary mortality is from metastatic pancreatic neuroendocrine disease with lethal onset beginning at around 22 weeks of age
• in rare instances, mice develop subcutaneous tumors and need to be euthanized at around 12-16 weeks of age and in even more rare cases, mice die as early as 8 weeks of age of unknown causes; these cases constitute about 12% of mice

homeostasis/metabolism
• mice show increased circulating glucagon levels at 4, 5 and 6 months but not at 2 months of age

growth/size/body
• 32% reduction in body weight of sick mutants

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
adenoma DOID:657 J:216559
pancreatic carcinoma DOID:4905 OMIM:260350
J:216559




Genotype
MGI:5796166
cn12
Allelic
Composition
Prkar1atm1.2Lsk/Prkar1a+
Rb1tm2Brn/Rb1+
Tg(Col1a1-cre)1Kry/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prkar1atm1.2Lsk mutation (1 available); any Prkar1a mutation (16 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Tg(Col1a1-cre)1Kry mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive to around 13.9 weeks
• treatment of mice with RANK-Fc prolongs survival to around 17.8 weeks

neoplasm
• mice develop osteosarcoma within 10.3 weeks of age
• tumors are marked by high TNFSF11 (RANKL)/low TNFRSF11A (RANK) levels
• treatment of mice with RANK-Fc for 52 weeks beginning at 12.6 weeks of age keeps mice tumor-free until 64.6 weeks of age

skeleton
• mice develop osteosarcoma within 10.3 weeks of age
• tumors are marked by high TNFSF11 (RANKL)/low TNFRSF11A (RANK) levels
• treatment of mice with RANK-Fc for 52 weeks beginning at 12.6 weeks of age keeps mice tumor-free until 64.6 weeks of age

cellular
• in a scratch wound healing assay, tumor cells show greater migration than tumor cells from conditional Rb1tm2Brn heterozygous Trp53tm1Brn homozygous double mutants

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
osteosarcoma DOID:3347 OMIM:259500
J:234128




Genotype
MGI:5796167
cn13
Allelic
Composition
Prkar1atm1.2Lsk/Prkar1a+
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Col1a1-cre)1Kry/0
Genetic
Background
involves: 129 * 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prkar1atm1.2Lsk mutation (1 available); any Prkar1a mutation (16 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Tg(Col1a1-cre)1Kry mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice do not live longer than 11 weeks
• treatment of mice with RANK-Fc prolongs survival to around to around 13.3 weeks

neoplasm
• mice develop osteosarcoma within 6.3 weeks of age
• tumors are marked by high (TNFSF11) RANKL/low (TNFRSF11A) RANK levels
• treatment of mice with RANK-Fc starting at 2.4 weeks of age suppresses tumor growth
• mice develop tumors 4.3 weeks after the discontinuation of RANK-Fc treatment and large numbers of osteoclasts are seen lining the boundary of tumor cells and adjacent osteopetrotic bone

skeleton
• mice develop osteosarcoma within 6.3 weeks of age
• tumors are marked by high (TNFSF11) RANKL/low (TNFRSF11A) RANK levels
• treatment of mice with RANK-Fc starting at 2.4 weeks of age suppresses tumor growth
• mice develop tumors 4.3 weeks after the discontinuation of RANK-Fc treatment and large numbers of osteoclasts are seen lining the boundary of tumor cells and adjacent osteopetrotic bone

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
osteosarcoma DOID:3347 OMIM:259500
J:234128




Genotype
MGI:5460854
cn14
Allelic
Composition
Calcatm1.1(cre/ERT2)Ptch/Calca+
Trp53tm1Brn/Trp53tm1Brn
Rb1tm2Brn/Rb1tm2Brn
Ptentm1Hwu/Ptentm1Hwu
Genetic
Background
involves: 129 * 129P2/OlaHsd * 129S4/SvJae * BALB/c * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Calcatm1.1(cre/ERT2)Ptch mutation (0 available); any Calca mutation (16 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (78 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• all mice develop thyroid tumors

mortality/aging
• death within 3 months of tamoxifen treatment

respiratory system
• small cell lung tumors 2.5 months after tamoxifen treatment
• increased proliferation of pulmonary neuroendocrine cells

neoplasm
• all mice develop thyroid tumors
• increased invasiveness at 2.5 months after tamoxifen treatment
• small cell lung tumors 2.5 months after tamoxifen treatment




Genotype
MGI:5563244
cn15
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (765 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor

neoplasm
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor




Genotype
MGI:5563247
cn16
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (765 available)
Ptentm1Mro mutation (1 available); any Pten mutation (78 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor

neoplasm
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor




Genotype
MGI:5519100
cn17
Allelic
Composition
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6J * CD-1 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• low penetrance (8.33%) of osteosarcomas with a long latency of 338 days of age on average

neoplasm
• low penetrance (8.33%) of osteosarcomas with a long latency of 338 days of age on average




Genotype
MGI:5519099
cn18
Allelic
Composition
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6J * CD-1 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• complete penetrance of osteosarcomas with an average latency of 292 days

mortality/aging
• mice die from around 250 to 375 days of age

neoplasm
• tumors show metastasis, most frequently to the lung and then the liver
• complete penetrance of osteosarcomas with an average latency of 292 days




