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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Krastm4Tyj
targeted mutation 4, Tyler Jacks
MGI:2429948
Summary 231 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
ht1
Krastm4Tyj/Kras+ involves: 129S4/SvJae MGI:3716404
cn2
Krastm4Tyj/Krastm4Tyj B6.129S4-Krastm4Tyj MGI:5440073
cn3
Krastm4Tyj/Kras+ B6.129S4-Krastm4Tyj MGI:5304807
cn4
Krastm4Tyj/Kras+ either: (involves: 129S4/SvJae) or (involves: 129S4/SvJae * C3H/HeJ) MGI:4836591
cn5
Krastm4Tyj/Kras+ involves: 129S4/SvJae MGI:3842379
cn6
Krastm4Tyj/Kras+ involves: 129S4/SvJae * C57BL/6 MGI:5528689
cn7
Krastm4Tyj/Kras+ involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5659878
cn8
Krastm4Tyj/Kras+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
129.Cg-Krastm4Tyj Ptentm2.1Ppp Tg(Tpo-cre)1Shk MGI:5897668
cn9
Krastm4Tyj/Kras+
Tg(TPO-cre)1Shk/0
129.Cg-Krastm4Tyj Tg(Tpo-cre)1Shk MGI:5897670
cn10
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
B6.129-Krastm4Tyj Tgfbr2tm1.2Hlm MGI:5304695
cn11
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
B6.Cg-Krastm4Tyj Map2k7tm1.1Twad/Map2k7tm1.2Twad MGI:4948962
cn12
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
B6.Cg-Krastm4Tyj Ptf1atm1.1(cre)Cvw MGI:3836557
cn13
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(MUC1)79.24Gend/0
B6.Cg-Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend MGI:3836556
cn14
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
B6J.Cg-Tg(Tyr-cre/ERT2)13Bos Cdkn2atm2.1Nesh Krastm4Tyj MGI:5752237
cn15
Apctm2Rak/Apctm2Rak
Krastm4Tyj/Kras+
involves: 129 * 129S4/SvJae * C57BL/6J * SJL MGI:5432240
cn16
Krastm4Tyj/Kras+
Tg(Gfap-cre)77.6Mvs/0
involves: 129 * BALB/c * C57BL/6NHsd MGI:4849444
cn17
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308946
cn18
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308961
cn19
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308962
cn20
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308963
cn21
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308954
cn22
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308951
cn23
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308959
cn24
Krastm4Tyj/Kras+
Tg(Scgb1a1-cre)1Kkw/?
involves: 129 * C57BL/6 * FVB/N MGI:3624415
cn25
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
involves: 129 * C57BL/6NCrl * FVB/N MGI:6296002
cn26
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Prdm1tm1Clme/Prdm1tm1Clme
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
involves: 129 * C57BL/6NCrl * FVB/N MGI:6296000
cn27
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129 * FVB/N MGI:3695424
cn28
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129 * FVB/N MGI:3695421
cn29
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129 * FVB/N MGI:3695428
cn30
Albtm1(cre/ERT2)Mtz/Alb+
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae MGI:6256733
cn31
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:4948964
cn32
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5510703
cn33
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716963
cn34
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716966
cn35
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716968
cn36
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5562914
cn37
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7tm1.1Ysun
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5562910
cn38
Krastm4Tyj/Kras+
Raf1tm2Bacc/Raf1tm2Bacc
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5510702
cn39
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:4441491
cn40
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Shhtm2(cre/ERT2)Cjt/Shh+
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac MGI:5298088
cn41
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Krt19tm1(cre/ERT)Ggu/Krt19+
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac MGI:5298083
cn42
Krastm4Tyj/Kras+
Krt19tm1(cre/ERT)Ggu/Krt19+
Ptentm2Mak/Ptentm2Mak
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac MGI:6256734
cn43
Hprttm1(CAG-BRF1)Gu/Hprt+
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * 129S7/SvEvBrd * FVB/N MGI:6403693
cn44
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
cn45
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
cn46
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
cn47
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
cn48
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
cn49
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
cn50
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441492
cn51
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441490
cn52
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441488
cn53
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441486
cn54
Krastm4Tyj/Kras+
Myod1tm1.1(cre/ERT,TVA)Gcg/Myod1+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5547939
cn55
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5528686
cn56
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5559052
cn57
Krastm4Tyj/Kras+
Lrrc17tm1Nik/Lrrc17+
Srpk2tm1Nik/Srpk2+
Tg(Mx1-cre)1Cgn/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA MGI:4460775
cn58
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Tg(Trp53)bSrn/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA MGI:4948965
cn59
Krastm4Tyj/Kras+
Ptentm2Mak/Pten+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:6256732
cn60
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428907
cn61
Krastm4Tyj/Krastm4Tyj
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:4819844
cn62
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:6256730
cn63
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428898
cn64
Cdkn2atm2.1Nesh/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835045
cn65
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:5486065
cn66
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835041
cn67
Krastm4Tyj/Kras+
Tg(CAG-Bgeo,-tsA58T)T26Ichi/0
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5604750
cn68
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5659893
cn69
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Gev/Trp53tm1Gev
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5635880
cn70
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:3776026
cn71
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6N * FVB/N MGI:6377667
cn72
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre/ERT)20Efu/0
involves: 129P2/OlaHsd * 129S4/SvJae * CD-1 MGI:5298084
cn73
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:4835046
cn74
Apctm2.1Cip/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:3776028
cn75
Cdkn2atm2Brn/Cdkn2atm2Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB/N MGI:5484548
cn76
Krastm4Tyj/Kras+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Meox2tm1(cre)Sor/Meox2+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * FVB/N MGI:3716399
cn77
Brca2tm1Cam/Brca2tm1Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940102
cn78
Brca2tm1Brn/Brca2tm1Cam
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940096
cn79
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:5486056
cn80
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3032576
cn81
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3695431
cn82
Krastm4Tyj/Krastm4Tyj
Bhlha15tm3(cre/ERT2)Skz/Bhlha15+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3821739
cn83
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3695432
cn84
Krastm4Tyj/Kras+
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4839215
cn85
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4839216
cn86
Bak1tm1Thsn/Bak1tm1Thsn
Baxtm1Sjk/Baxtm2Sjk
Krastm4Tyj/Kras+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5559061
cn87
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/Gt(ROSA)26Sor+
Tg(Flt3-cre)#Ccb/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:6273518
cn88
Gfi1tm6.1(GFI1)Tmo/Gfi1tm6.1(GFI1)Tmo
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA MGI:5468271
cn89
Gfi1tm5.1(GFI1*)Tmo/Gfi1tm5.1(GFI1*)Tmo
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA MGI:5468269
cn90
Gfi1tm5.1(GFI1*)Tmo/Gfi1+
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA MGI:5468270
cn91
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3695568
cn92
Krastm4Tyj/Kras+
Tg(Erbb2*)#Maed/0
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6J MGI:6192639
cn93
Krastm4Tyj/Krastm4Tyj
Trim33tm1Los/Trim33tm1Los
Tg(Pdx1-cre)89.1Dam/0
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 * DBA/2 MGI:4355873
cn94
Krastm4Tyj/Kras+
Tg(Prm-cre)58Og/0
involves: 129S4/SvJae MGI:3716392
cn95
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
involves: 129S4/SvJae MGI:3716965
cn96
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
involves: 129S4/SvJae MGI:3716967
cn97
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
involves: 129S4/SvJae MGI:3776023
cn98
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm3(CAG-luc)Tyj/Gt(ROSA)26Sor+
involves: 129S4/SvJae MGI:3818747
cn99
Krastm4Tyj/Krastm4Tyj
Tg(Cela1-cre/ERT)1Dam/0
involves: 129S4/SvJae MGI:3821750
cn100
Krastm4Tyj/Kras+
Rb1tm3Tyj/Rb1tm3Tyj
involves: 129S4/SvJae MGI:3842377
cn101
Krastm4Tyj/Kras+
Rbl2tm2Tyj/Rbl2tm2Tyj
involves: 129S4/SvJae MGI:3842378
cn102
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Scgb1a1-rtTA)1Jaw/0
involves: 129S4/SvJae MGI:4368025
cn103
Krastm4Tyj/Krastm4Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae MGI:4818400
cn104
Fastm1Ach/Fastm1Ach
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae MGI:5014515
cn105
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae MGI:5014516
cn106
Krastm4Tyj/Kras+
Trp53tm4Att/Trp53tm4Att
involves: 129S4/SvJae MGI:5140101
cn107
Gt(ROSA)26Sortm1(RAC1*)Jkis/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
involves: 129S4/SvJae MGI:5437472
cn108
Krastm4Tyj/Kras+
Trp53tm1Lejo/Trp53tm1Lejo
involves: 129S4/SvJae MGI:5441555
cn109
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
involves: 129S4/SvJae MGI:5491219
cn110
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Tg(Cela1-cre/ERT)1Dam/0
involves: 129S4/SvJae MGI:5510699
cn111
Krastm4Tyj/Kras+
Tg(Cela1-cre/ERT)1Dam/0
involves: 129S4/SvJae MGI:5510700
cn112
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae MGI:5510701
cn113
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scribtm1.1Phum
involves: 129S4/SvJae MGI:5638045
cn114
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scrib+
involves: 129S4/SvJae MGI:5638047
cn115
Gt(ROSA)26Sortm1(Notch1)Dam/Gt(ROSA)26Sor+
Krastm4Tyj/Krastm4Tyj
Tg(Cela1-cre/ERT)1Dam/0
involves: 129S4/SvJae * 129S4/SvJaeSor MGI:3821751
cn116
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Pms2tm2(cre)Lisk/Pms2tm2(cre)Lisk
involves: 129S4/SvJae * 129S4/SvJaeSor MGI:5543250
cn117
Krastm4Tyj/Kras+
Meox2tm1(cre)Sor/Meox2+
involves: 129S4/SvJae * 129S4/SvJaeSor MGI:3716398
cn118
Gt(ROSA)26Sortm1(Notch1)Dam/Gt(ROSA)26Sor+
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6 * CBA MGI:3821752
cn119
Cdkn2atm1.1Gsu/Cdkn2atm1.1Gsu
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6J * FVB/N MGI:5502380
cn120
Krastm4Tyj/Kras+
Shhtm2(cre/ERT2)Cjt/Shh+
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5298087
