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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Krastm4Tyj
targeted mutation 4, Tyler Jacks
MGI:2429948
Summary 203 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+
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
B6.129-Krastm4Tyj Tgfbr2tm1.2Hlm MGI:5304695
cn9
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
B6.Cg-Krastm4Tyj Map2k7tm1.1Twad/Map2k7tm1.2Twad MGI:4948962
cn10
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
B6.Cg-Krastm4Tyj Ptf1atm1.1(cre)Cvw MGI:3836557
cn11
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
cn12
Apctm2Rak/Apctm2Rak
Krastm4Tyj/Kras+
involves: 129 * 129S4/SvJae * C57BL/6J * SJL MGI:5432240
cn13
Krastm4Tyj/Kras+
Tg(Gfap-cre)77.6Mvs/0
involves: 129 * BALB/c * C57BL/6NHsd MGI:4849444
cn14
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308959
cn15
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308961
cn16
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308962
cn17
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308963
cn18
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308946
cn19
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308951
cn20
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308954
cn21
Krastm4Tyj/Kras+
Tg(Scgb1a1-cre)1Kkw/?
involves: 129 * C57BL/6 * FVB/N MGI:3624415
cn22
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129 * FVB/N MGI:3695428
cn23
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129 * FVB/N MGI:3695421
cn24
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129 * FVB/N MGI:3695424
cn25
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Krt19tm1(cre/ERT)Ggu/Krt19+
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae MGI:5298083
cn26
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Shhtm2(cre/ERT2)Cjt/Shh+
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae MGI:5298088
cn27
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:4948964
cn28
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716963
cn29
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5562914
cn30
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7tm1.1Ysun
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5562910
cn31
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5510703
cn32
Krastm4Tyj/Kras+
Raf1tm2Bacc/Raf1tm2Bacc
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5510702
cn33
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716966
cn34
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716968
cn35
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:4441491
cn36
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441490
cn37
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441492
cn38
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
cn39
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441486
cn40
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5528686
cn41
Krastm4Tyj/Kras+
Myod1tm1.1(cre/ERT,TVA)Gcg/Myod1+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5547939
cn42
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5559052
cn43
Krastm4Tyj/Kras+
Lrrc17tm1Nik/Lrrc17+
Srpk2tm1Nik/Srpk2+
Tg(Mx1-cre)1Cgn/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA MGI:4460775
cn44
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Tg(Trp53)bSrn/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA MGI:4948965
cn45
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Alb-cre)21Mgn/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428907
cn46
Krastm4Tyj/Krastm4Tyj
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Tg(Alb-cre)21Mgn/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:4819844
cn47
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Alb-cre)21Mgn/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428898
cn48
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:5486065
cn49
Krastm4Tyj/Kras+
Tg(CAG-Bgeo,-tsA58T)T26Ichi/0
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5604750
cn50
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:3776026
cn51
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5659893
cn52
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Gev/Trp53tm1Gev
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5635880
cn53
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre/ERT)20Efu/0
involves: 129P2/OlaHsd * 129S4/SvJae * CD-1 MGI:5298084
cn54
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:4835041
cn55
Cdkn2atm2.1Nesh/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:4835045
cn56
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:4835046
cn57
Apctm2.1Cip/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:3776028
cn58
Cdkn2atm2Brn/Cdkn2atm2Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB/N MGI:5484548
cn59
Krastm4Tyj/Kras+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Meox2tm1(cre)Sor/Meox2+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * FVB/N MGI:3716399
cn60
Brca2tm1Cam/Brca2tm1Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940102
cn61
Brca2tm1Brn/Brca2tm1Cam
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940096
cn62
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:5486056
cn63
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3695431
cn64
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3695432
cn65
Krastm4Tyj/Kras+
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4839215
cn66
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4839216
cn67
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3032576
cn68
Bak1tm1Thsn/Bak1tm1Thsn
Baxtm1Sjk/Baxtm2Sjk
Krastm4Tyj/Kras+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5559061
cn69
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
cn70
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
cn71
Gfi1tm5.1(GFI1*)Tmo/Gfi1+
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA MGI:5468270
cn72
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3695568
cn73
Krastm4Tyj/Kras+
Shhtm2(cre/ERT2)Cjt/Shh+
involves: 129S2/SvPas * 129S4/SvJae MGI:5298087
cn74
Krastm4Tyj/Kras+
Krt19tm1(cre/ERT)Ggu/Krt19+
involves: 129S2/SvPas * 129S4/SvJae MGI:5298082
cn75
Krastm4Tyj/Krastm4Tyj
Trim33tm1Los/Trim33tm1Los
Tg(Pdx1-cre)89.1Dam/0
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 * DBA/2 MGI:4355873
cn76
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
involves: 129S4/SvJae MGI:3776023
cn77
Krastm4Tyj/Krastm4Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae MGI:4818400
cn78
Krastm4Tyj/Kras+
Rbl2tm2Tyj/Rbl2tm2Tyj
involves: 129S4/SvJae MGI:3842378
cn79
Krastm4Tyj/Kras+
Rb1tm3Tyj/Rb1tm3Tyj
involves: 129S4/SvJae MGI:3842377
cn80
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scrib+
involves: 129S4/SvJae MGI:5638047
cn81
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scribtm1.1Phum
involves: 129S4/SvJae MGI:5638045
cn82
Krastm4Tyj/Krastm4Tyj
Tg(Ela1-cre/ERT)1Dam/0
involves: 129S4/SvJae MGI:3821750
cn83
Krastm4Tyj/Krastm4Tyj
Bhlha15tm3(cre/ERT2)Skz/Bhlha15+
involves: 129S4/SvJae MGI:3821739
cn84
Fastm1Ach/Fastm1Ach
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae MGI:5014515
cn85
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae MGI:5014516
cn86
Krastm4Tyj/Kras+
Trp53tm4Att/Trp53tm4Att
involves: 129S4/SvJae MGI:5140101
cn87
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm3(CAG-luc)Tyj/Gt(ROSA)26Sor+
involves: 129S4/SvJae MGI:3818747
cn88
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae MGI:5510701
cn89
Krastm4Tyj/Kras+
Tg(Ela1-cre/ERT)1Dam/0
involves: 129S4/SvJae MGI:5510700
cn90
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Scgb1a1-rtTA)1Jaw/0
involves: 129S4/SvJae MGI:4368025
cn91
Gt(ROSA)26Sortm1(RAC1*)Jkis/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
involves: 129S4/SvJae MGI:5437472
cn92
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Tg(Ela1-cre/ERT)1Dam/0
involves: 129S4/SvJae MGI:5510699
cn93
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
involves: 129S4/SvJae MGI:3716967
cn94
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
involves: 129S4/SvJae MGI:5491219
cn95
Krastm4Tyj/Kras+
Tg(Prm-cre)58Og/0
involves: 129S4/SvJae MGI:3716392
cn96
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
involves: 129S4/SvJae MGI:3716965
cn97
Krastm4Tyj/Kras+
Trp53tm1Lejo/Trp53tm1Lejo
involves: 129S4/SvJae MGI:5441555
cn98
Krastm4Tyj/Kras+
Meox2tm1(cre)Sor/Meox2+
involves: 129S4/SvJae * 129S4/SvJaeSor MGI:3716398
cn99
Gt(ROSA)26Sortm1(Notch1)Dam/Gt(ROSA)26Sor+
Krastm4Tyj/Krastm4Tyj
Tg(Ela1-cre/ERT)1Dam/0
involves: 129S4/SvJae * 129S4/SvJaeSor MGI:3821751
cn100
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Pms2tm2(cre)Lisk/Pms2tm2(cre)Lisk
involves: 129S4/SvJae * 129S4/SvJaeSor MGI:5543250
cn101
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
cn102
Cdkn2atm1.1Gsu/Cdkn2atm1.1Gsu
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6J * FVB/N MGI:5502380
cn103
Krastm4Tyj/Kras+
Pik3r1tm1Lca/Pik3r1tm1Lca
Pik3r2tm1Lca/Pik3r2tm1Lca
involves: 129S4/SvJae * 129S6/SvEvTac MGI:3834443
cn104
Gt(ROSA)26Sortm2(Pik3ca*)Dsa/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5510696
cn105
Krastm4Tyj/Kras+
Pik3r1tm1Lca/Pik3r1+
Pik3r2tm1Lca/Pik3r2tm1Lca
involves: 129S4/SvJae * 129S6/SvEvTac MGI:3834445
cn106
Krastm4Tyj/Kras+
Stk11tm1.2Rdp/Stk11tm1.2Rdp
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5515885
cn107
Krastm4Tyj/Kras+
Pik3r2tm1Lca/Pik3r2tm1Lca
involves: 129S4/SvJae * 129S6/SvEvTac MGI:3834444
cn108
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
cn109
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
cn110
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Vil-cre)20Syr/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5013409
cn111
Krastm4Tyj/Kras+
Stk11tm1.1Rdp/Stk11tm1.2Rdp
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659881
cn112
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659896
cn113
Krastm4Tyj/Kras+
Stk11tm1.1Rdp/Stk11tm1.1Rdp
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659880
cn114
Gt(ROSA)26Sortm1(Tva)Dsa/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6J MGI:3814193
cn115
Fgfr3tm4Cxd/Fgfr3+
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N MGI:5141739
cn116
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N MGI:5502381
cn117
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
cn118
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Amhr2tm3(cre)Bhr/Amhr2+
involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 MGI:5432231
cn119
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Tg(CYP19A1-cre)1Jri/0
involves: 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5432224
cn120
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * 129X1/SvJ * FVB/N MGI:5141743
cn121
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * BALB/c * C57BL/6 MGI:5013916
cn122
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA MGI:3035835
cn123
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA MGI:5013917
cn124
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Gfap-cre)77.6Mvs/0
involves: 129S4/SvJae * BALB/c * C57BL/6NHsd MGI:4849441
cn125
Krastm4Tyj/Kras+
Tg(Tek-cre)12Flv/0
involves: 129S4/SvJae * C3H * C57BL/6 MGI:3716393
cn126
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
involves: 129S4/SvJae * C57BL/6 MGI:5559056
cn127
Krastm4Tyj/Kras+
Plcl1tm1.1Matk/Plcl1tm1.1Matk
involves: 129S4/SvJae * C57BL/6 MGI:5607955
cn128
Krastm4Tyj/Kras+
Tg(IVL-cre/ERT2)1Blpn/0
involves: 129S4/SvJae * C57BL/6 MGI:5298090
cn129
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
involves: 129S4/SvJae * C57BL/6 MGI:5528687
cn130
Krastm4Tyj/Kras+
Siva1tm1.1Att/Siva1tm1.2Att
involves: 129S4/SvJae * C57BL/6 MGI:5659853
cn131
Braftm2Cpri/Braf+
Krastm4Tyj/Kras+
involves: 129S4/SvJae * C57BL/6 MGI:5440071
cn132
Krastm4Tyj/Kras+
Tg(MUC1)79.24Gend/0
involves: 129S4/SvJae * C57BL/6 MGI:4411919
cn133
Krastm4Tyj/Kras+
Siva1tm1.2Att/Siva1+
involves: 129S4/SvJae * C57BL/6 MGI:5659856
cn134
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Scgb1a1-cre)1Tauc/0
involves: 129S4/SvJae * C57BL/6 MGI:4943568
cn135
Krastm4Tyj/Kras+
Ralatm1.2Cjm/Ralatm1.2Cjm
Ralbtm1.1Cjm/Ralbtm1.2Cjm
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5505293
cn136
Krastm4Tyj/Kras+
Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL/J MGI:5556244
cn137
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3821753
cn138
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:2687206
cn139
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3695430
cn140
Krastm4Tyj/Kras+
Tg(Fabp7-cre)2Gtm/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3810650
cn141
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:5582314
cn142
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:5441554
cn143
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:2687217
cn144
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:5308806
cn145
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:5308964
cn146
Krastm4Tyj/Kras+
Tg(KRT14-cre/ERT)20Efu/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N MGI:5659911
cn147
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
cn148
Krastm4Tyj/Kras+
Tg(Alb-cre)21Mgn/0
involves: 129S4/SvJae * C57BL/6 * DBA MGI:5428897
cn149
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4355875
cn150
Braftm1Rima/Braf+
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)1Lru/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4458349
cn151
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4355874
cn152
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5705328
cn153
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5705321
cn154
Brca1tm1Thl/Brca1tm2.1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494465
cn155
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4941337
cn156
Gt(ROSA)26Sortm1(MYC/ERT2)Gev/Gt(ROSA)26Sortm1(MYC/ERT2)Gev
Krastm4Tyj/Krastm4Tyj
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:3821936
cn157
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm3Tyj/Trp53+
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4940098
cn158
Brca1tm1Thl/Brca1tm3.1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494462
cn159
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4941336
cn160
Brca1tm1Thl/Brca1tm1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494464
cn161
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae * C57BL/6J MGI:4836596
cn162
Krastm4Tyj/Kras+
Stk11tm1.1Gne/Stk11tm1.1Gne
involves: 129S4/SvJae * C57BL/6N MGI:5484547
cn163
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3821738
cn164
Krastm4Tyj/Kras+
Tg(Krt1-15-cre/PGR)22Cot/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:5298086
cn165
Krastm4Tyj/Krastm4Tyj
Tg(Ela1-cre/ERT2)1Stof/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3821737
cn166
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * FVB MGI:4835047
cn167
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * FVB MGI:4835044
cn168
Krastm4Tyj/Kras+
Tg(MMTV-cre)4Mam/0
involves: 129S4/SvJae * FVB MGI:3044680
cn169
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Usp9x+
involves: 129S4/SvJae * FVB/N MGI:5438091
cn170
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * FVB/N MGI:5494463
cn171
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * FVB/N MGI:3044567
cn172
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Y
involves: 129S4/SvJae * FVB/N MGI:5438090
cn173
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * FVB/N MGI:5141740
cn174
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/?
involves: 129S4/SvJae * FVB/N MGI:3032575
cn175
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * FVB/N MGI:5141742
cn176
Krastm4Tyj/Kras+
Tg(Pbsn-cre)20Fwan/0
involves: 129S4/SvJae * FVB/NCrl MGI:5300203
cn177
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scribtm1.1Phum
Tg(Pbsn-cre)20Fwan/0
involves: 129S4/SvJae * FVB/NCrl MGI:5300204
cn178
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scrib+
Tg(Pbsn-cre)20Fwan/0
involves: 129S4/SvJae * FVB/NCrl MGI:5300205
cn179
Krastm4Tyj/Kras+
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
Trp53tm5Tyj/Trp53+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 MGI:5317170
cn180
Krastm4Tyj/Kras+
Sftpctm1(cre/ERT2)Blh/Sftpc+
Trp53tm5Tyj/Trp53+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 MGI:5317171
cn181
Krastm4Tyj/Krastm4Tyj
Ugdhtm1.1Xzh/Ugdhtm1.1Xzh
Tg(Wnt1-cre)11Rth/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * CBA/J MGI:5430385
cn182
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3695569
cn183
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3695567
cn184
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:3695426
cn185
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:3695429
cn186
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:3695422
cn187
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940100
cn188
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940099
cn189
Krastm4Tyj/Kras+
Mapk8tm1Wag/Mapk8+
Mapk9tm1Mka/Mapk9tm1Mka
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:4948963
cn190
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182tm1.1Dgk
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704424
cn191
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
cn192
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182+
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704427
cn193
Krastm4Tyj/Kras+
Pax7tm2.1(cre/ERT2)Fan/Pax7+
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129X1/SvJ * C57BL/6 MGI:5547938
cn194
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714153
cn195
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1b+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714154
cn196
Pggt1btm1Mbrg/Pggt1btm1Mbrg
Krastm4Tyj/Kras+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714152
cn197
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722605
cn198
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm3Glo
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722604
cn199
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722603
cn200
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Krastm4Tyj/Kras+
involves: 129/Sv * 129S4/SvJae * C57BL/6 * FVB/N * SJL MGI:5659895
cn201
Krastm4Tyj/Kras+
Tg(SFTPC-rtTA)5Jaw/0
Tg(tetO-cre)1Jaw/0
involves: 129/Sv * C57BL/6 MGI:3716394
cn202
Krastm4Tyj/Kras+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * C57BL/6 * FVB * ICR MGI:3722600
cn203
Krastm4Tyj/Kras+
Trp53tm3Glo/Trp53+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * C57BL/6 * FVB * ICR MGI:3722602


