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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Pdx1-cre)6Tuv
transgene insertion 6, David A Tuveson
MGI:3032531
Summary 50 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Gt(ROSA)26Sortm1(Neurog3*S183A*S187A)Axbe/?
Tg(Pdx1-cre)6Tuv/?
B6.Cg-Gt(ROSA)26Sortm1(Neurog3*S183A*S187A)Axbe Tg(Pdx1-cre)6Tuv MGI:5604879
cn2
Cdh1tm2Kem/Cdh1tm2Kem
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129 * C57BL/6 * FVB/N MGI:5634407
cn3
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129 * C57BL/6 * FVB/N MGI:5634400
cn4
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Prdm1tm1Clme/Prdm1tm1Clme
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
involves: 129 * C57BL/6NCrl * FVB/N MGI:6296000
cn5
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
involves: 129 * C57BL/6NCrl * FVB/N MGI:6296002
cn6
Cdh1tm2Kem/Cdh1+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5634406
cn7
Krastm4Tyj/Kras+
Tg(CAG-Bgeo,-tsA58T)T26Ichi/0
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5604750
cn8
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Gev/Trp53tm1Gev
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5635880
cn9
Cdkn2atm2Brn/Cdkn2atm2Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB/N MGI:5484548
cn10
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5634408
cn11
Brca2tm1Cam/Brca2tm1Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940102
cn12
Brca2tm1Brn/Brca2tm1Cam
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940096
cn13
Brca2tm1Cam/Brca2tm1Brn
Tg(Pdx1-cre)6Tuv/0
Trp53tm3Tyj/Trp53+
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940104
cn14
Brca2tm1Cam/Brca2tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6 * FVB/N MGI:4940106
cn15
Tg(CAG-Bgeo,-tsA58T)T26Ichi/0
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:5604751
cn16
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw/0
Tg(Pdx1-cre)6Tuv/0
Tg(tetO-MYC)36Bop/0
involves: 129P2/OlaHsd * FVB/N MGI:5521486
cn17
Ctnnb1tm4Wbm/Ctnnb1tm4Wbm
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * FVB/N MGI:3773346
cn18
Sox17tm1Jaw/Sox17tm1Sjm
Tg(Pdx1-cre)6Tuv/0
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * FVB/N MGI:4356150
cn19
Sox17tm2Sjm/Sox17+
Tg(Pdx1-cre)6Tuv/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:6113948
cn20
Prdm1tm1Clme/Prdm1tm1Clme
Tg(Pdx1-cre)6Tuv/0
involves: 129S1/Sv * 129X1/SvJ * FVB/N MGI:6295997
cn21
Cdkn2atm1.1Gsu/Cdkn2atm1.1Gsu
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6J * FVB/N MGI:5502380
cn22
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Hmga2tm1.1Mmw/Hmga2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * FVB/N MGI:6295996
cn23
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N MGI:5502381
cn24
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
cn25
Brca1tm1Thl/Brca1tm2.1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494465
cn26
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4941336
cn27
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4941337
cn28
Brca1tm1Thl/Brca1tm1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494464
cn29
Brca1tm1Thl/Brca1tm3.1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494462
cn30
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm3Tyj/Trp53+
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4940098
cn31
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/?
involves: 129S4/SvJae * FVB/N MGI:3032575
cn32
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * FVB/N MGI:5494463
cn33
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Usp9x+
involves: 129S4/SvJae * FVB/N MGI:5438091
cn34
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Y
involves: 129S4/SvJae * FVB/N MGI:5438090
cn35
Krastm4Tyj/Kras+
Rab11fip1tm1.1Jicn/Rab11fip1tm1.1Jicn
Tg(Pdx1-cre)6Tuv/0
Trp53tm2.1Tyj/Trp53+
involves: 129S4/SvJae * FVB/N MGI:6113915
cn36
Cdkn2atm1.1Gsu/Cdkn2atm1.1Gsu
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJaeSor * C57BL/6J * FVB/N MGI:5502379
cn37
Nkx2-2tm5.1Suss/Nkx2-2tm5.1Suss
Tg(Pdx1-cre)6Tuv/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/N * NTac:NIHBS * SJL MGI:5544101
cn38
Sox17tm1Jaw/Sox17tm1Jaw
Tg(Pdx1-cre)6Tuv/0
involves: 129S6/SvEvTac * FVB/N MGI:4356152
cn39
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940100
cn40
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940099
cn41
Grb10tm1.1Fliu/Grb10tm1.1Fliu
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * C57BL/6 * FVB/N MGI:5569766
cn42
Wlstm1.1Lan/Wlstm1.1Lan
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * FVB/N * SJL MGI:4838406
cn43
Apctm2Rak/Apc+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * FVB/N * SJL MGI:5898453
cn44
Cdkn2atm1Rdp/Cdkn2a+
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw/0
Tg(Pdx1-cre)6Tuv/0
Tg(tetO-MYC)36Bop/0
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * FVB/N * SJL MGI:5521487
cn45
Apctm2Rak/Apctm2Rak
Tg(Pdx1-cre)6Tuv/0
involves: 129/Sv * C57BL/6J * FVB/N * SJL MGI:5898452
cn46
Smotm1Amc/Smotm1Amc
Tg(Pdx1-cre)6Tuv/0
involves: 129X1/SvJ * FVB/N MGI:4356154
cn47
Senp1tm1.1Eyeh/Senp1+
Tg(Pdx1-cre)6Tuv/0
involves: C57BL/6 MGI:5883577
cn48
Senp1tm1.1Eyeh/Senp1tm1.1Eyeh
Tg(Pdx1-cre)6Tuv/0
involves: C57BL/6 MGI:5883576
cn49
Hmgb1tm1.1Dltg/Hmgb1tm1.1Dltg
Tg(Pdx1-cre)6Tuv/0
involves: C57BL/6 * FVB/N MGI:5704414
cx50
Epha2tm1Jrui/Epha2tm1Jrui
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2.1Tyj/Trp53+
involves: 129S/SvEv * 129S4/SvJae * FVB/N MGI:6113916