cn121
Krastm4Tyj/Kras+
Stk11tm1.2Rdp/Stk11tm1.2Rdp
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5515885
cn122
Krastm4Tyj/Kras+
Pik3r1tm1Lca/Pik3r1+
Pik3r2tm1Lca/Pik3r2tm1Lca
involves: 129S4/SvJae * 129S6/SvEvTac MGI:3834445
cn123
Krastm4Tyj/Kras+
Krt19tm1(cre/ERT)Ggu/Krt19+
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5298082
cn124
Gt(ROSA)26Sortm2(Pik3ca*)Dsa/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5510696
cn125
Krastm4Tyj/Kras+
Pik3r2tm1Lca/Pik3r2tm1Lca
involves: 129S4/SvJae * 129S6/SvEvTac MGI:3834444
cn126
Krastm4Tyj/Kras+
Pik3r1tm1Lca/Pik3r1tm1Lca
Pik3r2tm1Lca/Pik3r2tm1Lca
involves: 129S4/SvJae * 129S6/SvEvTac MGI:3834443
cn127
Col1a1tm5(tetO-GFP/RNAi:Cdkn2a)Slowe/Col1a1+
Gt(ROSA)26Sortm1(Luc)Kael/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Krastm4Tyj/Kras+
Tg(Scgb1a1-rtTA)1Jaw/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 MGI:4999988
cn128
Krastm4Tyj/Kras+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL/J MGI:5556259
cn129
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Hmga2tm1.1Mmw/Hmga2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * FVB/N MGI:6295996
cn130
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Vil1-cre)20Syr/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5013409
cn131
Krastm4Tyj/Kras+
Stk11tm1.1Rdp/Stk11tm1.1Rdp
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659880
cn132
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659896
cn133
Krastm4Tyj/Kras+
Stk11tm1.1Rdp/Stk11tm1.2Rdp
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659881
cn134
Gt(ROSA)26Sortm1(Tva)Dsa/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6J MGI:3814193
cn135
Fgfr3tm4Cxd/Fgfr3+
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N MGI:5141739
cn136
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm1(sb13)Tuv/Gt(ROSA)26Sor+
Tg(Pdx1-cre)6Tuv/0
TgTn(sb-T2/Onc)#Dla/0
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N MGI:5438089
cn137
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N MGI:5502381
cn138
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Amhr2tm3(cre)Bhr/Amhr2+
involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 MGI:5432231
cn139
Brf1tm1Arte/Brf1tm1Arte
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S7/SvEvBrd * FVB/N MGI:6403690
cn140
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Tg(CYP19A1-cre)1Jri/0
involves: 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5432224
cn141
Ctnnb1tm1Mmt/Ctnnb1tm1Mmt
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * 129X1/SvJ * FVB/N MGI:5790500
cn142
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * 129X1/SvJ * FVB/N MGI:5141743
cn143
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * BALB/c * C57BL/6 MGI:5013916
cn144
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA MGI:5013917
cn145
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA MGI:3035835
cn146
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Gfap-cre)77.6Mvs/0
involves: 129S4/SvJae * BALB/c * C57BL/6NHsd MGI:4849441
cn147
Krastm4Tyj/Kras+
Tg(Tek-cre)12Flv/0
involves: 129S4/SvJae * C3H * C57BL/6 MGI:3716393
cn148
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Scgb1a1-cre)1Tauc/0
involves: 129S4/SvJae * C57BL/6 MGI:4943568
cn149
Braftm2Cpri/Braf+
Krastm4Tyj/Kras+
involves: 129S4/SvJae * C57BL/6 MGI:5440071
cn150
Krastm4Tyj/Kras+
Tg(MUC1)79.24Gend/0
involves: 129S4/SvJae * C57BL/6 MGI:4411919
cn151
Krastm4Tyj/Kras+
Siva1tm1.2Att/Siva1+
involves: 129S4/SvJae * C57BL/6 MGI:5659856
cn152
Krastm4Tyj/Kras+
Siva1tm1.1Att/Siva1tm1.2Att
involves: 129S4/SvJae * C57BL/6 MGI:5659853
cn153
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
involves: 129S4/SvJae * C57BL/6 MGI:5528687
cn154
Krastm4Tyj/Kras+
Plcl1tm1.1Matk/Plcl1tm1.1Matk
involves: 129S4/SvJae * C57BL/6 MGI:5607955
cn155
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
involves: 129S4/SvJae * C57BL/6 MGI:5559056
cn156
Krastm4Tyj/Kras+
Tg(IVL-cre/ERT2)1Blpn/0
involves: 129S4/SvJae * C57BL/6 MGI:5298090
cn157
Krastm4Tyj/Kras+
Ralatm1.2Cjm/Ralatm1.2Cjm
Ralbtm1.1Cjm/Ralbtm1.2Cjm
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5505293
cn158
Krastm4Tyj/Kras+
Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL/J MGI:5556244
cn159
Fbxw7tm1Iken/Fbxw7+
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA MGI:6157295
cn160
Fbxw7tm1Iken/Fbxw7tm1Iken
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA MGI:6157296
cn161
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:5441554
cn162
Krastm4Tyj/Kras+
Tg(Fabp7-cre,-lacZ)3Gtm/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3810650
cn163
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3695430
cn164
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:2687206
cn165
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3821753
cn166
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:5582314
cn167
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:2687217
cn168
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:5308806
cn169
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:5308964
cn170
Krastm4Tyj/Kras+
Tg(KRT14-cre/ERT)20Efu/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N MGI:5659911
cn171
Krastm4Tyj/Kras+
Tg(CAG-HPV16E6E7,-luc)#Mspi/0
Tg(KRT14-cre/ERT)20Efu/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N * FVB/NJ MGI:5659910
cn172
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA MGI:5428897
cn173
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5705328
cn174
Braftm1Rima/Braf+
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)1Lru/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4458349
cn175
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4355874
cn176
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4355875
cn177
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5705321
cn178
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * C57BL/6 * FVB MGI:4835044
cn179
Brca1tm1Thl/Brca1tm2.1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494465
cn180
Brca1tm1Thl/Brca1tm1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494464
cn181
Brca1tm1Thl/Brca1tm3.1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494462
cn182
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm3Tyj/Trp53+
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4940098
cn183
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4941337
cn184
Gt(ROSA)26Sortm1(MYC/ERT2)Gev/Gt(ROSA)26Sortm1(MYC/ERT2)Gev
Krastm4Tyj/Krastm4Tyj
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:3821936
cn185
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4941336
cn186
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae * C57BL/6J MGI:4836596
cn187
Chaf1btm2c(EUCOMM)Hmgu/Chaf1b+
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * C57BL/6J * C57BL/6N * CBA/J MGI:6267351
cn188
Krastm4Tyj/Kras+
Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6J * SJL/J MGI:5298086
cn189
Krastm4Tyj/Kras+
Stk11tm1.1Gne/Stk11tm1.1Gne
involves: 129S4/SvJae * C57BL/6N MGI:5484547
cn190
Krastm4Tyj/Krastm4Tyj
Tg(Cela1-cre/ERT2)1Stof/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3821737
cn191
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3821738
cn192
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * FVB MGI:4835047
cn193
Krastm4Tyj/Kras+
Tg(MMTV-cre)4Mam/0
involves: 129S4/SvJae * FVB MGI:3044680
cn194
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Y
involves: 129S4/SvJae * FVB/N MGI:5438090
cn195
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * FVB/N MGI:5141740
cn196
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * FVB/N MGI:5141742
cn197
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * FVB/N MGI:5494463
cn198
Krastm4Tyj/Kras+
Rab11fip1tm1.1Jicn/Rab11fip1tm1.1Jicn
Tg(Pdx1-cre)6Tuv/0
Trp53tm2.1Tyj/Trp53+
involves: 129S4/SvJae * FVB/N MGI:6113915
cn199
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/?
involves: 129S4/SvJae * FVB/N MGI:3032575
cn200
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * FVB/N MGI:3044567
cn201
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Usp9x+
involves: 129S4/SvJae * FVB/N MGI:5438091
cn202
Krastm4Tyj/Kras+
Tg(Tg-cre/ERT2)#Mmcm/0
involves: 129S4/SvJae * FVB/NCr MGI:5780080
cn203
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scribtm1.1Phum
Tg(Pbsn-cre)20Fwan/0
involves: 129S4/SvJae * FVB/NCrl MGI:5300204
cn204
Krastm4Tyj/Kras+
Tg(Pbsn-cre)20Fwan/0
involves: 129S4/SvJae * FVB/NCrl MGI:5300203
cn205
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scrib+
Tg(Pbsn-cre)20Fwan/0
involves: 129S4/SvJae * FVB/NCrl MGI:5300205
cn206
Krastm4Tyj/Kras+
Sftpctm1(cre/ERT2)Blh/Sftpc+
Trp53tm5Tyj/Trp53+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 MGI:5317171
cn207
Krastm4Tyj/Kras+
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
Trp53tm5Tyj/Trp53+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 MGI:5317170
cn208
Krastm4Tyj/Krastm4Tyj
Ugdhtm1.1Xzh/Ugdhtm1.1Xzh
H2az2Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * CBA/J MGI:5430385
cn209
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3695569
cn210
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3695567
cn211
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:3695426
cn212
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:3695429
cn213
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:3695422
cn214
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940100
cn215
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940099
cn216
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
cn217
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182+
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704427
cn218
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182tm1.1Dgk
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704424
cn219
Krastm4Tyj/Kras+
Mapk8tm1Wag/Mapk8+
Mapk9tm1Mka/Mapk9tm1Mka
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:4948963
cn220
Krastm4Tyj/Kras+
Pax7tm2.1(cre/ERT2)Fan/Pax7+
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129X1/SvJ * C57BL/6 MGI:5547938
cn221
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1b+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714154
cn222
Pggt1btm1Mbrg/Pggt1btm1Mbrg
Krastm4Tyj/Kras+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714152
cn223
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714153
cn224
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722603
cn225
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722605
cn226
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm3Glo
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722604
cn227
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Krastm4Tyj/Kras+
involves: 129/Sv * 129S4/SvJae * C57BL/6 * FVB/N * SJL MGI:5659895
cn228
Krastm4Tyj/Kras+
Tg(SFTPC-rtTA)5Jaw/0
Tg(tetO-cre)1Jaw/0
involves: 129/Sv * C57BL/6 MGI:3716394
cn229
Krastm4Tyj/Kras+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * C57BL/6 * FVB * ICR MGI:3722600
cn230
Krastm4Tyj/Kras+
Trp53tm3Glo/Trp53+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * C57BL/6 * FVB * ICR MGI:3722602
cx231
Epha2tm1Jrui/Epha2tm1Jrui
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2.1Tyj/Trp53+
involves: 129S/SvEv * 129S4/SvJae * FVB/N MGI:6113916