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 (4 available); any Kras mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 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)
• 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)
• 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) (J:207982)
• 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 (J:207982)
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) (J:207982)
• 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 (J:207982)
• a few adenocarcinomas develop in mice following Ad-Cre administration (J:207982)
• a few adenocarcinomas develop in mice following Ad-Cre administration (J:207982)

Mouse Models of Human Disease
OMIM ID Ref(s)
Lung Cancer 211980 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 (4 available); any Kras mutation (30 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 (J:187371)
• primary mouse embryonic fibroblast treated with adenoviral-cre exhibit enhanced growth rate compared with wild-type cells (J:187371)




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 (4 available); any Kras mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 79 days (J:177379)
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 79 days (J:177379)

tumorigenesis
• 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 (J:177379)
• 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 (J:177379)
• 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 (J:177379)
• 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 (J:177379)




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 (4 available); any Kras mutation (30 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 (J:96296)
• 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 (J:96296)

growth/size/body
• 47% of mutants develop peritoneal endometriosis following ovarian intrabursal injection of an adenovirus expressing Cre (J:96296)
• however, mice injected with adenovirus expressing Cre directly into the peritoneum do not develop peritoneal endometriosis (J:96296)
• 47% of mutants develop peritoneal endometriosis following ovarian intrabursal injection of an adenovirus expressing Cre (J:96296)
• however, mice injected with adenovirus expressing Cre directly into the peritoneum do not develop peritoneal endometriosis (J:96296)