Genotype
MGI:5796161
cn19
Allelic
Composition
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Col1a1-cre)1Kry/0
Genetic
Background
involves: 129 * 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Tg(Col1a1-cre)1Kry mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive up to 38.1 weeks of age

neoplasm
• mice develop osteosarcoma by 20 weeks of age

skeleton
• mice develop osteosarcoma by 20 weeks of age




Genotype
MGI:5796164
cn20
Allelic
Composition
Rb1tm2Brn/Rb1+
Trp53tm1Brn/Trp53tm1Brn
Tg(Col1a1-cre)1Kry/0
Genetic
Background
involves: 129 * 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Tg(Col1a1-cre)1Kry mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive up to 55.4 weeks of age

neoplasm
• mice develop osteosarcoma by 35 weeks of age
• tumors are marked by low TNFSF11 (RANKL)/high TNFRSF11A (RANK) levels

skeleton
• mice develop osteosarcoma by 35 weeks of age
• tumors are marked by low TNFSF11 (RANKL)/high TNFRSF11A (RANK) levels




Genotype
MGI:5460840
cn21
Allelic
Composition
Calcatm1.1(cre/ERT2)Ptch/Calca+
Trp53tm1Brn/Trp53tm1Brn
Rb1tm2Brn/Rb1tm2Brn
Genetic
Background
involves: 129 * 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Calcatm1.1(cre/ERT2)Ptch mutation (0 available); any Calca mutation (16 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• all mice develop thyroid tumors

mortality/aging
• death within 6-7 months of tamoxifen treatment

respiratory system
• small cell lung tumors 5-6 months after tamoxifen treatment in 4 of 32 mice examined, all with pulmonary neuroendocrine cells hyperplasia as well
• pulmonary neuroendocrine cells hyperplasia 5-6 months after tamoxifen treatment in 16 of 32 mice examined
• increased proliferation of pulmonary neuroendocrine cells

neoplasm
• all mice develop thyroid tumors
• small cell lung tumors 5-6 months after tamoxifen treatment in 4 of 32 mice examined, all with pulmonary neuroendocrine cells hyperplasia as well




Genotype
MGI:5437518
cn22
Allelic
Composition
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Gfap-cre)2Brn/0
Genetic
Background
involves: 129 * 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Tg(Gfap-cre)2Brn mutation (1 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:3813634
cn23
Allelic
Composition
Pgrtm2(cre)Lyd/Pgr+
Ptentm1Hwu/Ptentm1Hwu
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pgrtm2(cre)Lyd mutation (0 available); any Pgr mutation (50 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (78 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• impaired survival is seen beginning around 2 months of age
• death appears to result from excessive bleeding due to invasion of uterine blood vessels by tumor cells

reproductive system
• hyperplasia progresses to carcinoma by 3 weeks of age
• by P10, luminal and glandular epithelial hyperplasia are seen
• enlarged relative to conditional mutants that are wild type for Trp53

neoplasm
• hyperplasia progresses to carcinoma by 3 weeks of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
endometrial cancer DOID:1380 OMIM:608089
J:139053




Genotype
MGI:5308962
cn24
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (56 available)
Krastm4Tyj mutation (9 available); any Kras mutation (56 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 13.1 weeks
• 25% of tumors exhibit sarcomatoid carcinoma histology
• 75% of tumors exhibit well differentiated ductal adenocarcinoma histology

neoplasm
• mutants develop pancreatic tumors with an average latency of 13.1 weeks
• 25% of tumors exhibit sarcomatoid carcinoma histology
• 75% of tumors exhibit well differentiated ductal adenocarcinoma histology
• 25% of tumors exhibit metastasis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:108298




Genotype
MGI:5308961
cn25
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (56 available)
Krastm4Tyj mutation (9 available); any Kras mutation (56 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 14.7 weeks
• 19% of tumors exhibit sarcomatoid differentiation
• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology

neoplasm
• mutants develop pancreatic tumors with an average latency of 14.7 weeks
• 19% of tumors exhibit sarcomatoid differentiation
• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology
• 25% of tumors exhibit metastasis




Genotype
MGI:5308959
cn26
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (56 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 21.8 weeks
• 100% of tumors are well differentiated ductal adenocarcinomas

neoplasm
• mutants develop pancreatic tumors with an average latency of 21.8 weeks
• 100% of tumors are well differentiated ductal adenocarcinomas
• 33% of tumors exhibit metastasis




Genotype
MGI:5308954
cn27
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (56 available)
Krastm4Tyj mutation (9 available); any Kras mutation (56 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 7.2 weeks
• 60% of tumors exhibit anaplastic carcinoma histology
• 40% of tumors exhibit well differentiated ductal adenocarcinoma histology

neoplasm
• mutants develop pancreatic tumors with an average latency of 7.2 weeks
• 60% of tumors exhibit anaplastic carcinoma histology
• 40% of tumors exhibit well differentiated ductal adenocarcinoma histology
• 20% of tumors exhibit metastasis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:108298




Genotype
MGI:5308951
cn28
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (56 available)
Krastm4Tyj mutation (9 available); any Kras mutation (56 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 6.5 weeks
• 20% of tumors exhibit anaplastic carcinoma histology
• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology

neoplasm
• mutants develop pancreatic tumors with an average latency of 6.5 weeks
• 20% of tumors exhibit anaplastic carcinoma histology
• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:108298




Genotype
MGI:5308946
cn29
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (56 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 6.2 weeks
• mutants exhibit rapid pancreatic ductal adenocaracinoma progression, developing lethal tumors by 8 weeks of age
• 100% of tumors are well differentiated ductal adenocarcinomas

neoplasm
• mutants develop pancreatic tumors with an average latency of 6.2 weeks
• mutants exhibit rapid pancreatic ductal adenocaracinoma progression, developing lethal tumors by 8 weeks of age
• 100% of tumors are well differentiated ductal adenocarcinomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:108298