Genotype
MGI:3716404
ht1
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• treatment with adenoviral Cre to induce oncogenic Kras expression results in lung tumor development, but causes a lower tumor burden and decreased overall tumor area compared to induced mutants on a Spry2-null background (J:119477)
• 20% and 100% of mice develop lung lesions at 6 weeks and 20 weeks, respectively, post intranasal adenoviral cre administration (J:216266)
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre)
• treatment with MLN4924, a small molecular inhibitor of NAE, beginning at 13 weeks after Ad-Cre administration reduces tumor burden, with a reduction in both number of hyperplastic areas and adenomas and size of the tumors
• a few adenocarcinomas develop in mice following Ad-Cre administration

neoplasm
• treatment with adenoviral Cre to induce oncogenic Kras expression results in lung tumor development, but causes a lower tumor burden and decreased overall tumor area compared to induced mutants on a Spry2-null background (J:119477)
• 20% and 100% of mice develop lung lesions at 6 weeks and 20 weeks, respectively, post intranasal adenoviral cre administration (J:216266)
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre)
• treatment with MLN4924, a small molecular inhibitor of NAE, beginning at 13 weeks after Ad-Cre administration reduces tumor burden, with a reduction in both number of hyperplastic areas and adenomas and size of the tumors
• a few adenocarcinomas develop in mice following Ad-Cre administration

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:207982




Genotype
MGI:5440073
cn2
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Genetic
Background
B6.129S4-Krastm4Tyj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• primary mouse embryonic fibroblast treated with adenoviral-cre exhibit enhanced growth rate compared with wild-type cells




Genotype
MGI:5304807
cn3
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
B6.129S4-Krastm4Tyj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction

mortality/aging
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 79 days

neoplasm
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction




Genotype
MGI:4836591
cn4
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
either: (involves: 129S4/SvJae) or (involves: 129S4/SvJae * C3H/HeJ)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• after ovarian intrabursal injection of an adenovirus expressing Cre, mutants develop benign ovarian endometriosis-like lesions, however no invasive ovarian tumors are seen up to 10 months following adenoviral injection

growth/size/body
• 47% of mutants develop peritoneal endometriosis following ovarian intrabursal injection of an adenovirus expressing Cre
• however, mice injected with adenovirus expressing Cre directly into the peritoneum do not develop peritoneal endometriosis

reproductive system
• after ovarian intrabursal injection of an adenovirus expressing Cre, mutants develop benign ovarian endometriosis-like lesions, however no invasive ovarian tumors are seen up to 10 months following adenoviral injection

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
endometriosis DOID:289 J:96296