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 (J:96296)
• 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 (J:96296)

Mouse Models of Human Disease
OMIM ID Ref(s)
Endometriosis, Susceptibility to, 1 131200 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 (4 available); any Kras mutation (30 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 (J:147590)
• median life span of cre adenovirus-treated mice is 32 weeks (J:147590)

tumorigenesis
• tumors from cre adenovirus-treated mice exhibit increased cell proliferation compared to in tumors from Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice (J:147590)
• tumors from cre adenovirus-treated mice exhibit increased cell proliferation compared to in tumors from Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice (J:147590)
• cre adenovirus-treated mice develop smaller tumors than in cre adenovirus-treated Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice (J:147590)
• cre adenovirus-treated mice develop smaller tumors than in cre adenovirus-treated Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice (J:147590)
• 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)
• 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)
• 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 (J:158937)
• presence of atypical adenomatous hyperplasia after Cre-adenovirus treatment (J:158937)
• the most common lesion is adenocarcinoma after Cre-adenovirus treatment (J:158937)
• the most common lesion is adenocarcinoma after Cre-adenovirus treatment (J:158937)
• in cre adenovirus-treated mice (J:147590)
• in cre adenovirus-treated mice (J:147590)

respiratory system
• in cre adenovirus-treated mice (J:147590)
• in cre adenovirus-treated mice (J:147590)
• cre adenovirus-treated mice develop bronchiolar hyperplasia and dysplasia unlike wild-type mice (J:147590)
• cre adenovirus-treated mice develop bronchiolar hyperplasia and dysplasia unlike wild-type mice (J:147590)
• in cre adenovirus-treated mice (J:147590)
• in cre adenovirus-treated mice (J:147590)
• presence of epithelial hyperplasia after Cre-adenovirus treatment (J:158937)
• presence of epithelial hyperplasia after Cre-adenovirus treatment (J:158937)

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 (J:154046)
• 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 (J:154046)

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 (J:154046)
• 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 (J:154046)

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 (J:154046)
• 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 (J:154046)




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 (4 available); any Kras mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus (J:203686)
• lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus (J:203686)

Mouse Models of Human Disease
OMIM ID Ref(s)
Lung Cancer 211980 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 (4 available); any Kras mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
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 (J:124682)
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a median survival of 24 weeks after ad-cre inoculation (J:124682)

tumorigenesis
• mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness (J:124682)
• all tumors of ad-cre inoculated mice are adenocarincomas (J:124682)
• metastasis or local invasion is not seen in ad-cre inoculated mice (J:124682)
• mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness (J:124682)
• all tumors of ad-cre inoculated mice are adenocarincomas (J:124682)
• metastasis or local invasion is not seen in ad-cre inoculated mice (J:124682)




Genotype
MGI:5304695
cn8
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 (4 available); any Kras mutation (30 available)
Tgfbr2tm1.2Hlm mutation (0 available); any Tgfbr2 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 43 days (J:177379)
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 43 days (J:177379)

tumorigenesis
• tumors of Cre adenoviral treated mutants show transmural invasion of vessels and pleural invasion, and regional metastases to mediastinal lymph nodes (J:177379)
• tumors of Cre adenoviral treated mutants show transmural invasion of vessels and pleural invasion, and regional metastases to mediastinal lymph nodes (J:177379)
• 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 (J:177379)
• 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 (J:177379)
• 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 (J:177379)
• 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 (J:177379)

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 (J:177379)
• 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 (J:177379)
• 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 (J:177379)
• 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 (J:177379)
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit a lower myeloid cell population in the lungs than controls (J:177379)
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit a lower myeloid cell population in the lungs than controls (J:177379)

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 (J:177379)
• 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 (J:177379)
• 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 (J:177379)
• 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 (J:177379)
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit a lower myeloid cell population in the lungs than controls (J:177379)
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit a lower myeloid cell population in the lungs than controls (J:177379)

Mouse Models of Human Disease
OMIM ID Ref(s)
Lung Cancer 211980 J:177379




Genotype
MGI:4948962
cn9
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 (4 available); any Kras mutation (30 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
mortality/aging

tumorigenesis
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice (J:170904)
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice (J:170904)

cellular
• following adenovirus cre infection, mice exhibit impaired DNA damage response compared with control mice (J:170904)
• following adenovirus cre infection, mice exhibit impaired DNA damage response compared with control mice (J:170904)

homeostasis/metabolism
• following adenovirus cre infection, mice exhibit impaired DNA damage response compared with control mice (J:170904)
• following adenovirus cre infection, mice exhibit impaired DNA damage response compared with control mice (J:170904)




Genotype
MGI:3836557
cn10
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 (4 available); any Kras mutation (30 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 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 (J:138959)
• 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 (J:138959)
• pancreatic tumors exhibit higher proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes (J:138959)
• pancreatic tumors exhibit higher proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes (J:138959)
• in 8 of 10 mice at 26 weeks (J:138959)
• in 8 of 10 mice at 26 weeks (J:138959)
• at 6 weeks of age (J:138959)
• at 6 weeks of age (J:138959)

endocrine/exocrine glands
• pancreatic weight is greater than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes (J:138959)
• pancreatic weight is greater than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes (J:138959)




Genotype
MGI:3836556
cn11
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 (4 available); any Kras mutation (30 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (6 available)
Tg(MUC1)79.24Gend mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 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 (J:138959)
• 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 (J:138959)
• pancreatic tumors exhibit lower proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend heterozygotes (J:138959)
• pancreatic tumors exhibit lower proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend heterozygotes (J:138959)
• in 1 of 10 mice at 26 weeks (J:138959)
• in 1 of 10 mice at 26 weeks (J:138959)




Genotype
MGI:5432240
cn12
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 (0 available); any Apc mutation (53 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 64% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are adenomas (J:156532)
• 64% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are adenomas (J:156532)
• 36% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are carcinomas (J:156532)
• 36% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are carcinomas (J:156532)
• 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 (J:156532)
• 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 (J:156532)
• 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 (J:156532)
• rapamycin treatment of mutants with tumors does not result in tumor regression (J:156532)
• 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 (J:156532)
• rapamycin treatment of mutants with tumors does not result in tumor regression (J:156532)

Mouse Models of Human Disease
OMIM ID Ref(s)
Colorectal Cancer; CRC 114500 J:156532




Genotype
MGI:4849444
cn13
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 (4 available); any Kras mutation (30 available)
Tg(Gfap-cre)77.6Mvs mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• mutants do not develop tumors (J:154673)
• mutants do not develop tumors (J:154673)




Genotype
MGI:5308959
cn14
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 (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)89.1Dam mutation (0 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 33% of tumors exhibit metastasis (J:108298)
• 33% of tumors exhibit metastasis (J:108298)
• mutants develop pancreatic tumors with an average latency of 21.8 weeks (J:108298)
• mutants develop pancreatic tumors with an average latency of 21.8 weeks (J:108298)
• 100% of tumors are well differentiated ductal adenocarcinomas (J:108298)
• 100% of tumors are well differentiated ductal adenocarcinomas (J:108298)




Genotype
MGI:5308961
cn15
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 (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)89.1Dam mutation (0 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 25% of tumors exhibit metastasis (J:108298)
• 25% of tumors exhibit metastasis (J:108298)
• mutants develop pancreatic tumors with an average latency of 14.7 weeks (J:108298)
• 19% of tumors exhibit sarcomatoid differentiation (J:108298)
• mutants develop pancreatic tumors with an average latency of 14.7 weeks (J:108298)
• 19% of tumors exhibit sarcomatoid differentiation (J:108298)
• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)
• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)




Genotype
MGI:5308962
cn16
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 (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)89.1Dam mutation (0 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 25% of tumors exhibit metastasis (J:108298)
• 25% of tumors exhibit metastasis (J:108298)
• mutants develop pancreatic tumors with an average latency of 13.1 weeks (J:108298)
• 25% of tumors exhibit sarcomatoid carcinoma histology (J:108298)
• mutants develop pancreatic tumors with an average latency of 13.1 weeks (J:108298)
• 25% of tumors exhibit sarcomatoid carcinoma histology (J:108298)
• 75% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)
• 75% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)

Mouse Models of Human Disease
OMIM ID Ref(s)
Pancreatic Cancer 260350 J:108298




Genotype
MGI:5308963
cn17
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 (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)89.1Dam mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 33% of tumors exhibit metastasis (J:108298)
• 33% of tumors exhibit metastasis (J:108298)
• mutants develop pancreatic tumors with an average latency of 18.3 weeks (J:108298)
• 100% of tumors are sarcomatoid in histology (J:108298)
• mutants develop pancreatic tumors with an average latency of 18.3 weeks (J:108298)
• 100% of tumors are sarcomatoid in histology (J:108298)