Genotype
MGI:5604879
cn1
Allelic
Composition
Gt(ROSA)26Sortm1(Neurog3*S183A*S187A)Axbe/?
Tg(Pdx1-cre)6Tuv/?
Genetic
Background
B6.Cg-Gt(ROSA)26Sortm1(Neurog3*S183A*S187A)Axbe Tg(Pdx1-cre)6Tuv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Neurog3*S183A*S187A)Axbe mutation (0 available); any Gt(ROSA)26Sor mutation (493 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• beta cells, identified by immunostaining for insulin, occupied a greater proportional area of pancreas sections from adult mice bearing both the conditional Neurog3 knock-in and the embryonically expressed (E9.5-E12.5) pancreatic progenitor cell-specific cre recombinase transgene than in sections from control mice with only the conditional allele (highly significant at p = 0.007 (<= 0.01) by Student's unpaired t test).




Genotype
MGI:5634407
cn2
Allelic
Composition
Cdh1tm2Kem/Cdh1tm2Kem
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (119 available)
Smad4tm2.1Cxd mutation (1 available); any Smad4 mutation (13 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop gastric adenocarcinomas with a median tumor-free survival of 9.4 months but do not develop distant metastases

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




Genotype
MGI:5634400
cn3
Allelic
Composition
Cdh1tm2Kem/Cdh1+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (119 available)
Smad4tm2.1Cxd mutation (1 available); any Smad4 mutation (13 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 36% of mice develop duodenal adenocarcinomas
• 84% of mice develop spontaneous tumors in the glandular stomach with a median tumor-free survival of 8 months
• gastric tumors resemble diffuse-type gastric adenocarcinomas, are E-cadherin-negative, and are invasive into the muscle layers and regional lymph nodes
• intramucosal adenocarcinomas with signet ring cell feature is seen in 2 of 4 mice at 6 months of age
• gastric premalignant lesions such as atrophic gastritis, metaplasia or dysplasia are not seen at 4 and 5 months of age

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

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

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
stomach cancer DOID:10534 OMIM:137215
OMIM:613659
J:212549