Genotype
MGI:5543693
cn30
Allelic
Composition
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Tg(Vil1-cre/ERT2)23Syr/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * C57BL/6 * CD-1 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csnk1a1tm1.1Ybn mutation (1 available); any Csnk1a1 mutation (35 available)
Tg(Vil1-cre/ERT2)23Syr mutation (1 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• after 2 weeks of tamoxifen treatment

neoplasm
• widespread high-grade dysplasia and numerous intramucosal carcinomas invading the lamina propria in most of the small-bowel crypts and villi within 2 weeks of tamoxifen treatment

digestive/alimentary system
• increased proliferation after tamoxifen treatment throughout the crypt-villus axis

cellular
• in the gut of tamoxifen treated mice but no more so than in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Tg(Vil-cre/ERT2)23Syr mice
• increased proliferation after tamoxifen treatment throughout the crypt-villus axis




Genotype
MGI:5543694
cn31
Allelic
Composition
Csnk1a1tm1.1Ybn/Csnk1a1+
Tg(Vil1-cre/ERT2)23Syr/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * C57BL/6 * CD-1 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csnk1a1tm1.1Ybn mutation (1 available); any Csnk1a1 mutation (35 available)
Tg(Vil1-cre/ERT2)23Syr mutation (1 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• within 6 months, 7 of 9 tamoxifen-treated mice develop invasive carcinomas that permeates the bowel muscular wall into the subserosal fat with some involvement of the serosal surface (stage T4)




Genotype
MGI:5634401
cn32
Allelic
Composition
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (167 available)
Smad4tm2.1Cxd mutation (2 available); any Smad4 mutation (35 available)
Tg(Vil1-cre)20Syr mutation (3 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.2 months of age and no distant metastases are seen

neoplasm
• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.2 months of age and no distant metastases are seen




Genotype
MGI:5431947
cn33
Allelic
Composition
Ptentm1Rdp/Ptentm1Rdp
Smad4tm1Rdp/Smad4tm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Rdp mutation (0 available); any Pten mutation (78 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (35 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• tumors are more aggressive than in mutant mice wild-type for Smad4

reproductive system
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• tumors are more aggressive than in mutant mice wild-type for Smad4

mortality/aging
• survival time is shorter than in mutant mice wild-type for Smad4
• median survival time of 17.05 weeks

neoplasm
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• tumors are more aggressive than in mutant mice wild-type for Smad4
• bone metastases are seen in some (3 of 24) mice unlike in mutant mice wild-type for Smad4




Genotype
MGI:5634403
cn34
Allelic
Composition
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(MMTV-cre)7Mul/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (167 available)
Smad4tm2.1Cxd mutation (2 available); any Smad4 mutation (35 available)
Tg(MMTV-cre)7Mul mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• mice develop mammary gland carcinoma with a median tumor-free survival of 10.4 months of age
• tumors are invasive ductal carcinomas with a squamous component, however lobular carcinomas are not seen

endocrine/exocrine glands
• mice develop mammary gland carcinoma with a median tumor-free survival of 10.4 months of age
• tumors are invasive ductal carcinomas with a squamous component, however lobular carcinomas are not seen

neoplasm
• mice develop mammary gland carcinoma with a median tumor-free survival of 10.4 months of age
• tumors are invasive ductal carcinomas with a squamous component, however lobular carcinomas are not seen
• 33% of mice show lung metastasis




Genotype
MGI:5634400
cn35
Allelic
Composition
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (167 available)
Smad4tm2.1Cxd mutation (2 available); any Smad4 mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 36% of mice develop duodenal adenocarcinomas
• 84% of mice develop spontaneous tumors in the glandular stomach with a median tumor-free survival of 8 months
• gastric tumors resemble diffuse-type gastric adenocarcinomas, are E-cadherin-negative, and are invasive into the muscle layers and regional lymph nodes
• intramucosal adenocarcinomas with signet ring cell feature is seen in 2 of 4 mice at 6 months of age
• gastric premalignant lesions such as atrophic gastritis, metaplasia or dysplasia are not seen at 4 and 5 months of age

mortality/aging
• most common cause of death is duodenal obstruction, followed by gastric outlet obstruction

neoplasm
• 36% of mice develop duodenal adenocarcinomas
• 84% of mice develop spontaneous tumors in the glandular stomach with a median tumor-free survival of 8 months
• gastric tumors resemble diffuse-type gastric adenocarcinomas, are E-cadherin-negative, and are invasive into the muscle layers and regional lymph nodes
• intramucosal adenocarcinomas with signet ring cell feature is seen in 2 of 4 mice at 6 months of age
• gastric premalignant lesions such as atrophic gastritis, metaplasia or dysplasia are not seen at 4 and 5 months of age
• 3 of 21 mice with gastric adenocarcinomas develop lung metastases
• metastatic lesions have similar cytologic features to primary gastric tumors
• 8% of mice exhibit adenocarcinomas in the pancreas, most likely due to invasion of the primary duodenal or gastric adenocarcinomas
• 24% of mice develop forestomach squamous cell carcinomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
stomach cancer DOID:10534 OMIM:613659
J:212549