Genotype
MGI:5308946
cn18
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 (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)89.1Dam mutation (0 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mutants develop pancreatic tumors with an average latency of 6.2 weeks (J:108298)
• mutants develop pancreatic tumors with an average latency of 6.2 weeks (J:108298)
• mutants exhibit rapid pancreatic ductal adenocaracinoma progression, developing lethal tumors by 8 weeks of age (J:108298)
• 100% of tumors are well differentiated ductal adenocarcinomas (J:108298)
• mutants exhibit rapid pancreatic ductal adenocaracinoma progression, developing lethal tumors by 8 weeks of age (J:108298)
• 100% of tumors are well differentiated ductal adenocarcinomas (J:108298)

Mouse Models of Human Disease
OMIM ID Ref(s)
Pancreatic Cancer 260350 J:108298




Genotype
MGI:5308951
cn19
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 (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)89.1Dam mutation (0 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mutants develop pancreatic tumors with an average latency of 6.5 weeks (J:108298)
• 20% of tumors exhibit anaplastic carcinoma histology (J:108298)
• mutants develop pancreatic tumors with an average latency of 6.5 weeks (J:108298)
• 20% of tumors exhibit anaplastic carcinoma histology (J:108298)
• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)
• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)

Mouse Models of Human Disease
OMIM ID Ref(s)
Pancreatic Cancer 260350 J:108298




Genotype
MGI:5308954
cn20
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 (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)89.1Dam mutation (0 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 20% of tumors exhibit metastasis (J:108298)
• 20% of tumors exhibit metastasis (J:108298)
• mutants develop pancreatic tumors with an average latency of 7.2 weeks (J:108298)
• 60% of tumors exhibit anaplastic carcinoma histology (J:108298)
• mutants develop pancreatic tumors with an average latency of 7.2 weeks (J:108298)
• 60% of tumors exhibit anaplastic carcinoma histology (J:108298)
• 40% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)
• 40% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)

Mouse Models of Human Disease
OMIM ID Ref(s)
Pancreatic Cancer 260350 J:108298




Genotype
MGI:3624415
cn21
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 (4 available); any Kras mutation (30 available)
Tg(Scgb1a1-cre)1Kkw mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• early mortality with a median survival of 8 weeks (J:107260)
• early mortality with a median survival of 8 weeks (J:107260)

tumorigenesis
• progressive phenotype characterized by cellular atypia, adenoma, and ultimately adenocarcinoma in CC10 positive cells of bronchial epithelia (J:107260)
• progressive phenotype characterized by cellular atypia, adenoma, and ultimately adenocarcinoma in CC10 positive cells of bronchial epithelia (J:107260)

immune system
• a robust inflammatory response characterized by an abundant infiltration of alveolar macrophages and neutrophils (J:107260)
• a robust inflammatory response characterized by an abundant infiltration of alveolar macrophages and neutrophils (J:107260)




Genotype
MGI:3695428
cn22
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 (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (6 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average tumor-free survival is 8.8 weeks (J:116130)
• average tumor-free survival is 8.8 weeks (J:116130)

tumorigenesis
• 4 of 4 mice develop pancreatic ductal adenocarcinoma (J:116130)
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4 (J:116130)
• tumor fibrosis is increased compared to mice wild-type for Smad4 (J:116130)
• 4 of 4 mice develop pancreatic ductal adenocarcinoma (J:116130)
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4 (J:116130)
• tumor fibrosis is increased compared to mice wild-type for Smad4 (J:116130)




Genotype
MGI:3695421
cn23
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 (4 available); any Kras mutation (30 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (6 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 (J:116130)
• average tumor-free survival is 15.7 weeks (J:116130)
• mice die between 8 and 24 weeks of age (J:116130)
• average tumor-free survival is 15.7 weeks (J:116130)

tumorigenesis
• 12 of 12 mice develop intraductal papillary mucinous neoplasms (J:116130)
• 12 of 12 mice develop intraductal papillary mucinous neoplasms (J:116130)
• 2 of 12 mice develop pancreatic ductal adenocarcinoma (J:116130)
• 2 of 12 mice develop pancreatic ductal adenocarcinoma (J:116130)

endocrine/exocrine glands
• seen in all mice (J:116130)
• seen in all mice (J:116130)




Genotype
MGI:3695424
cn24
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 (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (6 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average tumor-free survival is 14 weeks (J:116130)
• average tumor-free survival is 14 weeks (J:116130)

tumorigenesis
• 5 of 13 mice develop intraductal papillary mucinous neoplasms (J:116130)
• tumor fibrosis is increased compared to mice wild-type for Smad4 (J:116130)
• 5 of 13 mice develop intraductal papillary mucinous neoplasms (J:116130)
• tumor fibrosis is increased compared to mice wild-type for Smad4 (J:116130)
• 12 of 13 mice develop pancreatic ductal adenocarcinoma (J:116130)
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4 (J:116130)
• 12 of 13 mice develop pancreatic ductal adenocarcinoma (J:116130)
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4 (J:116130)




Genotype
MGI:5298083
cn25
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Krt19tm1(cre/ERT)Ggu/Krt19+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Krt19tm1(cre/ERT)Ggu mutation (0 available); any Krt19 mutation (2 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 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 (J:172048)
• tamoxifen treated mice die within 2 months from intestinal cancers before developing skin tumors (J:172048)

tumorigenesis
• 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 (J:172048)
• 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 (J:172048)
• most tumors that develop are benign (J:172048)
• most tumors that develop are benign (J:172048)
• some tumors that develop are invasive squamous cell carcinomas (SCCs) (J:172048)
• some tumors that develop are invasive squamous cell carcinomas (SCCs) (J:172048)
• tamoxifen treated mice develop terminal intestinal carcinomas with 2 months of treatment (J:172048)
• tamoxifen treated mice develop terminal intestinal carcinomas with 2 months of treatment (J:172048)

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 (J:172048)
• 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 (J:172048)
• most tumors that develop are benign (J:172048)
• most tumors that develop are benign (J:172048)
• some tumors that develop are invasive squamous cell carcinomas (SCCs) (J:172048)
• some tumors that develop are invasive squamous cell carcinomas (SCCs) (J:172048)




Genotype
MGI:5298088
cn26
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Shhtm2(cre/ERT2)Cjt/Shh+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Shhtm2(cre/ERT2)Cjt mutation (1 available); any Shh mutation (25 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 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 (J:172048)
• no macroscopic or microscopic skin tumors are observed up to 4 months after tamoxifen treatment (J:172048)




Genotype
MGI:4948964
cn27
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 (4 available); any Kras mutation (30 available)
Map2k7tm1.1Twad mutation (0 available); any Map2k7 mutation (5 available)
Map2k7tm1.2Twad mutation (0 available); any Map2k7 mutation (5 available)
Trp53tm1Tyj mutation (9 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice (J:170904)
• however, tumorigenesis is the same as in Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice (J:170904)
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice (J:170904)
• however, tumorigenesis is the same as in Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice (J:170904)
• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice (J:170904)
• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice (J:170904)




Genotype
MGI:3716963
cn28
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 (4 available); any Kras mutation (30 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• following cre-adenovirus treatment, all mice develop primary lung tumors (J:103407)
• following cre-adenovirus treatment, lung tumors resemble those found in Krastm4Tyj heterozygotes (J:103407)
• following cre-adenovirus treatment, tumors occupy 24% of lung space (J:103407)
• following cre-adenovirus treatment, all mice develop primary lung tumors (J:103407)
• following cre-adenovirus treatment, lung tumors resemble those found in Krastm4Tyj heterozygotes (J:103407)
• following cre-adenovirus treatment, tumors occupy 24% of lung space (J:103407)
• 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 (J:103407)
• 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 (J:103407)




Genotype
MGI:5562914
cn29
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 (4 available); any Kras mutation (30 available)
Rnf7Gt(XE423)Byg mutation (0 available); any Rnf7 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of Ad-Cre treated mice is 27.6 weeks, with all mice dying by 33 weeks (J:207982)
• median survival time of Ad-Cre treated mice is 27.6 weeks, with all mice dying by 33 weeks (J:207982)

tumorigenesis
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) (J:207982)
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) (J:207982)
• a few adenocarcinomas develop in mice following Ad-Cre administration (J:207982)
• a few adenocarcinomas develop in mice following Ad-Cre administration (J:207982)




Genotype
MGI:5562910
cn30
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 (4 available); any Kras mutation (30 available)
Rnf7Gt(XE423)Byg mutation (0 available); any Rnf7 mutation (14 available)
Rnf7tm1.1Ysun mutation (0 available); any Rnf7 mutation (14 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 (J:207982)
• median survival time of Ad-Cre treated mice is 37.9 weeks, with most mice dying by 60 weeks (J:207982)

tumorigenesis
• 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 (J:207982)
• hyperplasia or adenomas from Ad-Cre treated mice show reduced proliferation compared to single Kras homozygotes (J:207982)
• 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 (J:207982)
• hyperplasia or adenomas from Ad-Cre treated mice show reduced proliferation compared to single Kras homozygotes (J:207982)