Genotype
MGI:3842379
cn5
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median life span of cre adenovirus-treated mice is 32 weeks

neoplasm
• tumors from cre adenovirus-treated mice exhibit increased cell proliferation compared to in tumors from Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice
• cre adenovirus-treated mice develop smaller tumors than in cre adenovirus-treated Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice
• mice treated with adenovirus cre develop lung lesions in 4 to 6 months (J:147590)
• cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia (J:147590)
• cre adenovirus-treated mice develop fewer tumors than in Krastm4Tyj/Kras+ Rb1tm3Tyj/Rb1tm3Tyj mice (J:147590)
• large tumors easily visible on the surface of the lungs at eight weeks after Cre-adenovirus treatment (J:158937)
• presence of atypical adenomatous hyperplasia after Cre-adenovirus treatment
• the most common lesion is adenocarcinoma after Cre-adenovirus treatment
• in cre adenovirus-treated mice

respiratory system
• mice treated with adenovirus cre develop lung lesions in 4 to 6 months (J:147590)
• cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia (J:147590)
• cre adenovirus-treated mice develop fewer tumors than in Krastm4Tyj/Kras+ Rb1tm3Tyj/Rb1tm3Tyj mice (J:147590)
• large tumors easily visible on the surface of the lungs at eight weeks after Cre-adenovirus treatment (J:158937)
• presence of atypical adenomatous hyperplasia after Cre-adenovirus treatment
• the most common lesion is adenocarcinoma after Cre-adenovirus treatment
• in cre adenovirus-treated mice
• in cre adenovirus-treated mice
• cre adenovirus-treated mice develop bronchiolar hyperplasia and dysplasia unlike wild-type mice
• in cre adenovirus-treated mice
• presence of epithelial hyperplasia after Cre-adenovirus treatment

immune system
• following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice

hematopoietic system
• following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice

reproductive system
• following injection of a cre adenovirus in the ovarian bursa, mice develop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Krastm4Tyj micefollowing injection of a cre adenovirus in the ovarian bursa, mice develop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Krastm4Tyj mice




Genotype
MGI:5528689
cn6
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus

neoplasm
• lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:203686




Genotype
MGI:5659878
cn7
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness
• all tumors of ad-cre inoculated mice are adenocarincomas
• metastasis or local invasion is not seen in ad-cre inoculated mice

mortality/aging
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a median survival of 24 weeks after ad-cre inoculation

neoplasm
• mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness
• all tumors of ad-cre inoculated mice are adenocarincomas
• metastasis or local invasion is not seen in ad-cre inoculated mice




Genotype
MGI:5897668
cn8
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
Genetic
Background
129.Cg-Krastm4Tyj Ptentm2.1Ppp Tg(Tpo-cre)1Shk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (39 available)
Tg(TPO-cre)1Shk mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% of mice die within 7 weeks from birth and none survive over 4 months of age
• treatment with LY294002, an inhibitor of PI3K, twice a week starting at 3 weeks of age prolongs survival of mice

endocrine/exocrine glands
• mice develop thyroids 200- to 500-fold larger than controls
• mice rapidly develop thyroid follicular carcinomas
• 30-90% of the thyroid glands are replaced by microfollicular to solid areas, indicating thyroid follicular cancer, including capsular, muscle, and vascular invasion

homeostasis/metabolism

neoplasm
• mice rapidly develop thyroid follicular carcinomas
• 30-90% of the thyroid glands are replaced by microfollicular to solid areas, indicating thyroid follicular cancer, including capsular, muscle, and vascular invasion
• all mice surviving at least 12 weeks develop thyroglobulin-positive lung metastases




Genotype
MGI:5897670
cn9
Allelic
Composition
Krastm4Tyj/Kras+
Tg(TPO-cre)1Shk/0
Genetic
Background
129.Cg-Krastm4Tyj Tg(Tpo-cre)1Shk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(TPO-cre)1Shk mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• mice are indistinguishable from wild-type mice and show no alterations of the thyroid gland




Genotype
MGI:5304695
cn10
Allelic
Composition
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
Genetic
Background
B6.129-Krastm4Tyj Tgfbr2tm1.2Hlm
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tgfbr2tm1.2Hlm mutation (0 available); any Tgfbr2 mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop tumors similar to human mixed subtype adenocarcinomas; they show progression of a pure noninvasive lung adenocarcinoma to an adenocarcinoma with mixed invasive morphology and metastatic potential
• tumors of mutants treated with Cre adenovirus show evidence of inflammatory cell recruitment and tumor microenvironment remodeling with neoangiogenesis not seen in homozygous cre adenovirus treated Krastm4Tyj mice

mortality/aging
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 43 days

neoplasm
• tumors of Cre adenoviral treated mutants show transmural invasion of vessels and pleural invasion, and regional metastases to mediastinal lymph nodes
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop tumors similar to human mixed subtype adenocarcinomas; they show progression of a pure noninvasive lung adenocarcinoma to an adenocarcinoma with mixed invasive morphology and metastatic potential
• tumors of mutants treated with Cre adenovirus show evidence of inflammatory cell recruitment and tumor microenvironment remodeling with neoangiogenesis not seen in homozygous cre adenovirus treated Krastm4Tyj mice

hematopoietic system
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit and increase in B cells in the lungs compared to homozygous cre adenovirus treated Krastm4Tyj mice
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit and increase in T cells in the lungs compared to homozygous cre adenovirus treated Krastm4Tyj mice
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit a lower myeloid cell population in the lungs than controls

immune system
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit and increase in B cells in the lungs compared to homozygous cre adenovirus treated Krastm4Tyj mice
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit and increase in T cells in the lungs compared to homozygous cre adenovirus treated Krastm4Tyj mice
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit a lower myeloid cell population in the lungs than controls

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:177379




Genotype
MGI:4948962
cn11
Allelic
Composition
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Genetic
Background
B6.Cg-Krastm4Tyj Map2k7tm1.1Twad/Map2k7tm1.2Twad
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Map2k7tm1.1Twad mutation (0 available); any Map2k7 mutation (5 available)
Map2k7tm1.2Twad mutation (0 available); any Map2k7 mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice

mortality/aging

neoplasm
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice

cellular
• following adenovirus cre infection, mice exhibit impaired DNA damage response compared with control mice

homeostasis/metabolism
• following adenovirus cre infection, mice exhibit impaired DNA damage response compared with control mice




Genotype
MGI:3836557
cn12
Allelic
Composition
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
B6.Cg-Krastm4Tyj Ptf1atm1.1(cre)Cvw
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• pancreatic weight is greater than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes

neoplasm
• pancreatic tumors exhibit higher proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes
• at 34 weeks of age, 4 of 10 mice develop metastasis to the lung and liver compared to 6 of 10 metastasis at 48 weeks in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes

endocrine/exocrine glands
• pancreatic weight is greater than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes
• pancreatic tumors exhibit higher proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes




Genotype
MGI:3836556
cn13
Allelic
Composition
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(MUC1)79.24Gend/0
Genetic
Background
B6.Cg-Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (18 available)
Tg(MUC1)79.24Gend mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• pancreatic tumors exhibit lower proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend heterozygotes (J:138959)
• mice exhibit carcinoma in situ in the pancreas (J:234412)
• mice exhibit high-grade PanIN lesions and carcinoma in situ, associated with disorganized glandular epithelium (J:234412)
• mice treated with gemcitabine exhibit normal pancreatic glandular structure 26 weeks after the beginning of treatment (J:234412)
• at 48 weeks, 6 of 10 mice develop metastasis to the lung and liver compared to 4 of 10 metastasis at 34 weeks of age in Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend heterozygotes

endocrine/exocrine glands
• pancreatic tumors exhibit lower proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend heterozygotes (J:138959)
• mice exhibit carcinoma in situ in the pancreas (J:234412)
• mice exhibit high-grade PanIN lesions and carcinoma in situ, associated with disorganized glandular epithelium (J:234412)
• mice treated with gemcitabine exhibit normal pancreatic glandular structure 26 weeks after the beginning of treatment (J:234412)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
adenoma DOID:657 J:138959
pancreatic carcinoma DOID:4905 OMIM:260350
J:234412