Genotype
MGI:5634407
cn36
Allelic
Composition
Cdh1tm2Kem/Cdh1tm2Kem
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (167 available)
Smad4tm2.1Cxd mutation (2 available); any Smad4 mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop gastric adenocarcinomas with a median tumor-free survival of 9.4 months but do not develop distant metastases

neoplasm
• mice develop gastric adenocarcinomas with a median tumor-free survival of 9.4 months but do not develop distant metastases




Genotype
MGI:5293779
cn37
Allelic
Composition
Mettm1Sst/Mettm1Sst
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mettm1Sst mutation (1 available); any Met mutation (48 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
N
• ovarian surface epithelium cells transfected with a cre-expressing adenovirus exhibit reduced invasion compared with cells from Trp53tm1Brn homozygotes transfected with a lacZ-expressing adenoviru




Genotype
MGI:5825466
cn38
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Trp53tm1Brn/Trp53tm1Brn
Tg(Nes-cre/ERT2,-ALPP)1Sbk/0
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (4 available); any Pten mutation (78 available)
Tg(Nes-cre/ERT2,-ALPP)1Sbk mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 100% of mice induced with tamoxifen at P0 and P1 develop medulloblastoma with a median onset of morbidity of 63 days of age
• medullablastomas of tamoxifen treated mice show extensive and abnormal vascularization and highly differentiated tumor cells surrounding a perivascular tumor stem cell niche that is not seen in single Trp53 conditional mutants
• blood clots are often seen in the lumen of abnormal blood vessels
• medulloblastoma initiates from a perivascular tumor stem cell niche
• medulloblastomas of tamoxifen treated mice acquire somatic inactivation of Ptch1 and show expression signatures of sonic hedgehog subgroup medulloblastoma
• 18 of 26 mice treated with tamoxifen at P0 and P1 develop gliomas in the forebrain and brain stem

nervous system
• 100% of mice induced with tamoxifen at P0 and P1 develop medulloblastoma with a median onset of morbidity of 63 days of age
• medullablastomas of tamoxifen treated mice show extensive and abnormal vascularization and highly differentiated tumor cells surrounding a perivascular tumor stem cell niche that is not seen in single Trp53 conditional mutants
• blood clots are often seen in the lumen of abnormal blood vessels
• medulloblastoma initiates from a perivascular tumor stem cell niche
• medulloblastomas of tamoxifen treated mice acquire somatic inactivation of Ptch1 and show expression signatures of sonic hedgehog subgroup medulloblastoma
• 18 of 26 mice treated with tamoxifen at P0 and P1 develop gliomas in the forebrain and brain stem
• cerebellum at P21 of mice treated with tamoxifen at birth shows disrupted lamination and abundant Ki67+ proliferative cells throughout the cerebellum , which are concentrated around blood vessels either under the pial surface or in the parenchyma

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:237990




Genotype
MGI:3712022
cn39
Allelic
Composition
Braftm1Mmcm/Braf+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (44 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 8 weeks after adenoCre treatment, lungs show rapid cancer progression with increased proliferation compared to Trp53-sufficient mice
• tumors show nodules composed of central papillary structures with solid peripheral areas
• all double mutants show increased proliferation, and cells show altered nuclear morphology, while Trp53 conditional single mutants have normal lung phenotypes
• 2/5 mice are found to have prominent adenocarcinomas, composed of glandular structures lined by atypical cells with enlarged nuclei, hyperchromasia, contour irregularities, and prominent nucleoli
• large areas of necrosis are present in adenocarcinomas, with evidence of lymphatic and vascular invasion

respiratory system
• 8 weeks after adenoCre treatment, lungs show rapid cancer progression with increased proliferation compared to Trp53-sufficient mice
• tumors show nodules composed of central papillary structures with solid peripheral areas
• all double mutants show increased proliferation, and cells show altered nuclear morphology, while Trp53 conditional single mutants have normal lung phenotypes
• 2/5 mice are found to have prominent adenocarcinomas, composed of glandular structures lined by atypical cells with enlarged nuclei, hyperchromasia, contour irregularities, and prominent nucleoli
• large areas of necrosis are present in adenocarcinomas, with evidence of lymphatic and vascular invasion
• 8 weeks after Cre treatment, some small airways display papillary hyperplasia, not seen in Braf-conditional mice




Genotype
MGI:3696696
cn40
Allelic
Composition
Brca1tm1Brn/Brca1tm1Brn
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Brn mutation (2 available); any Brca1 mutation (94 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• after adenoviral cre treatment, double mutant OSE cells show significantly enhanced proliferation compared to control cells




Genotype
MGI:5704166
cn41
Allelic
Composition
Rb1tm2Brn/Rb1+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• in some mice treated with a cre-expressing adenovirus
• small in some mice treated with a cre-expressing adenovirus

neoplasm
• some mice treated with a cre-expressing adenovirus exhibit metastasis in the mediastinum, ovary and adrenal gland
• in some mice treated with a cre-expressing adenovirus
• small in some mice treated with a cre-expressing adenovirus