Genotype
MGI:5510703
cn31
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 (4 available); any Kras mutation (30 available)
Ptf1atm1(cre)Hnak mutation (0 available); any Ptf1a mutation (6 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
Trp53tm2Tyj mutation (2 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• however, treatment with a potent and selective oral pan class I PI3K inhibitor (GDC 0941) blocks tumor growth (J:197054)
• however, treatment with a potent and selective oral pan class I PI3K inhibitor (GDC 0941) blocks tumor growth (J:197054)




Genotype
MGI:5510702
cn32
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 (4 available); any Kras mutation (30 available)
Ptf1atm1(cre)Hnak mutation (0 available); any Ptf1a mutation (6 available)
Raf1tm2Bacc mutation (0 available); any Raf1 mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• as in Krastm4Tyj Ptf1atm1(cre)Hnak double heterozygotes (J:197054)
• as in Krastm4Tyj Ptf1atm1(cre)Hnak double heterozygotes (J:197054)




Genotype
MGI:3716966
cn33
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 (4 available); any Kras mutation (30 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
Trp53tm2Tyj mutation (2 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• at 19 weeks following cre-adenovirus treatment, sinonasal adenocarninomas develop in 64% of mice (J:103407)
• at 19 weeks following cre-adenovirus treatment, sinonasal adenocarninomas develop in 64% of mice (J:103407)
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)




Genotype
MGI:3716968
cn34
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 (4 available); any Kras mutation (30 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• following cre-adenovirus treatment, a subset of tumors are highly invasive and grow into the hilus, heart, and overlying pleura (J:103407)
• following cre-adenovirus treatment, lymph node metastases are present in over 50% of mice (J:103407)
• following cre-adenovirus treatment, a subset of tumors are highly invasive and grow into the hilus, heart, and overlying pleura (J:103407)
• following cre-adenovirus treatment, lymph node metastases are present in over 50% of mice (J:103407)
• at 19 weeks following cre-adenovirus treatment, sinonasal adenocarninomas develop in 14% of mice (J:103407)
• at 19 weeks following cre-adenovirus treatment, sinonasal adenocarninomas develop in 14% of mice (J:103407)
• mice infected with low-titre (5X103) lentiviruses expressing Cre and Nfkbia have either a single lung adenocarcinoma or none at all (J:154041)
• mice infected with high-titre (5X104) lentiviruses expressing Cre and Nfkbia have 6-22 lung adenocarcinomas detected per mouse (J:154041)
• mice infected with low-titre (5X103) lentiviruses expressing Cre and Nfkbia have either a single lung adenocarcinoma or none at all (J:154041)
• mice infected with high-titre (5X104) lentiviruses expressing Cre and Nfkbia have 6-22 lung adenocarcinomas detected per mouse (J:154041)
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)
• 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)
• 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)
• 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)
• 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)
• 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)
• 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 (J:103407)
• mice do not survive to 26 weeks post cre-adenovirus treatment in contrast to Krastm4Tyj Trp53tm1Brn heterozygous mice (J:103407)

Mouse Models of Human Disease
OMIM ID Ref(s)
Lung Cancer 211980 J:103407 , J:154041 , J:195492 , J:203686




Genotype
MGI:4441491
cn35
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 (4 available); any Kras mutation (30 available)
Lyz2tm1(cre)Ifo mutation (7 available); any Lyz2 mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• the maximum survival is 24 days (J:158937)
• the maximum survival is 24 days (J:158937)

respiratory system
• lung weight is 10-fold higher than that in control mice at 3 weeks old (J:158937)
• lung weight is 10-fold higher than that in control mice at 3 weeks old (J:158937)

tumorigenesis




Genotype
MGI:4441490
cn36
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 (193 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (193 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Pggt1btm1.1Mbrg mutation (0 available); any Pggt1b mutation (15 available)
Pggt1btm1Mbrg mutation (0 available); any Pggt1b mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment (J:158937)
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment (J:158937)
• the lung surface of Cre-adenovirus treated mice is nearly indistinguishable from that of control mice (J:158937)
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment (J:158937)
• the lung surface of Cre-adenovirus treated mice is nearly indistinguishable from that of control mice (J:158937)
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment (J:158937)
• presence of small adenomas after Cre-adenovirus treatment (J:158937)
• presence of small adenomas after Cre-adenovirus treatment (J:158937)
• adenocarcinoma in 1 of 11 mice after Cre-adenovirus treatment (J:158937)
• adenocarcinoma in 1 of 11 mice after Cre-adenovirus treatment (J:158937)

respiratory system
• presence of epithelial hyperplasia after Cre-adenovirus treatment (J:158937)
• presence of epithelial hyperplasia after Cre-adenovirus treatment (J:158937)




Genotype
MGI:4441492
cn37
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 (193 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (193 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Lyz2tm1(cre)Ifo mutation (7 available); any Lyz2 mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• longer life span than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (>100 days in some cases) (J:158937)
• longer life span than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (>100 days in some cases) (J:158937)

respiratory system
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice but higher than in normal mice (J:158937)
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice but higher than in normal mice (J:158937)

tumorigenesis
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (J:158937)
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (J:158937)




Genotype
MGI:4441488
cn38
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 (193 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (193 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Lyz2tm1(cre)Ifo mutation (7 available); any Lyz2 mutation (9 available)
Pggt1btm1.1Mbrg mutation (0 available); any Pggt1b mutation (15 available)
Pggt1btm1Mbrg mutation (0 available); any Pggt1b mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median life span is 170 days (J:158937)
• longer median life span than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (170 vs. 22 days) (J:158937)
• median life span is 170 days (J:158937)
• longer median life span than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (170 vs. 22 days) (J:158937)

tumorigenesis
• 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 (J:158937)
• 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 (J:158937)
• lung weight and histology are indistinguishable from littermate control mice at 3-week old (J:158937)
• but eventually develop lung tumors at older age (J:158937)
• lung weight and histology are indistinguishable from littermate control mice at 3-week old (J:158937)
• but eventually develop lung tumors at older age (J:158937)




Genotype
MGI:4441486
cn39
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 (193 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (193 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 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 (J:158937)
• Cre-adenovirus treatment results in G2M cell-cycle arrest in embryonic fibroblasts (J:158937)




Genotype
MGI:5528686
cn40
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 (4 available); any Kras mutation (30 available)
Mapkapk2tm1.1Yaff mutation (0 available); any Mapkapk2 mutation (7 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus (J:203686)
• 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 (J:203686)
• 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 (J:203686)
• proportion of total lung tumor burden composed of Mapkapk2 (MK2-) null tumors is reduced from 39% to 11% following cisplatin treatment (J:203686)
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus (J:203686)
• 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 (J:203686)
• 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 (J:203686)
• proportion of total lung tumor burden composed of Mapkapk2 (MK2-) null tumors is reduced from 39% to 11% following cisplatin treatment (J:203686)




Genotype
MGI:5547939
cn41
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 (4 available); any Kras mutation (30 available)
Myod1tm1.1(cre/ERT,TVA)Gcg mutation (1 available); any Myod1 mutation (6 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 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 (J:205518)
• 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 (J:205518)
• tamoxifen treated mice develop sarcomas that are exclusively undifferentiated pleomorphic sarcomas (UPS), myogenic or nonmyogenic in type (J:205518)
• tumors can appear in the body wall, the extremities, or the head and neck region (J:205518)
• tamoxifen treated mice develop sarcomas that are exclusively undifferentiated pleomorphic sarcomas (UPS), myogenic or nonmyogenic in type (J:205518)
• tumors can appear in the body wall, the extremities, or the head and neck region (J:205518)




Genotype
MGI:5559052
cn42
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 (4 available); any Kras mutation (30 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 20% of mice with large extremity sarcomas develop metastasis to the lungs (J:125101)
• extremity sarcomas in mice injected with Ad-Cre invade adjacent skeletal muscle and uterine sarcomas invade the intestinal wall and pancreas (J:125101)
• extremity sarcomas in mice injected with Ad-Cre invade adjacent skeletal muscle and uterine sarcomas invade the intestinal wall and pancreas (J:125101)
• 20% of mice with large extremity sarcomas develop metastasis to the lungs (J:125101)
• 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)
• 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)
• gene expression analysis indicates that Ad-Cre induced sarcomas are undifferentiated pleomorphic sarcoma/malignant fibrous histiocytoma (J:155389)




Genotype
MGI:4460775
cn43
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 (4 available); any Kras mutation (30 available)
Lrrc17tm1Nik mutation (0 available); any Lrrc17 mutation (2 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 (J:161558)
• in pIpC-treated mice similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice (J:161558)

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 (J:161558)
• 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 (J:161558)

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 (J:161558)
• 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 (J:161558)
• in pIpC-treated mice similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice (J:161558)
• in pIpC-treated mice similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice (J:161558)
• 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 (J:161558)
• 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 (J:161558)