Genotype
MGI:5752237
cn14
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
B6J.Cg-Tg(Tyr-cre/ERT2)13Bos Cdkn2atm2.1Nesh Krastm4Tyj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (51 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Tyr-cre/ERT2)13Bos mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• mice treated with 4-hydroxytamoxifen (4-OHT) neonatally exhibit the presence of nevi and hyperpigmented regions on the paws and tails

integument
• mice treated with 4-OHT neonatally develop melanoma with 76% penetrance and a median latency of 36.3 weeks
• melanomas contain both spindle-cell and desmoplastic cell types with no overt signs of macrometastatic spread

neoplasm
• mice treated with 4-OHT neonatally develop melanoma with 76% penetrance and a median latency of 36.3 weeks
• melanomas contain both spindle-cell and desmoplastic cell types with no overt signs of macrometastatic spread

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
skin melanoma DOID:8923 OMIM:608035
OMIM:612263
J:220627




Genotype
MGI:5432240
cn15
Allelic
Composition
Apctm2Rak/Apctm2Rak
Krastm4Tyj/Kras+
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Rak mutation (1 available); any Apc mutation (59 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 64% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are adenomas

neoplasm
• 36% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are carcinomas
• 20% of mutants injected with an adenovirus expressing cre recombinase in the distal colon to inactivate Apc exhibit spontaneous gross liver metastases starting 24 weeks after adenoviral injection; these lesions are adenocarcinomas
• 96% of mutants injected with an adenovirus expressing cre recombinase in the distal colon to inactivate Apc develop distal colonic tumors as little as 3 weeks after viral administration
• rapamycin treatment of mutants with tumors does not result in tumor regression
• 64% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are adenomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
colorectal cancer DOID:9256 OMIM:114500
J:156532




Genotype
MGI:4849444
cn16
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Gfap-cre)77.6Mvs/0
Genetic
Background
involves: 129 * BALB/c * C57BL/6NHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Gfap-cre)77.6Mvs mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mutants do not develop tumors




Genotype
MGI:5308946
cn17
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 (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 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:5308961
cn18
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 (51 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 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:5308962
cn19
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 (51 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 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:5308963
cn20
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
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 (51 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 18.3 weeks
• 100% of tumors are sarcomatoid in histology

neoplasm
• mutants develop pancreatic tumors with an average latency of 18.3 weeks
• 100% of tumors are sarcomatoid in histology
• 33% of tumors exhibit metastasis




Genotype
MGI:5308954
cn21
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 (51 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 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
cn22
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 (51 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 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:5308959
cn23
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 (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 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:3624415
cn24
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Scgb1a1-cre)1Kkw/?
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Scgb1a1-cre)1Kkw mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• progressive phenotype characterized by cellular atypia, adenoma, and ultimately adenocarcinoma in CC10 positive cells of bronchial epithelia

mortality/aging
• early mortality with a median survival of 8 weeks

neoplasm
• progressive phenotype characterized by cellular atypia, adenoma, and ultimately adenocarcinoma in CC10 positive cells of bronchial epithelia

immune system
• a robust inflammatory response characterized by an abundant infiltration of alveolar macrophages and neutrophils




Genotype
MGI:6296002
cn25
Allelic
Composition
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
Genetic
Background
involves: 129 * C57BL/6NCrl * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (3 available); any Gt(ROSA)26Sor mutation (540 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• pancreas contains PanINs and adenocarcinoma
• pancreas contains PanINs and adenocarcinoma

neoplasm
• pancreas contains PanINs and adenocarcinoma
• pancreas contains PanINs and adenocarcinoma
• most mice develop metastases which are numerous and widespread in many different sites, including the lymph nodes, diaphragm, lungs, and liver
• all mice exhibit peritoneal disseminated tumor cells




Genotype
MGI:6296000
cn26
Allelic
Composition
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Prdm1tm1Clme/Prdm1tm1Clme
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
Genetic
Background
involves: 129 * C57BL/6NCrl * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (3 available); any Gt(ROSA)26Sor mutation (540 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Prdm1tm1Clme mutation (1 available); any Prdm1 mutation (19 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice exhibit a similar overall pancreatic tumor burden as KPCT (Krastm4Tyj/Kras+ Trp53tm2Tyj/Trp53+ Tg(Pdx1-cre)6Tuv/0 Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+) mice
• pancreas contains PanINs and adenocarcinoma that are similar to pancreatic ductal adenocarcinoma (PDAC) in KPCT mice
• only 3 of 14 mice develop metastases, with only half of mice showing peritoneal disseminated tumor cells
• cancer cells exhibit a higher mitotic index than KPCT mice
• pancreas contains PanINs and adenocarcinoma that are similar to PDAC in KPCT mice

mortality/aging
• mice exhibit a shorter survival than KPCT mice

endocrine/exocrine glands
• mice exhibit a similar overall pancreatic tumor burden as KPCT (Krastm4Tyj/Kras+ Trp53tm2Tyj/Trp53+ Tg(Pdx1-cre)6Tuv/0 Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+) mice
• pancreas contains PanINs and adenocarcinoma that are similar to pancreatic ductal adenocarcinoma (PDAC) in KPCT mice
• only 3 of 14 mice develop metastases, with only half of mice showing peritoneal disseminated tumor cells
• cancer cells exhibit a higher mitotic index than KPCT mice
• pancreas contains PanINs and adenocarcinoma that are similar to PDAC in KPCT mice




Genotype
MGI:3695424
cn27
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (51 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (18 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 12 of 13 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4

mortality/aging
• average tumor-free survival is 14 weeks

neoplasm
• 5 of 13 mice develop intraductal papillary mucinous neoplasms
• tumor fibrosis is increased compared to mice wild-type for Smad4
• 12 of 13 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4




Genotype
MGI:3695421
cn28
Allelic
Composition
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (18 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die between 8 and 24 weeks of age
• average tumor-free survival is 15.7 weeks

neoplasm
• 12 of 12 mice develop intraductal papillary mucinous neoplasms
• 2 of 12 mice develop pancreatic ductal adenocarcinoma

endocrine/exocrine glands
• seen in all mice
• 2 of 12 mice develop pancreatic ductal adenocarcinoma




Genotype
MGI:3695428
cn29
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (51 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (18 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 4 of 4 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4
• tumor fibrosis is increased compared to mice wild-type for Smad4

mortality/aging
• average tumor-free survival is 8.8 weeks

neoplasm
• 4 of 4 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4
• tumor fibrosis is increased compared to mice wild-type for Smad4




Genotype
MGI:6256733
cn30
Allelic
Composition
Albtm1(cre/ERT2)Mtz/Alb+
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Albtm1(cre/ERT2)Mtz mutation (1 available); any Alb mutation (36 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptentm2Mak mutation (4 available); any Pten mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma
• mice injected with tamoxifen at 8 weeks after birth develop multiple liver tumors that are all hepatocellular carcinoma and hepatocellular dysplasia, but not intrahepatic cholangiocarcinoma

liver/biliary system
• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma
• mice injected with tamoxifen at 8 weeks after birth develop multiple liver tumors that are all hepatocellular carcinoma and hepatocellular dysplasia, but not intrahepatic cholangiocarcinoma




Genotype
MGI:4948964
cn31
Allelic
Composition
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Map2k7tm1.1Twad mutation (0 available); any Map2k7 mutation (5 available)
Map2k7tm1.2Twad mutation (0 available); any Map2k7 mutation (5 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice
• however, tumorigenesis is the same as in Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice
• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice

neoplasm
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice
• however, tumorigenesis is the same as in Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice
• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice




Genotype
MGI:5510703
cn32
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (18 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• however, treatment with a potent and selective oral pan class I PI3K inhibitor (GDC 0941) blocks tumor growth

neoplasm
• however, treatment with a potent and selective oral pan class I PI3K inhibitor (GDC 0941) blocks tumor growth