Genotype
MGI:6296000
cn4
Allelic
Composition
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Prdm1tm1Clme/Prdm1tm1Clme
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
Genetic
Background
involves: 129 * C57BL/6NCrl * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (3 available); any Gt(ROSA)26Sor mutation (493 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Prdm1tm1Clme mutation (1 available); any Prdm1 mutation (19 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm2Tyj mutation (3 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice exhibit a similar overall pancreatic tumor burden as KPCT (Krastm4Tyj/Kras+ Trp53tm2Tyj/Trp53+ Tg(Pdx1-cre)6Tuv/0 Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+) mice
• pancreas contains PanINs and adenocarcinoma that are similar to pancreatic ductal adenocarcinoma (PDAC) in KPCT mice
• only 3 of 14 mice develop metastases, with only half of mice showing peritoneal disseminated tumor cells
• cancer cells exhibit a higher mitotic index than KPCT mice
• pancreas contains PanINs and adenocarcinoma that are similar to PDAC in KPCT mice

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

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




Genotype
MGI:6296002
cn5
Allelic
Composition
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
Genetic
Background
involves: 129 * C57BL/6NCrl * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (3 available); any Gt(ROSA)26Sor mutation (493 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm2Tyj mutation (3 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• pancreas contains PanINs and adenocarcinoma
• pancreas contains PanINs and adenocarcinoma

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




Genotype
MGI:5634406
cn6
Allelic
Composition
Cdh1tm2Kem/Cdh1+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdh1tm2Kem mutation (1 available); any Cdh1 mutation (119 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mice do not develop gastric adenocarcinomas




Genotype
MGI:5604750
cn7
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 (6 available); any Kras mutation (35 available)
Tg(CAG-Bgeo,-tsA58T)T26Ichi mutation (0 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice do not survive beyond P21

neoplasm
• 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
• at P16, pancreatic ductal adenocarcinoma progresses to occupy the whole pancreas and to invade the muscular wall of the duodenum
• PanIN-3 are detected in the pancreas with inflammation at P3 and P4

endocrine/exocrine glands
• invasive features of pancreatic ductal adenocarcinoma are seen containing acinoductal metaplasia at P5-P10
• 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
• at P16, pancreatic ductal adenocarcinoma progresses to occupy the whole pancreas and to invade the muscular wall of the duodenum
• PanIN-3 are detected in the pancreas with inflammation at P3 and P4

homeostasis/metabolism
• hemorrhagic ascites are seen by P16

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:214846




Genotype
MGI:5635880
cn8
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 (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Gev mutation (0 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice exhibit rapid development of pancreatic tumors within 8 weeks with features typical of human pancreatic adenocarcinoma
• 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
• mice treated with both ibrutinib and gemcitabine show extended survival compared to treatment with gemcitabine alone
• 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

neoplasm
• mice exhibit rapid development of pancreatic tumors within 8 weeks with features typical of human pancreatic adenocarcinoma
• 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
• mice treated with both ibrutinib and gemcitabine show extended survival compared to treatment with gemcitabine alone
• 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

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:220300




Genotype
MGI:5484548
cn9
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 (49 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 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
• however, no cysts develop

cellular
• after 5 days in culture, pancreatic explants exhibit irregular branching with increased proliferation




Genotype
MGI:5634408
cn10
Allelic
Composition
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smad4tm2.1Cxd mutation (1 available); any Smad4 mutation (13 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• in general, mice do not develop gastric adenocarcinomas, with only one mouse seen to develop it




Genotype
MGI:4940102
cn11
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 (3 available); any Brca2 mutation (33 available)
Brca2tm1Cam mutation (0 available); any Brca2 mutation (33 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 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

endocrine/exocrine glands
• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls
• 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
• mutants not succumbing to pancreatic insufficiency later develop pancreatic ductal adenocarcinomas with a moderate latency and incomplete penetrance (6 of 32 mutants)

mortality/aging
• mutants exhibit shortened pancreatic ductal adenocarcinoma-free survival