Genotype
MGI:4437461
cn42
Allelic
Composition
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• after a single ovarian intrabursal injection of an adenovirus expressing Cre, mutant females develop epithelial ovarian cancer similar in progression of disease in women, with ovarian neoplasms spreading, forming ascites and metastasizing to the contralateral ovary, the lung and the liver
• 39% are well-differentiated serous epithelial neoplasms of the ovary and 45% are poorly differentiated CK8-positive neoplasms of the ovary
• the ovarian cancer found after a single ovarian intrabursal injection of an adenovirus expressing Cre is characterisitic of serous adenocarcinoma

respiratory system
• mice treated with cre-expressing adenovirus median tumor-free survival is 210 days
• bronchioalveolar carcinomas in some mice treated with a cre-expressing adenovirus
• mice treated with a cre-expressing adenovirus exhibit multiple dysplastic foci of clustering small cells in the bronchial and bronchiolar mucosa (J:86077)
• mice treated with cre-expressing adenovirus exhibit dysplastic foci of clustering small cells in the bronchial and bronchiolar mucosa unlike in wild-type mice (J:157319)

endocrine/exocrine glands
• after a single ovarian intrabursal injection of an adenovirus expressing Cre, mutant females develop epithelial ovarian cancer similar in progression of disease in women, with ovarian neoplasms spreading, forming ascites and metastasizing to the contralateral ovary, the lung and the liver
• 39% are well-differentiated serous epithelial neoplasms of the ovary and 45% are poorly differentiated CK8-positive neoplasms of the ovary
• the ovarian cancer found after a single ovarian intrabursal injection of an adenovirus expressing Cre is characterisitic of serous adenocarcinoma
• medullary thyroid carcinomas in some mice treated with a cre-expressing adenovirus (J:86077)
• following treatment with cre-expressing adenovirus, 6 of 33 mice develop medullary thyroid carcinoma unlike wild-type mice (J:157319)

mortality/aging
• 97% of mice succumb to ovarian tumors at a median age of 227 days after after a single ovarian intrabusal injection of an adenovirus expressing Cre

neoplasm
• after a single ovarian intrabursal injection of an adenovirus expressing Cre, mutant females develop epithelial ovarian cancer similar in progression of disease in women, with ovarian neoplasms spreading, forming ascites and metastasizing to the contralateral ovary, the lung and the liver
• 39% are well-differentiated serous epithelial neoplasms of the ovary and 45% are poorly differentiated CK8-positive neoplasms of the ovary
• the ovarian cancer found after a single ovarian intrabursal injection of an adenovirus expressing Cre is characterisitic of serous adenocarcinoma
• medullary thyroid carcinomas in some mice treated with a cre-expressing adenovirus (J:86077)
• following treatment with cre-expressing adenovirus, 6 of 33 mice develop medullary thyroid carcinoma unlike wild-type mice (J:157319)
• various metastases in some mice treated with a cre-expressing adenovirus
• 15% of tumors that form in females after a single ovarian intrabursal injection of an adenovirus expressing Cre metastasized to the opposite ovary, 18% of tumors metastasized to the lung, and 6% of tumors metastasized to the liver
• mice treated with cre-expressing adenovirus median tumor-free survival is 210 days
• bronchioalveolar carcinomas in some mice treated with a cre-expressing adenovirus
• mice treated with a cre-expressing adenovirus exhibit multiple dysplastic foci of clustering small cells in the bronchial and bronchiolar mucosa (J:86077)
• mice treated with cre-expressing adenovirus exhibit dysplastic foci of clustering small cells in the bronchial and bronchiolar mucosa unlike in wild-type mice (J:157319)




Genotype
MGI:4437462
cn43
Allelic
Composition
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• mice treated with cre-expressing adenovirus median tumor-free survival is 475 days
• in some mice treated with a cre-expressing adenovirus (J:86077)
• in some mice following treatment with cre-expressing adenovirus (J:157319)
• large in 5 of 13 mice treated with a cre-expressing adenovirus (J:86077)
• in some mice following treatment with cre-expressing adenovirus (J:157319)

endocrine/exocrine glands
• medullary thyroid carcinomas in 2 of 13 mice treated with a cre-expressing adenovirus (J:86077)
• following treatment with cre-expressing adenovirus, 2 of 13 mice exhibit medullary thyroid carcinoma unlike wild-type mice (J:157319)

neoplasm
• medullary thyroid carcinomas in 2 of 13 mice treated with a cre-expressing adenovirus (J:86077)
• following treatment with cre-expressing adenovirus, 2 of 13 mice exhibit medullary thyroid carcinoma unlike wild-type mice (J:157319)
• mice treated with cre-expressing adenovirus median tumor-free survival is 475 days
• in some mice treated with a cre-expressing adenovirus (J:86077)
• in some mice following treatment with cre-expressing adenovirus (J:157319)
• large in 5 of 13 mice treated with a cre-expressing adenovirus (J:86077)
• in some mice following treatment with cre-expressing adenovirus (J:157319)




Genotype
MGI:5000480
cn44
Allelic
Composition
Trp53tm1Brn/Trp53+
Tg(MMTV-cre)#Tfln/0
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(MMTV-cre)#Tfln mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 92% of mice have mammary tumors
• many mice have tumors in more than one gland
• mammary tumors are either spindle/epithelial-mesenchymal transition or poorly differentiated adenocarcinoma

integument
• 92% of mice have mammary tumors
• many mice have tumors in more than one gland
• mammary tumors are either spindle/epithelial-mesenchymal transition or poorly differentiated adenocarcinoma

neoplasm
• 92% of mice have mammary tumors
• many mice have tumors in more than one gland
• mammary tumors are either spindle/epithelial-mesenchymal transition or poorly differentiated adenocarcinoma