Genotype
MGI:3716963
cn33
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• following cre-adenovirus treatment, all mice develop primary lung tumors
• following cre-adenovirus treatment, lung tumors resemble those found in Krastm4Tyj heterozygotes
• following cre-adenovirus treatment, tumors occupy 24% of lung space
• at 6 weeks following cre-adenovirus treatment, mice have lesions ranging from atypical adenomatous hyperplasia to small adenomas that are smaller than in Krastm4Tyj Trp53tm1Brn homozygotes

neoplasm
• following cre-adenovirus treatment, all mice develop primary lung tumors
• following cre-adenovirus treatment, lung tumors resemble those found in Krastm4Tyj heterozygotes
• following cre-adenovirus treatment, tumors occupy 24% of lung space
• at 6 weeks following cre-adenovirus treatment, mice have lesions ranging from atypical adenomatous hyperplasia to small adenomas that are smaller than in Krastm4Tyj Trp53tm1Brn homozygotes




Genotype
MGI:3716966
cn34
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes

neoplasm
• at 19 weeks following cre-adenovirus treatment, sinonasal adenocarninomas develop in 64% of mice
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes




Genotype
MGI:3716968
cn35
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes
• at 6 weeks following cre-adenovirus treatment, mice have lesions ranging from atypical adenomatous hyperplasia to small adenomas that are larger than in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus (J:203686)
• following cre-adenovirus treatment, all mice develop advanced pulmonary adenocarinomas (J:103407)
• following cre-adenovirus treatment, multiple tumors are present ranging from well-defined tumors to advanced highly dysplastic lesions containing large sheets of dysplastic cells, abnormal mitoses, and multinucleated giant cells (J:103407)
• seventeen weeks after infection with low-titre (5X103) cre lentiviruses, an average of 30 lung adenocarcinomas are detected per mouse (J:154041)
• seventeen weeks after infection with high-titre (5X104) cre lentiviruses, 90-131 lung adenocarcinomas are detected per mouse (J:154041)
• mice develop multiple, aggressive adenocarcinomas in the lungs bilaterally following intranasal delivery of an adenovirus expressing Cre recombinase (J:195492)
• tumor growth is reduced to a similar extent following either two 7.3 Gy fractions of radiation therapy or a single 11.6 Gy fraction (J:195492)
• tumors incorporate high levels of BrdU 4 hours after radiation treatment similarly to unirradiated tumors, indicating lack of an intact G1 cell-cycle checkpoint (J:195492)

neoplasm
• following cre-adenovirus treatment, a subset of tumors are highly invasive and grow into the hilus, heart, and overlying pleura
• following cre-adenovirus treatment, lymph node metastases are present in over 50% of mice
• at 19 weeks following cre-adenovirus treatment, sinonasal adenocarninomas develop in 14% of mice
• mice infected with low-titre (5X103) lentiviruses expressing Cre and Nfkbia have either a single lung adenocarcinoma or none at all
• mice infected with high-titre (5X104) lentiviruses expressing Cre and Nfkbia have 6-22 lung adenocarcinomas detected per mouse
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes
• at 6 weeks following cre-adenovirus treatment, mice have lesions ranging from atypical adenomatous hyperplasia to small adenomas that are larger than in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus (J:203686)
• following cre-adenovirus treatment, all mice develop advanced pulmonary adenocarinomas (J:103407)
• following cre-adenovirus treatment, multiple tumors are present ranging from well-defined tumors to advanced highly dysplastic lesions containing large sheets of dysplastic cells, abnormal mitoses, and multinucleated giant cells (J:103407)
• seventeen weeks after infection with low-titre (5X103) cre lentiviruses, an average of 30 lung adenocarcinomas are detected per mouse (J:154041)
• seventeen weeks after infection with high-titre (5X104) cre lentiviruses, 90-131 lung adenocarcinomas are detected per mouse (J:154041)
• mice develop multiple, aggressive adenocarcinomas in the lungs bilaterally following intranasal delivery of an adenovirus expressing Cre recombinase (J:195492)
• tumor growth is reduced to a similar extent following either two 7.3 Gy fractions of radiation therapy or a single 11.6 Gy fraction (J:195492)
• tumors incorporate high levels of BrdU 4 hours after radiation treatment similarly to unirradiated tumors, indicating lack of an intact G1 cell-cycle checkpoint (J:195492)

mortality/aging
• mice do not survive to 26 weeks post cre-adenovirus treatment in contrast to Krastm4Tyj Trp53tm1Brn heterozygous mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:103407 , J:154041 , J:195492 , J:203686




Genotype
MGI:5562914
cn36
Allelic
Composition
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Rnf7Gt(XE423)Byg mutation (0 available); any Rnf7 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre)
• a few adenocarcinomas develop in mice following Ad-Cre administration

mortality/aging
• median survival time of Ad-Cre treated mice is 27.6 weeks, with all mice dying by 33 weeks

neoplasm
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre)
• a few adenocarcinomas develop in mice following Ad-Cre administration




Genotype
MGI:5562910
cn37
Allelic
Composition
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7tm1.1Ysun
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Rnf7Gt(XE423)Byg mutation (0 available); any Rnf7 mutation (18 available)
Rnf7tm1.1Ysun mutation (0 available); any Rnf7 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of Ad-Cre treated mice is 37.9 weeks, with most mice dying by 60 weeks

neoplasm
• mice show reduced lung tumor burden following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) compared to single Kras homozygotes, however the number of hyperplastic loci is not affected
• hyperplasia or adenomas from Ad-Cre treated mice show reduced proliferation compared to single Kras homozygotes




Genotype
MGI:5510702
cn38
Allelic
Composition
Krastm4Tyj/Kras+
Raf1tm2Bacc/Raf1tm2Bacc
Ptf1atm1(cre)Hnak/Ptf1a+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (18 available)
Raf1tm2Bacc mutation (0 available); any Raf1 mutation (82 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• as in Krastm4Tyj Ptf1atm1(cre)Hnak double heterozygotes

neoplasm
• as in Krastm4Tyj Ptf1atm1(cre)Hnak double heterozygotes




Genotype
MGI:4441491
cn39
Allelic
Composition
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Lyz2tm1(cre)Ifo mutation (10 available); any Lyz2 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• lung weight is 10-fold higher than that in control mice at 3 weeks old

mortality/aging
• the maximum survival is 24 days

respiratory system
• lung weight is 10-fold higher than that in control mice at 3 weeks old

neoplasm




Genotype
MGI:5298088
cn40
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Shhtm2(cre/ERT2)Cjt/Shh+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Shhtm2(cre/ERT2)Cjt mutation (1 available); any Shh mutation (23 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
N
• no macroscopic or microscopic skin tumors are observed up to 4 months after tamoxifen treatment




Genotype
MGI:5298083
cn41
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Krt19tm1(cre/ERT)Ggu/Krt19+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Krt19tm1(cre/ERT)Ggu mutation (1 available); any Krt19 mutation (1 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• tamoxifen treated mice die within 2 months from intestinal cancers before developing skin tumors

digestive/alimentary system
• tamoxifen treated mice develop intestinal cancers

neoplasm
• tamoxifen treated mice develop intestinal cancers
• when back skin from mutant animals is grafted onto back skin of nude mice, all engrafted mice develop skin tumors, including ulcerative lesions (benign and squamous cell carcinomas) within 2 months of tamoxifen administration
• tamoxifen treated mice develop terminal intestinal carcinomas with 2 months of treatment

integument
• when back skin from mutant animals is grafted onto back skin of nude mice, all engrafted mice develop skin tumors, including ulcerative lesions (benign and squamous cell carcinomas) within 2 months of tamoxifen administration