Genotype
MGI:4948965
cn44
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 (4 available); any Kras mutation (30 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
tumorigenesis
N
• following adenovirus cre infection, mice exhibit the same tumor burden as in control mice (J:170904)
• following adenovirus cre infection, mice exhibit the same tumor burden as in control mice (J:170904)




Genotype
MGI:5428907
cn45
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Alb-cre)21Mgn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Alb-cre)21Mgn mutation (4 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival is 19 weeks of age (J:184949)
• mean survival is 19 weeks of age (J:184949)

tumorigenesis
• 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 (J:184949)
• 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 (J:184949)
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas (J:184949)
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas (J:184949)
• mutants develop intrahepatic cholangiocarcinoma as early as 9 weeks of age (J:184949)
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas (J:184949)
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy (J:184949)
• different grades of differentiation are seen in the same tumor (J:184949)
• different grades of differentiation are seen in the same tumor (J:184949)
• mutants develop intrahepatic cholangiocarcinoma as early as 9 weeks of age (J:184949)
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas (J:184949)
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy (J:184949)

cardiovascular system
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis (J:184949)
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis (J:184949)




Genotype
MGI:4819844
cn46
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Tg(Alb-cre)21Mgn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Alb-cre)21Mgn mutation (4 available)
Yap1tm1.1Dupa mutation (1 available); any Yap1 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis




Genotype
MGI:5428898
cn47
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Alb-cre)21Mgn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Alb-cre)21Mgn mutation (4 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival is 52 weeks of age (J:184949)
• mean survival is 52 weeks of age (J:184949)

tumorigenesis
• 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 (J:184949)
• 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 (J:184949)
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas (J:184949)
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas (J:184949)
• mutants develop intrahepatic cholangiocarcinoma as early as 32 weeks of age (J:184949)
• intrahepatic cholangiocarcinoma recapitulates the histologic and molecular features of multistage progression of human intrahepatic cholangiocarcinoma (J:184949)
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas (J:184949)
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy (J:184949)
• different grades of differentiation are seen in the same tumor (J:184949)
• mutants develop intrahepatic cholangiocarcinoma as early as 32 weeks of age (J:184949)
• intrahepatic cholangiocarcinoma recapitulates the histologic and molecular features of multistage progression of human intrahepatic cholangiocarcinoma (J:184949)
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas (J:184949)
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy (J:184949)
• different grades of differentiation are seen in the same tumor (J:184949)

cardiovascular system
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis (J:184949)
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis (J:184949)




Genotype
MGI:5486065
cn48
Allelic
Composition
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Sftpctm1.1(cre/ERT2)Ptch mutation (0 available); any Sftpc mutation (2 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• many mice do not survive to 13 weeks after tamoxifen treatment due to high tumor burden (J:195738)
• mice display leaky cre expression without tamoxifen treatment and survive a few months longer than tamoxifen-treated animals (J:195738)
• many mice do not survive to 13 weeks after tamoxifen treatment due to high tumor burden (J:195738)
• mice display leaky cre expression without tamoxifen treatment and survive a few months longer than tamoxifen-treated animals (J:195738)

tumorigenesis
• after tamoxifen treatment, mice show a more severe phenotype than animals with wild-type Trp53 (greater tumor size, tumor growth and tumor grade); by 3-4 weeks after tamoxifen treatment, several small adenomas of papillary nature are observed in alveoli (J:195738)
• at 10 weeks after tamoxifen injection, many alveoli have large tumors; tumors exhibit enlarged pleomorphic nuclei, aberrant mitosis; tumor giant cells are present (J:195738)
• after tamoxifen treatment, mice show a more severe phenotype than animals with wild-type Trp53 (greater tumor size, tumor growth and tumor grade); by 3-4 weeks after tamoxifen treatment, several small adenomas of papillary nature are observed in alveoli (J:195738)
• at 10 weeks after tamoxifen injection, many alveoli have large tumors; tumors exhibit enlarged pleomorphic nuclei, aberrant mitosis; tumor giant cells are present (J:195738)
• mice surviving to 13 weeks after tamoxifen treatment have adenocarcinomas in the alveoli of the lungs (J:195738)
• without tamoxifen treatment, mice develop invasive lung adenocarcinomas localized to the alveoli (J:195738)
• bronchioalveolar duct junctions (BADJs) appear normal ( in mice with or without tamoxifen treatment) (J:195738)
• mice surviving to 13 weeks after tamoxifen treatment have adenocarcinomas in the alveoli of the lungs (J:195738)
• without tamoxifen treatment, mice develop invasive lung adenocarcinomas localized to the alveoli (J:195738)
• bronchioalveolar duct junctions (BADJs) appear normal ( in mice with or without tamoxifen treatment) (J:195738)

respiratory system
• 8 days after tamoxifen treatment, extensive type II cell proliferation is observed compared to wild-type; however, proliferating bronchioalveolar stem cells (BASCs) are rarely observed (at 8 days, 3, 6, 10 and 13 weeks after tamoxifen treatment) (J:195738)
• tumor cells express type II cell markers and are highly proliferative, even without tamoxifen treatment (J:195738)
• 8 days after tamoxifen treatment, extensive type II cell proliferation is observed compared to wild-type; however, proliferating bronchioalveolar stem cells (BASCs) are rarely observed (at 8 days, 3, 6, 10 and 13 weeks after tamoxifen treatment) (J:195738)
• tumor cells express type II cell markers and are highly proliferative, even without tamoxifen treatment (J:195738)




Genotype
MGI:5604750
cn49
Allelic
Composition
Krastm4Tyj/Kras+
Tg(CAG-Bgeo,-tsA58T)T26Ichi/0
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(CAG-Bgeo,-tsA58T)T26Ichi mutation (0 available)
Tg(Pdx1-cre)6Tuv mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice do not survive beyond P21 (J:214846)
• mice do not survive beyond P21 (J:214846)

tumorigenesis
• mice develop highly aggressive adenocarcinoma with a ductal cell phenotype and inflammation resembling human pancreatic ductal adenocarcinoma within a short period (5 and 10 days after birth) and die within 3 weeks (J:214846)
• at P16, pancreatic ductal adenocarcinoma progresses to occupy the whole pancreas and to invade the muscular wall of the duodenum (J:214846)
• mice develop highly aggressive adenocarcinoma with a ductal cell phenotype and inflammation resembling human pancreatic ductal adenocarcinoma within a short period (5 and 10 days after birth) and die within 3 weeks (J:214846)
• at P16, pancreatic ductal adenocarcinoma progresses to occupy the whole pancreas and to invade the muscular wall of the duodenum (J:214846)
• PanIN-3 are detected in the pancreas with inflammation at P3 and P4 (J:214846)
• PanIN-3 are detected in the pancreas with inflammation at P3 and P4 (J:214846)

endocrine/exocrine glands
• invasive features of pancreatic ductal adenocarcinoma are seen containing acinoductal metaplasia at P5-P10 (J:214846)
• invasive features of pancreatic ductal adenocarcinoma are seen containing acinoductal metaplasia at P5-P10 (J:214846)

homeostasis/metabolism
• hemorrhagic ascites are seen by P16 (J:214846)
• hemorrhagic ascites are seen by P16 (J:214846)

Mouse Models of Human Disease
OMIM ID Ref(s)
Pancreatic Cancer 260350 J:214846




Genotype
MGI:3776026
cn50
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop widespread hyperplasia throughout the colonic epithelium (J:132357)
• colonic epithelium has a larger transit amplifying cell zone than wild-type; cells in the colonic epithelium have a higher mitotic index than in wild-type (J:132357)
• mice develop widespread hyperplasia throughout the colonic epithelium (J:132357)
• colonic epithelium has a larger transit amplifying cell zone than wild-type; cells in the colonic epithelium have a higher mitotic index than in wild-type (J:132357)
• hyperplasia is typified by extreme lengthening of the crypts (J:132357)
• hyperplasia is typified by extreme lengthening of the crypts (J:132357)
• large, prominent goblet cells develop in the colon (J:132357)
• large, prominent goblet cells develop in the colon (J:132357)

endocrine/exocrine glands
• hyperplasia is typified by extreme lengthening of the crypts (J:132357)
• hyperplasia is typified by extreme lengthening of the crypts (J:132357)




Genotype
MGI:5659893
cn51
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a mean survival of 14 weeks after ad-cre inoculation (J:124682)
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a mean survival of 14 weeks after ad-cre inoculation (J:124682)

tumorigenesis
• 4 of 9 (44%) ad-cre inoculated mice exhibit metastasis (J:124682)
• 4 of 9 (44%) ad-cre inoculated mice exhibit metastasis (J:124682)
• mice inoculated ad-cre by inhalation develop lung adenocarcinomas with high multiplicity (J:124682)
• mice inoculated ad-cre by inhalation develop lung adenocarcinomas with high multiplicity (J:124682)