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

cellular
• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls




Genotype
MGI:4940096
cn12
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 (3 available); any Brca2 mutation (33 available)
Brca2tm1Cam mutation (0 available); any Brca2 mutation (33 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm3Tyj mutation (2 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• about 18% of assessable tumor cases develop an acinar-cell carcinoma component of pancreatic tumors
• high penetrance (29 of 30 mutants) of pancreatic ductal adenocarcinomas

neoplasm
• about 18% of assessable tumor cases develop an acinar-cell carcinoma component of pancreatic tumors
• high penetrance (29 of 30 mutants) of pancreatic ductal adenocarcinomas

mortality/aging
• average survival time is 84 days, with a range of 48-110 days

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:166678




Genotype
MGI:4940104
cn13
Allelic
Composition
Brca2tm1Cam/Brca2tm1Brn
Tg(Pdx1-cre)6Tuv/0
Trp53tm3Tyj/Trp53+
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 (3 available); any Brca2 mutation (33 available)
Brca2tm1Cam mutation (0 available); any Brca2 mutation (33 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm3Tyj mutation (2 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• pancreatic insufficiency is occasionally observed in mutants

endocrine/exocrine glands
• pancreatic insufficiency is occasionally observed in mutants

mortality/aging
• premature death before 600 days of age due to lymphoid malignancies and sarcomas

neoplasm
• mutants develop lymphoid malignancies




Genotype
MGI:4940106
cn14
Allelic
Composition
Brca2tm1Cam/Brca2tm1Brn
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (3 available); any Brca2 mutation (33 available)
Brca2tm1Cam mutation (0 available); any Brca2 mutation (33 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• small fraction of mutants develop pancreatic insufficiency

endocrine/exocrine glands
• small fraction of mutants develop pancreatic insufficiency

mortality/aging
• premature death in the small fraction of mutants with pancreatic insufficiency




Genotype
MGI:5604751
cn15
Allelic
Composition
Tg(CAG-Bgeo,-tsA58T)T26Ichi/0
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-Bgeo,-tsA58T)T26Ichi mutation (0 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die within 200 days after birth, showing symptoms to that seen in wasting disease

endocrine/exocrine glands
• mice develop pancreatic acinar cell dysplasia by 22 weeks without PanIN formation
• pancreatic ductal system and ductal cells are atrophic by 22 weeks of age

digestive/alimentary system
• mice develop pancreatic acinar cell dysplasia by 22 weeks without PanIN formation
• pancreatic ductal system and ductal cells are atrophic by 22 weeks of age




Genotype
MGI:5521486
cn16
Allelic
Composition
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw/0
Tg(Pdx1-cre)6Tuv/0
Tg(tetO-MYC)36Bop/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw mutation (1 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Tg(tetO-MYC)36Bop mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice develop pancreatic tumors as early as 14 days post partum
• all mice develop pancreatic neoplasms in less than 5 months
• 43% of mutants develop only ductal lesions, 46% of mutants have both ductal lesions and poorly differentiated carcinomas, and 11% of mutants exhibit only poorly differentiated adenocarcinomas
• 40-50 day old mutants with palpable pancreatic neoplasms treated with doxycycline for 7 days show cancer regression, however tumor-associated stroma does not remodel/regress
• 43% of mutants develop only ductal lesions that include pancreatic intraepithelial neoplasia (PanINs) and invasive pancreatic ductal adenocarcinomas (PDACs) with sporadic metastasis to the liver
• 11% of mutants exhibit exclusively poorly differentiated adenocarcinomas that can metastasize to the liver, diaphragm, and lung
• 46% of mutants have both ductal lesions and poorly differentiated carcinomas, with a few mutants having moderately differentiated lesions that have an acinar-like appearance
• 43% of mutants develop only ductal lesions that include pancreatic intraepithelial neoplasia (PanINs) and invasive pancreatic ductal adenocarcinoma (PDACs) with sporadic metastasis to the liver

mortality/aging
• mutants become moribund before they develop large tumors

neoplasm
• mice develop pancreatic tumors as early as 14 days post partum
• all mice develop pancreatic neoplasms in less than 5 months
• 43% of mutants develop only ductal lesions, 46% of mutants have both ductal lesions and poorly differentiated carcinomas, and 11% of mutants exhibit only poorly differentiated adenocarcinomas
• 40-50 day old mutants with palpable pancreatic neoplasms treated with doxycycline for 7 days show cancer regression, however tumor-associated stroma does not remodel/regress
• 43% of mutants develop only ductal lesions that include pancreatic intraepithelial neoplasia (PanINs) and invasive pancreatic ductal adenocarcinomas (PDACs) with sporadic metastasis to the liver
• 11% of mutants exhibit exclusively poorly differentiated adenocarcinomas that can metastasize to the liver, diaphragm, and lung
• 46% of mutants have both ductal lesions and poorly differentiated carcinomas, with a few mutants having moderately differentiated lesions that have an acinar-like appearance
• 43% of mutants develop only ductal lesions that include pancreatic intraepithelial neoplasia (PanINs) and invasive pancreatic ductal adenocarcinoma (PDACs) with sporadic metastasis to the liver
• pancreatic ductal adenocarcinomas metastasize to the liver, diaphragm, and lung