Genotype
MGI:6256734
cn42
Allelic
Composition
Krastm4Tyj/Kras+
Krt19tm1(cre/ERT)Ggu/Krt19+
Ptentm2Mak/Ptentm2Mak
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Krt19tm1(cre/ERT)Ggu mutation (1 available); any Krt19 mutation (1 available)
Ptentm2Mak mutation (4 available); any Pten mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice administered tamoxifen at 8 weeks of age show a median survival of 30 days after tamoxifen injection

digestive/alimentary system
• colonic serrated epithelial changes in tamoxifen treated mice
• hyperplastic changes of gastric mucosa in tamoxifen treated mice

endocrine/exocrine glands
• extrahepatic bile duct is rigid and dilated in tamoxifen treated mice
• papillary hyperplasia of the extrahepatic biliary tract
• papillary hyperplasia of the gallbladder in tamoxifen treated mice
• gallbladder and cystic duct are rigid and dilated in tamoxifen treated mice
• in tamoxifen treated mice
• PanIN-like lesions and hyperplasia in the pancreatic ducts in tamoxifen treated mice
• however, no obvious tumors are seen in mice administered tamoxifen at 8 weeks of age

immune system
• obstructive pneumonia in tamoxifen treated mice

liver/biliary system
• extrahepatic bile duct is rigid and dilated in tamoxifen treated mice
• papillary hyperplasia of the extrahepatic biliary tract
• papillary hyperplasia of the gallbladder in tamoxifen treated mice
• gallbladder and cystic duct are rigid and dilated in tamoxifen treated mice
• in tamoxifen treated mice
• liver of tamoxifen treated mice shows pre-malignant papillary ductal lesions in periportal areas

neoplasm
• PanIN-like lesions and hyperplasia in the pancreatic ducts in tamoxifen treated mice
• however, no obvious tumors are seen in mice administered tamoxifen at 8 weeks of age

respiratory system
• obstructive pneumonia in tamoxifen treated mice
• papillary hyperplasia of bronchial epithelia in tamoxifen treated mice
• respiratory failure by lung lesions in tamoxifen treated mice




Genotype
MGI:6403693
cn43
Allelic
Composition
Hprttm1(CAG-BRF1)Gu/Hprt+
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hprttm1(CAG-BRF1)Gu mutation (0 available); any Hprt mutation (35 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• as in mice lacking the BRF1 knock-in

neoplasm
• as in mice lacking the BRF1 knock-in

homeostasis/metabolism
• tRNA levels are increased in the pancreas

endocrine/exocrine glands
• as in mice lacking the BRF1 knock-in

cellular
• tRNA levels are increased in the pancreas




Genotype
MGI:6377664
cn44
Allelic
Composition
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd9tm1c(EUCOMM)Hmgu mutation (0 available); any Cd9 mutation (96 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (6 available); any Gt(ROSA)26Sor mutation (540 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele

neoplasm
• at 8 weeks, not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele
• increased tumor weight compared to in mice homozygous for a conditional allele
• compared to in mice homozygous for a conditional allele

endocrine/exocrine glands
• at 8 weeks, not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele
• increased tumor weight compared to in mice homozygous for a conditional allele




Genotype
MGI:6377668
cn45
Allelic
Composition
Cd9tm1c(EUCOMM)Hmgu/Cd9tm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd9tm1c(EUCOMM)Hmgu mutation (0 available); any Cd9 mutation (96 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (6 available); any Gt(ROSA)26Sor mutation (540 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• as severe as in mice wild-type for Cd9

neoplasm
• at 8 weeks, more severe than in mice heterozygous for the Cd9 conditional allele

endocrine/exocrine glands
• at 8 weeks, more severe than in mice heterozygous for the Cd9 conditional allele




Genotype
MGI:6377665
cn46
Allelic
Composition
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd9tm1c(EUCOMM)Hmgu mutation (0 available); any Cd9 mutation (96 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (6 available); any Gt(ROSA)26Sor mutation (540 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele




Genotype
MGI:6377669
cn47
Allelic
Composition
Cd9tm1c(EUCOMM)Hmgu/Cd9tm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd9tm1c(EUCOMM)Hmgu mutation (0 available); any Cd9 mutation (96 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (6 available); any Gt(ROSA)26Sor mutation (540 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• as severe as in mice wild-type for Cd9




Genotype
MGI:6377672
cn48
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (6 available); any Gt(ROSA)26Sor mutation (540 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die by 8 weeks of age




Genotype
MGI:6377671
cn49
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (6 available); any Gt(ROSA)26Sor mutation (540 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die by 30 weeks of age

neoplasm

endocrine/exocrine glands




Genotype
MGI:4441492
cn50
Allelic
Composition
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fntbtm1.1Mbrg mutation (0 available); any Fntb mutation (194 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (194 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Lyz2tm1(cre)Ifo mutation (10 available); any Lyz2 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice but higher than in normal mice

mortality/aging
• longer life span than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (>100 days in some cases)

respiratory system
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice but higher than in normal mice

neoplasm
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice




Genotype
MGI:4441490
cn51
Allelic
Composition
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fntbtm1.1Mbrg mutation (0 available); any Fntb mutation (194 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (194 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Pggt1btm1.1Mbrg mutation (0 available); any Pggt1b mutation (10 available)
Pggt1btm1Mbrg mutation (0 available); any Pggt1b mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment
• the lung surface of Cre-adenovirus treated mice is nearly indistinguishable from that of control mice
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment
• presence of small adenomas after Cre-adenovirus treatment
• adenocarcinoma in 1 of 11 mice after Cre-adenovirus treatment

respiratory system
• the lung surface of Cre-adenovirus treated mice is nearly indistinguishable from that of control mice
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment
• presence of small adenomas after Cre-adenovirus treatment
• adenocarcinoma in 1 of 11 mice after Cre-adenovirus treatment
• presence of epithelial hyperplasia after Cre-adenovirus treatment




Genotype
MGI:4441488
cn52
Allelic
Composition
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fntbtm1.1Mbrg mutation (0 available); any Fntb mutation (194 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (194 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Lyz2tm1(cre)Ifo mutation (10 available); any Lyz2 mutation (15 available)
Pggt1btm1.1Mbrg mutation (0 available); any Pggt1b mutation (10 available)
Pggt1btm1Mbrg mutation (0 available); any Pggt1b mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• lung weight and histology are indistinguishable from littermate control mice at 3-week old
• but eventually develop lung tumors at older age

mortality/aging
• median life span is 170 days
• longer median life span than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (170 vs. 22 days)

neoplasm
• lung weight and histology are indistinguishable from littermate control mice at 3-week old, compare with lung weight is 10-fold higher in Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice
• lung weight and histology are indistinguishable from littermate control mice at 3-week old
• but eventually develop lung tumors at older age




Genotype
MGI:4441486
cn53
Allelic
Composition
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fntbtm1.1Mbrg mutation (0 available); any Fntb mutation (194 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (194 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• Cre-adenovirus treatment results in G2M cell-cycle arrest in embryonic fibroblasts




Genotype
MGI:5547939
cn54
Allelic
Composition
Krastm4Tyj/Kras+
Myod1tm1.1(cre/ERT,TVA)Gcg/Myod1+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Myod1tm1.1(cre/ERT,TVA)Gcg mutation (1 available); any Myod1 mutation (5 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• when mice older than 6 weeks are given systemic tamoxifen treatment by intraperitoneal delivery, mice develop multiple tumors at clinically relevant sites with a median tumor free survival of 153 days (longer latency than Pax7CE mutants
• tamoxifen treated mice develop sarcomas that are exclusively undifferentiated pleomorphic sarcomas (UPS), myogenic or nonmyogenic in type
• tumors can appear in the body wall, the extremities, or the head and neck region




Genotype
MGI:5528686
cn55
Allelic
Composition
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Mapkapk2tm1.1Yaff mutation (1 available); any Mapkapk2 mutation (13 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus
• tumor burden progresses from 11% of lung (6 weeks) to 45% at experimental endpoint (12+ weeks) in the presence of a Cre-recombinase expressing adenovirus
• Mapkap2 expressing tumors (MK2+) represent a higher proportion of tumor burden, however over time the proportion of these tumors decreases and the proportion of Mapkapk2 (MK2-) null tumors increases in the presence of a Cre-recombinase expressing adenovirus
• proportion of total lung tumor burden composed of Mapkapk2 (MK2-) null tumors is reduced from 39% to 11% following cisplatin treatment

neoplasm
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus
• tumor burden progresses from 11% of lung (6 weeks) to 45% at experimental endpoint (12+ weeks) in the presence of a Cre-recombinase expressing adenovirus
• Mapkap2 expressing tumors (MK2+) represent a higher proportion of tumor burden, however over time the proportion of these tumors decreases and the proportion of Mapkapk2 (MK2-) null tumors increases in the presence of a Cre-recombinase expressing adenovirus
• proportion of total lung tumor burden composed of Mapkapk2 (MK2-) null tumors is reduced from 39% to 11% following cisplatin treatment