Genotype
MGI:5825464
cn45
Allelic
Composition
Trp53tm1Brn/Trp53tm1Brn
Tg(Nes-cre/ERT2,-ALPP)1Sbk/0
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre/ERT2,-ALPP)1Sbk mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 53% of mice induced with tamoxifen at P0 and P1 develop non-CNS tumors or other type of brain tumors
• 53% of mice induced with tamoxifen at P0 and P1 develop non-CNS tumors or other type of brain tumors
• 47% of mice induced with tamoxifen at P0 and P1 develop medulloblastoma with a median onset of morbidity of 135 days

nervous system
• 53% of mice induced with tamoxifen at P0 and P1 develop non-CNS tumors or other type of brain tumors
• 47% of mice induced with tamoxifen at P0 and P1 develop medulloblastoma with a median onset of morbidity of 135 days




Genotype
MGI:5475383
cn46
Allelic
Composition
Bcl11atm2.1Peli/Bcl11atm2.1Peli
Trp53tm1Brn/Trp53tm1Brn
Gt(ROSA)26Sortm2(cre/ERT2)Brn/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl11atm2.1Peli mutation (0 available); any Bcl11a mutation (25 available)
Gt(ROSA)26Sortm2(cre/ERT2)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (765 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• early B cell development is rescued in tamoxifen treated mice
• reduced LSK and lymphoid-primed multipotent progenitors in tamoxifen-treated mice
• tamoxifen-treated LSK cells exhibit a complete loss of lymphoid development

immune system
N
• early B cell development is rescued in tamoxifen treated mice




Genotype
MGI:3710322
cn47
Allelic
Composition
Cdkn2ctm1Bbd/Cdkn2ctm1Bbd
Trp53tm1Brn/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2ctm1Bbd mutation (1 available); any Cdkn2c mutation (13 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 4/4 of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age

neoplasm
• 4/4 of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:102702




Genotype
MGI:3813635
cn48
Allelic
Composition
Pgrtm2(cre)Lyd/Pgr+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pgrtm2(cre)Lyd mutation (0 available); any Pgr mutation (50 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
N
• unlike mice with conditional loss of Pten, endometrial morphology and histology appear normal through 5 months of age




Genotype
MGI:6448982
cn49
Allelic
Composition
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Trp53tm1Brn/Trp53tm1Brn
Tg(Vil1-cre/ERT2)23Syr/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csnk1a1tm1.1Ybn mutation (1 available); any Csnk1a1 mutation (35 available)
Tg(Vil1-cre/ERT2)23Syr mutation (1 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased proliferation in the entire bowel
• distal gut dysplasia appears later than in mice with Trp53tm2.1Tyj (containing the R172H missense mutation)
• jejunal and ileal organoids exhibit increased proliferation, decreased differentiation, and resemble highly dysplastic spheroids
• high-grade dysplasia in the entire bowel

endocrine/exocrine glands

cellular
• increased proliferation in the entire bowel
• distal gut dysplasia appears later than in mice with Trp53tm2.1Tyj (containing the R172H missense mutation)




Genotype
MGI:5648533
cn50
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (765 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (21 available)
Tg(tetO-Kras*G12D)#Rdp mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age
• tumors exhibit features of human PDAC, including glandular tumor structures, exuberant stroma, local invasion into surrounding structures such as the duodenum, and distant metastases to the liver and lung
• mice show rapid tumor regression staring 48 hours and peaking at 72 hours following doxycycline withdrawal, with a reduction in tumor mass of about 50% after 1 week of doxycycline withdrawal; tumor regression is accompanied by decreased tumor cell proliferation and increased apoptosis
• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro

neoplasm
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age
• tumors exhibit features of human PDAC, including glandular tumor structures, exuberant stroma, local invasion into surrounding structures such as the duodenum, and distant metastases to the liver and lung
• mice show rapid tumor regression staring 48 hours and peaking at 72 hours following doxycycline withdrawal, with a reduction in tumor mass of about 50% after 1 week of doxycycline withdrawal; tumor regression is accompanied by decreased tumor cell proliferation and increased apoptosis
• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:186194




Genotype
MGI:5634406
cn51
Allelic
Composition
Cdh1tm2Kem/Cdh1+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (167 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mice do not develop gastric adenocarcinomas




Genotype
MGI:5648534
cn52
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras*G12D)#Rdp/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (765 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (21 available)
Tg(tetO-Kras*G12D)#Rdp mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) at a median age of 7.9 weeks following doxycycline treatment at 3 weeks of age

neoplasm
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) at a median age of 7.9 weeks following doxycycline treatment at 3 weeks of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:186194




Genotype
MGI:4453164
cn53
Allelic
Composition
Ptch1tm1Cklr/Ptch1+
Trp53tm1Brn/?
Pax7tm1(cre)Mrc/Pax7+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pax7tm1(cre)Mrc mutation (3 available); any Pax7 mutation (35 available)
Ptch1tm1Cklr mutation (1 available); any Ptch1 mutation (89 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• earlier tumor onset, from 32 to 65 days of age
• bortezomib treated mice have better survival

neoplasm
• earlier tumor onset, from 32 to 65 days of age
• bortezomib treated mice have better survival




Genotype
MGI:3844658
cn54
Allelic
Composition
Myf6tm1(cre)Mrc/Myf6+
Pax3tm1Mrc/Pax3tm1Mrc
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myf6tm1(cre)Mrc mutation (0 available); any Myf6 mutation (14 available)
Pax3tm1Mrc mutation (1 available); any Pax3 mutation (41 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• 2 in 5 mice develop an rhabdomyosarcoma by day 75 to 91

neoplasm
• 2 in 5 mice develop an rhabdomyosarcoma by day 75 to 91

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
alveolar rhabdomyosarcoma DOID:4051 OMIM:268220
J:93444