Genotype
MGI:5635880
cn52
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Gev/Trp53tm1Gev
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)6Tuv mutation (1 available)
Trp53tm1Gev mutation (0 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mice exhibit rapid development of pancreatic tumors within 8 weeks with features typical of human pancreatic adenocarcinoma (J:220300)
• tumors treated with ibrutinib show a reduction in proliferation rate and tumor fibrosis, inhibition of mast cell degranulation, and reduction in CD11b+ and F4/80+ macrophages and mice show increased survival (J:220300)
• mice treated with both ibrutinib and gemcitabine show extended survival compared to treatment with gemcitabine alone (J:220300)
• mice treated with a daily injection of cromolyn, a blocker of mast cell degranulation and inflammogen release, starting at 8 weeks of age show a reduction in F4/80+ cells and CD11b+ cells in the tumor stroma (J:220300)
• mice exhibit rapid development of pancreatic tumors within 8 weeks with features typical of human pancreatic adenocarcinoma (J:220300)
• tumors treated with ibrutinib show a reduction in proliferation rate and tumor fibrosis, inhibition of mast cell degranulation, and reduction in CD11b+ and F4/80+ macrophages and mice show increased survival (J:220300)
• mice treated with both ibrutinib and gemcitabine show extended survival compared to treatment with gemcitabine alone (J:220300)
• mice treated with a daily injection of cromolyn, a blocker of mast cell degranulation and inflammogen release, starting at 8 weeks of age show a reduction in F4/80+ cells and CD11b+ cells in the tumor stroma (J:220300)

Mouse Models of Human Disease
OMIM ID Ref(s)
Pancreatic Cancer 260350 J:220300




Genotype
MGI:5298084
cn53
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre/ERT)20Efu/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(KRT14-cre/ERT)20Efu mutation (1 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• lesions are squamous cell carcinomas (SCCs)characterized by fibroblast-like shaped cells and disruption of basal lamina (J:172048)
• numerous microscopic and small invasive SCCs are observed in the dermis of the back skin in addition to the macroscopic lesions (J:172048)
• lesions are squamous cell carcinomas (SCCs)characterized by fibroblast-like shaped cells and disruption of basal lamina (J:172048)
• numerous microscopic and small invasive SCCs are observed in the dermis of the back skin in addition to the macroscopic lesions (J:172048)

integument
• within 2 months of tamoxifen treatment, animals develop rapidly growing ulcerative skin lesions in the back skin (J:172048)
• within 2 months of tamoxifen treatment, animals develop rapidly growing ulcerative skin lesions in the back skin (J:172048)
• lesions are squamous cell carcinomas (SCCs)characterized by fibroblast-like shaped cells and disruption of basal lamina (J:172048)
• numerous microscopic and small invasive SCCs are observed in the dermis of the back skin in addition to the macroscopic lesions (J:172048)
• lesions are squamous cell carcinomas (SCCs)characterized by fibroblast-like shaped cells and disruption of basal lamina (J:172048)
• numerous microscopic and small invasive SCCs are observed in the dermis of the back skin in addition to the macroscopic lesions (J:172048)




Genotype
MGI:4835041
cn54
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (0 available); any Cdkn2a mutation (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Tyr-cre/ERT2)13Bos mutation (2 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice treated with tamoxifen neonatally die within 14 weeks of treatment due to aggressive melanomas with spindle-like morphology unlike control mice in which only one mouse develops melanoma over a period of 60 weeks (J:164588)
• all mice treated with tamoxifen neonatally die within 14 weeks of treatment due to aggressive melanomas with spindle-like morphology unlike control mice in which only one mouse develops melanoma over a period of 60 weeks (J:164588)

tumorigenesis
• tumor growth is more aggressive than in Cdkn2atm1Rdp/Cdkn2atm1Rdp Tg(Tyr-HRAS)60Lc mice (J:164588)
• tumor growth is more aggressive than in Cdkn2atm1Rdp/Cdkn2atm1Rdp Tg(Tyr-HRAS)60Lc mice (J:164588)
• tamoxifen-treated mice develop melanomas with spindle-like morphology (J:164588)
• tamoxifen-treated mice develop melanomas with spindle-like morphology (J:164588)
• all mice treated with tamoxifen neonatally die within 14 weeks of treatment due to aggressive melanomas with spindle-like morphology unlike control mice in which only one mouse develops melanoma over a period of 60 weeks (J:164588)
• tumors in tamoxifen-treated mice occur on the flank, ear, and tail (J:164588)
• the number of tumors in tamoxifen-treated mice is greater than in similarly treated Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Tg(Tyr-cre/ERT2)13Bos mice or Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos mice (J:164588)
• by 15 weeks, 17 of 27 adult mice treated with tamoxifen develop melanomas at the site of application and depilation (J:164588)
• however, no uveal tumors are observed (J:164588)
• all mice treated with tamoxifen neonatally die within 14 weeks of treatment due to aggressive melanomas with spindle-like morphology unlike control mice in which only one mouse develops melanoma over a period of 60 weeks (J:164588)
• tumors in tamoxifen-treated mice occur on the flank, ear, and tail (J:164588)
• the number of tumors in tamoxifen-treated mice is greater than in similarly treated Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Tg(Tyr-cre/ERT2)13Bos mice or Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos mice (J:164588)
• by 15 weeks, 17 of 27 adult mice treated with tamoxifen develop melanomas at the site of application and depilation (J:164588)
• however, no uveal tumors are observed (J:164588)

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice (J:164588)
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice (J:164588)
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice (J:164588)
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice (J:164588)




Genotype
MGI:4835045
cn55
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (0 available); any Cdkn2a mutation (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Tyr-cre/ERT2)13Bos mutation (2 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• tamoxifen-treated mice develop melanomas with spindle-like morphology (J:164588)
• tamoxifen-treated mice develop melanomas with spindle-like morphology (J:164588)
• 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 (J:164588)
• 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 (J:164588)

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice (J:164588)
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice (J:164588)
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice (J:164588)
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice (J:164588)




Genotype
MGI:4835046
cn56
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Tyr-cre/ERT2)13Bos mutation (2 available)
Trp53tm1Brn mutation (6 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• tamoxifen-treated mice develop melanomas with spindle-like morphology (J:164588)
• tamoxifen-treated mice develop melanomas with spindle-like morphology (J:164588)
• 5 of 11 mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology at a longer latency (median latency 31 weeks) than in Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1BrnTg(Tyr-cre/ERT2)13Bos mice (median latency 14 weeks) (J:164588)
• 5 of 11 mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology at a longer latency (median latency 31 weeks) than in Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1BrnTg(Tyr-cre/ERT2)13Bos mice (median latency 14 weeks) (J:164588)

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice (J:164588)
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice (J:164588)
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice (J:164588)
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice (J:164588)




Genotype
MGI:3776028
cn57
Allelic
Composition
Apctm2.1Cip/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2.1Cip mutation (2 available); any Apc mutation (53 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• animals have greatly reduced life-span compared to mutants expressing wild-type Kras (J:132357)
• animals have greatly reduced life-span compared to mutants expressing wild-type Kras (J:132357)

tumorigenesis
• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio (J:132357)
• mice have more tumors than mutants expressing wild-type Kras (J:132357)
• terminally differentiated cells are absent from tumors (J:132357)
• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio (J:132357)
• mice have more tumors than mutants expressing wild-type Kras (J:132357)
• terminally differentiated cells are absent from tumors (J:132357)




Genotype
MGI:5484548
cn58
Allelic
Composition
Cdkn2atm2Brn/Cdkn2atm2Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2Brn mutation (2 available); any Cdkn2a mutation (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)6Tuv mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• after 5 days in culture, pancreatic explants exhibit irregular branching and disorganization with increased proliferation, pseudostratification, nuclear crowding and elongation resembling precancerous lesions (J:195229)
• however, no cysts develop (J:195229)
• after 5 days in culture, pancreatic explants exhibit irregular branching and disorganization with increased proliferation, pseudostratification, nuclear crowding and elongation resembling precancerous lesions (J:195229)
• however, no cysts develop (J:195229)

cellular
• after 5 days in culture, pancreatic explants exhibit irregular branching with increased proliferation (J:195229)
• after 5 days in culture, pancreatic explants exhibit irregular branching with increased proliferation (J:195229)




Genotype
MGI:3716399
cn59
Allelic
Composition
Krastm4Tyj/Kras+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Meox2tm1(cre)Sor/Meox2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Meox2tm1(cre)Sor mutation (2 available); any Meox2 mutation (4 available)
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• lungs at E12.5 show increased branching compared to Kras; Meox2-cre, Spry2-wild-type lungs; bronchi number is increased, but is still less than age-matched wild-type (J:119477)
• lungs at E12.5 show increased branching compared to Kras; Meox2-cre, Spry2-wild-type lungs; bronchi number is increased, but is still less than age-matched wild-type (J:119477)