Genotype
MGI:5559052
cn56
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• extremity sarcomas in mice injected with Ad-Cre invade adjacent skeletal muscle and uterine sarcomas invade the intestinal wall and pancreas
• 20% of mice with large extremity sarcomas develop metastasis to the lungs
• 90% of mice injected intramuscularly with an adenovirus expressing Cre recombinase (Ad-Cre) into the extremities develop soft tissue sarcomas after a median time of 3 months (J:125101)
• high penetrance of soft tissue sarcomas also develops after injection of Ad-Cre into the uterus (J:125101)
• soft tissue sarcomas present as large solitary masses originating at the site of Ad-Cre injection, and are high-grade spindle cell neoplasms (J:125101)
• sarcomas show myofibroblastic differentiation with intracytoplasmic filaments with densities (J:125101)
• gene expression analysis indicates that Ad-Cre induced sarcomas are undifferentiated pleomorphic sarcoma/malignant fibrous histiocytoma (J:155389)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
malignant fibrous histiocytoma DOID:1907 J:155389
sarcoma DOID:1115 J:125101 , J:204376 , J:155389




Genotype
MGI:4460775
cn57
Allelic
Composition
Krastm4Tyj/Kras+
Lrrc17tm1Nik/Lrrc17+
Srpk2tm1Nik/Srpk2+
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Lrrc17tm1Nik mutation (0 available); any Lrrc17 mutation (4 available)
Srpk2tm1Nik mutation (0 available); any Srpk2 mutation (11 available)
Tg(Mx1-cre)1Cgn mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in pIpC-treated mice similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice

immune system
• pIpC-treated mice develop myeloproliferative disorder with anemia unlike wild-type mice that is similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice

hematopoietic system
• bone marrow cells from pIpC-treated mice spontaneous form colony forming units-granulocyte and macrophage (CFU-GM) in the absence of cytokines unlike wild-type cells
• in pIpC-treated mice similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice
• pIpC-treated mice develop myeloproliferative disorder with anemia unlike wild-type mice that is similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice




Genotype
MGI:4948965
cn58
Allelic
Composition
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Tg(Trp53)bSrn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Map2k7tm1.1Twad mutation (0 available); any Map2k7 mutation (5 available)
Map2k7tm1.2Twad mutation (0 available); any Map2k7 mutation (5 available)
Tg(Trp53)bSrn mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• following adenovirus cre infection, mice exhibit the same tumor burden as in control mice




Genotype
MGI:6256732
cn59
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm2Mak/Pten+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptentm2Mak mutation (4 available); any Pten mutation (39 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• some lesions are diagnosed as intrahepatic cholangiocarcinoma by the appearance of adenocarcinoma showing tubular and/or papillary structures with a fibrous stroma; these tumor cells show loss of Pten expression
• mice develop liver tumors at 6 months of age, showing obvious symptoms after 7 months with abdominal distension due to multiple tumors at later stages
• mice develop liver tumors with both hepatocyte and cholangiocyte differentiation
• majority of large nodules are hepatocellular dysplasia, a precursor lesion of hepatocellular carcinoma

liver/biliary system
• some lesions are diagnosed as intrahepatic cholangiocarcinoma by the appearance of adenocarcinoma showing tubular and/or papillary structures with a fibrous stroma; these tumor cells show loss of Pten expression
• mice develop liver tumors at 6 months of age, showing obvious symptoms after 7 months with abdominal distension due to multiple tumors at later stages
• mice develop liver tumors with both hepatocyte and cholangiocyte differentiation
• majority of large nodules are hepatocellular dysplasia, a precursor lesion of hepatocellular carcinoma




Genotype
MGI:5428907
cn60
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• mutants develop intrahepatic cholangiocarcinoma as early as 9 weeks of age
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor

mortality/aging
• mean survival is 19 weeks of age

neoplasm
• mutants develop intrahepatic cholangiocarcinoma as early as 9 weeks of age
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor
• tumors are highly metastatic, with 75% of mutants having tumors showing invasion into adjacent organs such as the diaphragm, bowel, pancreas and stomach or distant metastasis to the lymph nodes, spleen, lungs, or peritoneal cavity
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas

cardiovascular system
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:184949




Genotype
MGI:4819844
cn61
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Yap1tm1.1Dupa mutation (2 available); any Yap1 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system

neoplasm




Genotype
MGI:6256730
cn62
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Ptentm2Mak mutation (4 available); any Pten mutation (39 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival is 46 days

growth/size/body
• seen in 5 month old mice
• all mice start to show abdominal distension at about 5 weeks of age, frequently accompanied by jaundice and weight loss
• distension is due to hepatic enlargement and/or hemorrhagic ascites

neoplasm
• tumors primarily show glandular morphology that resembles well-differentiated human cholangiocarcinoma and marker analysis indicates that tumors are intrahepatic cholangiocarcinoma
• in some cases, regions of moderately differentiated tumor with a cribriform appearance are seen
• no metastasis or invasion to other organs is seen
• tumors are frequently surrounded by dense fibrous stroma, indicating accumulation of fibrillar collagens
• stellate cells are activated and acquire a myofibroblast-like phenotype
• tumor cells show mucin production, a characteristic of epithelial cells in the bile duct
• multiple solid tumors with various sizes are seen throughout the liver
• invasive tumors are apparent after 7 weeks of age, with abundant desmoplastic stroma or desmoplasia

endocrine/exocrine glands
• various degrees of hyperplasia are seen in the bile ducts, characterized by increase in number and size and change in morphology, at 4 weeks of age
• at 5 weeks, a part of the hyperplastic ductal lesions at the hilum become enlarged and show a pattern of papillary growth

homeostasis/metabolism

liver/biliary system
• various degrees of hyperplasia are seen in the bile ducts, characterized by increase in number and size and change in morphology, at 4 weeks of age
• at 5 weeks, a part of the hyperplastic ductal lesions at the hilum become enlarged and show a pattern of papillary growth
• tumors primarily show glandular morphology that resembles well-differentiated human cholangiocarcinoma and marker analysis indicates that tumors are intrahepatic cholangiocarcinoma
• in some cases, regions of moderately differentiated tumor with a cribriform appearance are seen
• no metastasis or invasion to other organs is seen
• tumors are frequently surrounded by dense fibrous stroma, indicating accumulation of fibrillar collagens
• stellate cells are activated and acquire a myofibroblast-like phenotype
• tumor cells show mucin production, a characteristic of epithelial cells in the bile duct
• multiple solid tumors with various sizes are seen throughout the liver
• invasive tumors are apparent after 7 weeks of age, with abundant desmoplastic stroma or desmoplasia
• seen in 5 month old mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:254370




Genotype
MGI:5428898
cn63
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• mutants develop intrahepatic cholangiocarcinoma as early as 32 weeks of age
• intrahepatic cholangiocarcinoma recapitulates the histologic and molecular features of multistage progression of human intrahepatic cholangiocarcinoma
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor

mortality/aging
• mean survival is 52 weeks of age

neoplasm
• mutants develop intrahepatic cholangiocarcinoma as early as 32 weeks of age
• intrahepatic cholangiocarcinoma recapitulates the histologic and molecular features of multistage progression of human intrahepatic cholangiocarcinoma
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor
• tumors are highly metastatic, with tumors showing invasion into adjacent organs such as the diaphragm, bowel, pancreas and stomach or distant metastasis to the lymph nodes, spleen, lungs, or peritoneal cavity
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas

cardiovascular system
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:184949




Genotype
MGI:4835045
cn64
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (51 available)
Krastm4Tyj mutation (8 available); any Kras mutation (37 available)
Tg(Tyr-cre/ERT2)13Bos mutation (9 available)
Trp53tm1Brn mutation (14 available); any Trp53 mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen-treated mice develop melanomas with spindle-like morphology
• 3 of 7 (43%) mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology at a median latency greater than 52 weeks compared with Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos mice whose median latency is 14 weeks

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:5486065
cn65
Allelic
Composition