Genotype
MGI:3844657
cn55
Allelic
Composition
Myf6tm1(cre)Mrc/Myf6+
Pax3tm1Mrc/Pax3tm1Mrc
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myf6tm1(cre)Mrc mutation (0 available); any Myf6 mutation (14 available)
Pax3tm1Mrc mutation (1 available); any Pax3 mutation (41 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• 1 in 12 mice develop an rhabdomyosarcoma by day 202

neoplasm
• 1 in 12 mice develop an rhabdomyosarcoma by day 202

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
alveolar rhabdomyosarcoma DOID:4051 OMIM:268220
J:93444




Genotype
MGI:6246565
cn56
Allelic
Composition
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre/ERT)20Efu/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Csnk1a1tm1.1Ybn mutation (1 available); any Csnk1a1 mutation (35 available)
Tg(KRT14-cre/ERT)20Efu mutation (1 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Skin hyperpigmentation in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Tg(KRT14-cre/ERT)20Efu/0 mice but not in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Trp53tm1Brn/Trp53tm1Brn Tg(KRT14-cre/ERT)20Efu/0 mice

integument
• after tamoxifen i.p. treatment, the epidermis becomes dysplastic with no melanin deposition
• at day 28 after tamoxifen i.p. treatment, BrdU+ (proliferating) cells and beta-catenin nuclear staining are increased in the basal layer of the epidermis; however, most of the positive cells are multinucleated clumping cells indicating abnormal mitoses associated with epidermal dysplasia

pigmentation
N
• mice do NOT develop skin hyperpigmentation after tamoxifen i.p. treatment
• melanin is mainly distributed in the dermis and less in the epidermis, similar to control mice




Genotype
MGI:5796169
cn57
Allelic
Composition
Prkar1atm1.2Lsk/Prkar1a+
Tg(Col1a1-cre)1Kry/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prkar1atm1.2Lsk mutation (1 available); any Prkar1a mutation (16 available)
Tg(Col1a1-cre)1Kry mutation (2 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive to around 17 weeks of age

neoplasm
• mice develop osteosarcoma within 17 weeks of age
• multiple tumors among long bones, spine, jaw, and skull
• tumors are composed of malignant-appearing osteoblasts with woven bone as the predominant matrix and occasional chondroblastic or fibroblastic phenotype
• tumors are marked by high TNFSF11 (RANKL)/low TNFRSF11A (RANK) levels

skeleton
• mice develop osteosarcoma within 17 weeks of age
• multiple tumors among long bones, spine, jaw, and skull
• tumors are composed of malignant-appearing osteoblasts with woven bone as the predominant matrix and occasional chondroblastic or fibroblastic phenotype
• tumors are marked by high TNFSF11 (RANKL)/low TNFRSF11A (RANK) levels

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
osteosarcoma DOID:3347 OMIM:259500
J:234128




Genotype
MGI:5771803
cn58
Allelic
Composition
Smarcb1tm2Sho/Smarcb1+
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smarcb1tm2Sho mutation (0 available); any Smarcb1 mutation (19 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• excessive scratching behavior resulting in dermatitis around the neck, earlobes, and the flank region




Genotype
MGI:5771802
cn59
Allelic
Composition
Smarcb1tm2Sho/Smarcb1+
Trp53tm1Brn/Trp53+
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smarcb1tm2Sho mutation (0 available); any Smarcb1 mutation (19 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• excessive scratching behavior resulting in dermatitis around the neck, earlobes, and the flank region




Genotype
MGI:5771804
cn60
Allelic
Composition
Smarcb1tm2Sho/Smarcb1tm2Sho
Trp53tm1Brn/Trp53+
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smarcb1tm2Sho mutation (0 available); any Smarcb1 mutation (19 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• lesions in the white matter of the corpus callosum and cingulum

neoplasm
N
• no neoplastic growth is seen in the brain




Genotype
MGI:5771805
cn61
Allelic
Composition
Smarcb1tm2Sho/Smarcb1tm2Sho
Trp53tm1Brn/Trp53tm1Brn
Tg(GFAP-cre)#Gtm/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smarcb1tm2Sho mutation (0 available); any Smarcb1 mutation (19 available)
Tg(GFAP-cre)#Gtm mutation (0 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• many mice appear lethargic with hind limb paralysis
• severe scratching behavior
• mice exhibit intermittent episodes of tail extension and dystonic posturing of the body, frequently in response to handling
• motor coordination problems become evident from around 3 weeks of age
• abnormal posture of the hind limbs
• mice exhibit tumbling repeatedly during attempted locomotion; mice frequently fall over and repeatedly lift and replace the same paw in various positions during each stride
• severe ataxia
• mice exhibit a non-uniform gait, with uneven stride length and width, dragging of the hindpaws and an inability to keep the hindquarters upr
• uneven stride length
• many mice appear lethargic with hind limb paralysis
• mice exhibit clear seizures or intermittent electrographic seizures associated either with forelimb clonus, evolving into body jerking, and wild running or arrest of activity during the ictal EEG discharges

cellular
• altered granule neuron migration, with some granule neurons failing to migrate out of the external germinal layer, others remaining trapped in the molecular layer
• altered cerebellar granule neuron migration is already seen at 3 weeks of age