Genotype
MGI:4940102
cn60
Allelic
Composition
Brca2tm1Cam/Brca2tm1Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (2 available); any Brca2 mutation (33 available)
Brca2tm1Cam mutation (0 available); any Brca2 mutation (33 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)6Tuv mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• pancreatic insufficiency; spectrum of anomalies are seen from isolated paucity of the islets of Langerhans to complete fibro-inflammatory or cystic degeneration of both the endocrine and exocrine pancreas (J:166678)
• pancreatic insufficiency; spectrum of anomalies are seen from isolated paucity of the islets of Langerhans to complete fibro-inflammatory or cystic degeneration of both the endocrine and exocrine pancreas (J:166678)

endocrine/exocrine glands
• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls (J:166678)
• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls (J:166678)
• pancreatic insufficiency; spectrum of anomalies are seen from isolated paucity of the islets of Langerhans to complete fibro-inflammatory or cystic degeneration of both the endocrine and exocrine pancreas (J:166678)
• pancreatic insufficiency; spectrum of anomalies are seen from isolated paucity of the islets of Langerhans to complete fibro-inflammatory or cystic degeneration of both the endocrine and exocrine pancreas (J:166678)

mortality/aging
• mutants exhibit shortened pancreatic ductal adenocarcinoma-free survival (J:166678)
• mutants exhibit shortened pancreatic ductal adenocarcinoma-free survival (J:166678)

tumorigenesis
• mutants not succumbing to pancreatic insufficiency later develop pancreatic ductal adenocarcinomas with a moderate latency and incomplete penetrance (6 of 32 mutants) (J:166678)
• mutants not succumbing to pancreatic insufficiency later develop pancreatic ductal adenocarcinomas with a moderate latency and incomplete penetrance (6 of 32 mutants) (J:166678)

cellular
• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls (J:166678)
• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls (J:166678)




Genotype
MGI:4940096
cn61
Allelic
Composition
Brca2tm1Brn/Brca2tm1Cam
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (2 available); any Brca2 mutation (33 available)
Brca2tm1Cam mutation (0 available); any Brca2 mutation (33 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Tg(Pdx1-cre)6Tuv mutation (1 available)
Trp53tm3Tyj mutation (2 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• about 18% of assessable tumor cases develop an acinar-cell carcinoma component of pancreatic tumors (J:166678)
• about 18% of assessable tumor cases develop an acinar-cell carcinoma component of pancreatic tumors (J:166678)
• high penetrance (29 of 30 mutants) of pancreatic ductal adenocarcinomas (J:166678)
• high penetrance (29 of 30 mutants) of pancreatic ductal adenocarcinomas (J:166678)

mortality/aging
• average survival time is 84 days, with a range of 48-110 days (J:166678)
• average survival time is 84 days, with a range of 48-110 days (J:166678)

Mouse Models of Human Disease
OMIM ID Ref(s)
Pancreatic Cancer 260350 J:166678




Genotype
MGI:5486056
cn62
Allelic
Composition
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Sftpctm1.1(cre/ERT2)Ptch mutation (0 available); any Sftpc mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• airways and BADJs retain normal architecture (J:195738)
• by 18 weeks after tamoxifen treatment, numerous adenomas develop in alveoli; small numbers of cells with features of malignant transformation are observed in some lung sections (J:195738)
• tumors are usually found in proximity to the airways, bronchioalveolar duct junctions (BADJs), or surface of the lung, but lesions are not found in the BADJs (J:195738)
• tumor cells are highly proliferative (J:195738)
• by 18 weeks after tamoxifen treatment, numerous adenomas develop in alveoli; small numbers of cells with features of malignant transformation are observed in some lung sections (J:195738)
• tumors are usually found in proximity to the airways, bronchioalveolar duct junctions (BADJs), or surface of the lung, but lesions are not found in the BADJs (J:195738)
• tumor cells are highly proliferative (J:195738)
• airways and BADJs retain normal architecture (J:195738)




Genotype
MGI:3695431
cn63
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average tumor-free survival is 8.6 weeks (J:116130)
• average tumor-free survival is 8.6 weeks (J:116130)

tumorigenesis
• 6 of 6 mice develop pancreatic ductal adenocarcinoma (J:116130)
• 6 of 6 mice develop pancreatic ductal adenocarcinoma (J:116130)




Genotype
MGI:3695432
cn64
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (26 available)
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average tumor-free survival is 38 weeks (J:116130)
• average tumor-free survival is 38 weeks (J:116130)

tumorigenesis
• 6 of 10 mice develop pancreatic ductal adenocarcinoma (J:116130)
• 6 of 10 mice develop pancreatic ductal adenocarcinoma (J:116130)




Genotype
MGI:4839215
cn65
Allelic
Composition
Krastm4Tyj/Kras+
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Scgb1a1tm1.1(cre)Fjd mutation (0 available); any Scgb1a1 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average survival is 24 weeks (J:131721)
• average survival is 24 weeks (J:131721)

respiratory system
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles (J:131721)
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site (J:131721)
• however, no carcinomas are seen by 24 weeks of age (J:131721)
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles (J:131721)
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site (J:131721)
• however, no carcinomas are seen by 24 weeks of age (J:131721)

tumorigenesis
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles (J:131721)
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site (J:131721)
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles (J:131721)
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site (J:131721)
• atypical adenomatous hyperplasia lesions and adenomas (J:131721)
• atypical adenomatous hyperplasia lesions and adenomas (J:131721)




Genotype
MGI:4839216
cn66
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Ptentm1Hwu mutation (3 available); any Pten mutation (37 available)
Scgb1a1tm1.1(cre)Fjd mutation (0 available); any Scgb1a1 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival is 8 weeks (J:131721)
• mean survival is 8 weeks (J:131721)

immune system
• increase in inflammation in lesions compared to single Kras mutants, with an increase in neutrophil and endothelial cell infiltration; infiltration of these cells increases with malignant progression (J:131721)
• increase in inflammation in lesions compared to single Kras mutants, with an increase in neutrophil and endothelial cell infiltration; infiltration of these cells increases with malignant progression (J:131721)

respiratory system
• increase in inflammation in lesions compared to single Kras mutants, with an increase in neutrophil and endothelial cell infiltration; infiltration of these cells increases with malignant progression (J:131721)
• increase in inflammation in lesions compared to single Kras mutants, with an increase in neutrophil and endothelial cell infiltration; infiltration of these cells increases with malignant progression (J:131721)
• by 2 months of age, mutants exhibit tachypnea (J:131721)
• by 2 months of age, mutants exhibit tachypnea (J:131721)

tumorigenesis
• mutants have higher numbers of lesions and more extensive tumors than single Kras mutants (J:131721)
• mutants develop distinct bronchial and alveolar tumors (J:131721)
• mutants have higher numbers of lesions and more extensive tumors than single Kras mutants (J:131721)
• mutants develop distinct bronchial and alveolar tumors (J:131721)
• mutants develop lung lesions as early as 4 weeks of age including proliferative atypical adenomatous hyperplasia lesions (J:131721)
• mutants develop lung lesions as early as 4 weeks of age including proliferative atypical adenomatous hyperplasia lesions (J:131721)
• mutants develop lung lesions as early as 4 weeks of age that includes atypical papillary bronchiolar proliferation (J:131721)
• mutants develop lung lesions as early as 4 weeks of age that includes atypical papillary bronchiolar proliferation (J:131721)
• mucinous bronchioloalveolar cell carcinoma-like lesions, a subtype of lung adenocarcinoma (J:131721)
• mucinous bronchioloalveolar cell carcinoma-like lesions, a subtype of lung adenocarcinoma (J:131721)

growth/size/body
• by 2 months of age, mutants exhibit weight loss (J:131721)
• by 2 months of age, mutants exhibit weight loss (J:131721)




Genotype
MGI:3032576
cn67
Allelic
Composition
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (4 available); any Kras mutation (30 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• pancreatic ductal adenocarcinomas (J:87973)
• transitions of epithelium from cuboid to columnar as early as 2 weeks (J:87973)
• extra pancreatic tumors are rare (J:87973)
• number and extent of lesions increases with age (J:87973)
• by 7-10 months occasional animals with invasive and metastatic adenocarcinomas (J:87973)
• lesions eventually found in liver diaphragm and lungs (J:87973)
• pancreatic ductal adenocarcinomas (J:87973)
• transitions of epithelium from cuboid to columnar as early as 2 weeks (J:87973)
• extra pancreatic tumors are rare (J:87973)
• number and extent of lesions increases with age (J:87973)
• by 7-10 months occasional animals with invasive and metastatic adenocarcinomas (J:87973)
• lesions eventually found in liver diaphragm and lungs (J:87973)
• average cancer free survival is greater than 52 weeks and 2 of 9 mice develop pancreatic ductal adenocarcinoma (J:116130)
• average cancer free survival is greater than 52 weeks and 2 of 9 mice develop pancreatic ductal adenocarcinoma (J:116130)

endocrine/exocrine glands