growth/size/body
• body weight is reduced by about 40%

mortality/aging
• mice require water gel for survival

muscle
• mice exhibit intermittent episodes of tail extension and dystonic posturing of the body, frequently in response to handling

neoplasm
• mice develop brain tumors starting at around 1 month of age
• mice that die suddenly exhibit presence of high-grade, aggressive tumors that infiltrate and obliterate the surrounding cerebellar folia
• tumors appear to arise from the cerebellum
• tumors show hallmarks of atypical teratoid/rhabdoid tumor of the central nervous system

nervous system
• mice exhibit clear seizures or intermittent electrographic seizures associated either with forelimb clonus, evolving into body jerking, and wild running or arrest of activity during the ictal EEG discharges
• altered granule neuron migration, with some granule neurons failing to migrate out of the external germinal layer, others remaining trapped in the molecular layer
• altered cerebellar granule neuron migration is already seen at 3 weeks of age
• mice develop brain tumors starting at around 1 month of age
• mice that die suddenly exhibit presence of high-grade, aggressive tumors that infiltrate and obliterate the surrounding cerebellar folia
• tumors appear to arise from the cerebellum
• tumors show hallmarks of atypical teratoid/rhabdoid tumor of the central nervous system
• defects in white matter with complete loss of tissue in regions of white matter over time
• white matter fiber tracks are reduced
• loss of white matter is already seen at 3 weeks of age
• defects in the corpus callosum
• lesions in the corpus callosum are already seen at 3 weeks of age
• defects in the hippocampus
• reduced cerebral cortex is already seen at 3 weeks of age
• defects in the cytoarchitecture of the cerebellum
• progressive loss of cells and neuronal projections in the cerebellum
• the boundary between the internal granule layer and the molecular layer remains diffuse
• loss of oligodendrocytes with age
• high level of gliosis in the fiber tracks and in the molecular layer and in the remnants of the external germinal layer

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
central nervous system cancer DOID:3620 J:226786




Genotype
MGI:5790976
cn62
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Slc1a3tm1(cre/ERT2)Mgoe/Slc1a3+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJaeSor
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (765 available)
Ptentm1Mro mutation (1 available); any Pten mutation (78 available)
Slc1a3tm1(cre/ERT2)Mgoe mutation (0 available); any Slc1a3 mutation (51 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 3 of 16 mice injected with endoxifen develop glial tumors with lesions of different sizes and varying extents of infiltration
• small neoplastic lesions in endoxifen-induced mice arise from beneath the SVZ and extend into the striatum and dorsally into the corpus callosum
• larger tumors of endoxifen-induced mice show expansion into and a diffuse infiltration of the entire caudate nucleus
• some tumors contain areas of necrosis and occasional microvascular proliferations similar to those in malignant gliomas
• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas
• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas

nervous system
• 3 of 16 mice injected with endoxifen develop glial tumors with lesions of different sizes and varying extents of infiltration
• small neoplastic lesions in endoxifen-induced mice arise from beneath the SVZ and extend into the striatum and dorsally into the corpus callosum
• larger tumors of endoxifen-induced mice show expansion into and a diffuse infiltration of the entire caudate nucleus
• some tumors contain areas of necrosis and occasional microvascular proliferations similar to those in malignant gliomas
• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas
• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
high grade glioma DOID:3070 OMIM:PS137800
J:229481




Genotype
MGI:3710238
cn63
Allelic
Composition
Rb1tm1Tyj/Rb1tm2Brn
Rbl1tm1Tyj/Rbl1tm1Tyj
Trp53tm1Brn/Trp53tm1Brn
Tg(Chx10-EGFP/cre,-ALPP)2Clc/0
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm1Tyj mutation (5 available); any Rb1 mutation (84 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (84 available)
Rbl1tm1Tyj mutation (1 available); any Rbl1 mutation (47 available)
Tg(Chx10-EGFP/cre,-ALPP)2Clc mutation (1 available)
Trp53tm1Brn mutation (17 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• mice have much more aggressive, invasive form of retinoblastoma than Trp53-sufficient compound mutants; tumor size varies with age and genotype
• an early-stage tumor displayed a pronounced vitreal protrusion in one animal, and contained structures resembling neuronal processes like those in the plexiform layer of the normal retina
• in tumors, proteins usually found in amacrine/horizontal cells, including Gad65, Snap25, Calbindin, vGlut-1, E-cadherin, N-cadherin, synapsin, and Syntaxin-1 are expressed; these cells are considered to be differentiated
• cells positive for amacrine/horizontal cell markers (1.7-3.6 x 106 cells/tumor) are much more numerous than number of amacrine/horizontal cells in a normal retina
• regions of tumors negative for amacrine/horizontal markers contain more densely packed nuclei
• tumor cells that invade the anterior eye chamber beneath the cornea are densely packed stage II cells surrounded by sparse regions of plexus with no synaptic densities or vesiclesin in the plexus or rosettes of these cells
• tumor cells have abundant mitochondria and mitotic figures; some rosettes have a central plexus made up of large, undifferentiated processes, with other rosettes having a central plexus containing neurons and synapses
• areas of the plexus within the posterior chamber are composed of neuron-like processes having synaptic structures similar to horizontal/amacrine cells; this is seen in smaller areas of plexus in tumors
• processes are usually smaller in diameter (<0.5 um) but large ones of 1-3 um are observed occasionally; variety of synaptic arrangements occur and all types can be found in contacts among processes, while ribbon synapses are seen only in areas near photoreceptor cell bodies