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:197052




Genotype
MGI:3773346
cn17
Allelic
Composition
Ctnnb1tm4Wbm/Ctnnb1tm4Wbm
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm4Wbm mutation (1 available); any Ctnnb1 mutation (21 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Ctnnb1tm4Wbm/Ctnnb1tm4Wbm Tg(Pdx1-cre)6Tuv/? pancreata display extensive loss of exocrine tissue

mortality/aging
• shortened lifespan, with a median survival of 29 days, although some mice do survive more than 6 months

growth/size/body
• small body size at birth that persists into adulthood

endocrine/exocrine glands
• in 17% of mutants that survived beyond 3 months, the pancreas has a liver-like histology
• numerous tubular structures suggesting pancreas acinar to duct metaplasia, however islets are intact
• acinar hypoplasia is seen by E16.5 and by 2 months of age, there is a near complete absence of acinar cell structures
• pancreas weighs on average 30% less than wild-type
• increase in parenchymal fibrosis
• decrease in the proliferation rate of pancreatic exocrine progenitors
• variable degree of surrounding inflammatory infiltrate which becomes more severe by 1 month of age; inflammatory infiltrate is reminiscent of pancreatitis

immune system
• variable degree of surrounding inflammatory infiltrate which becomes more severe by 1 month of age; inflammatory infiltrate is reminiscent of pancreatitis

digestive/alimentary system
• numerous tubular structures suggesting pancreas acinar to duct metaplasia, however islets are intact
• acinar hypoplasia is seen by E16.5 and by 2 months of age, there is a near complete absence of acinar cell structures




Genotype
MGI:4356150
cn18
Allelic
Composition
Sox17tm1Jaw/Sox17tm1Sjm
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sox17tm1Jaw mutation (1 available); any Sox17 mutation (15 available)
Sox17tm1Sjm mutation (1 available); any Sox17 mutation (15 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• at E9.5, Ipfl (Pdx1)+ cells are found throughout the liver bud unlike in control mice
• at E10.0, the biliary primordium is absent unlike in control mice
• at E16.5

liver/biliary system
• at E9.5, Ipfl (Pdx1)+ cells are found throughout the liver bud unlike in control mice
• at E10.0, the biliary primordium is absent unlike in control mice
• at E16.5




Genotype
MGI:6113948
cn19
Allelic
Composition
Sox17tm2Sjm/Sox17+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sox17tm2Sjm mutation (1 available); any Sox17 mutation (15 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• embryos show varying degrees of shortening of the cystic duct
• epithelial deciduation in the gallbladder
• embryos show varying degrees of shortening of the gallbladder

immune system
• hepatitis in fetuses with normal or mild gallbladder abnormalities but not hepatitis in fetuses with complete lack of the gallbladder

liver/biliary system
• hepatitis in fetuses with normal or mild gallbladder abnormalities but not hepatitis in fetuses with complete lack of the gallbladder
• embryos exhibit biliary atresia-like phenotypes such as epithelial deciduation and bile duct stenosis/atresia
• embryos show varying degrees of shortening of the cystic duct
• epithelial deciduation in the gallbladder
• embryos show varying degrees of shortening of the gallbladder
• 4/55 embryos exhibit severe gross hepatic lesions
• bile duct stenosis




Genotype
MGI:6295997
cn20
Allelic
Composition
Prdm1tm1Clme/Prdm1tm1Clme
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prdm1tm1Clme mutation (1 available); any Prdm1 mutation (19 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• mice are viable and pancreata show no histologic changes




Genotype
MGI:5502380
cn21
Allelic
Composition
Cdkn2atm1.1Gsu/Cdkn2atm1.1Gsu
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1.1Gsu mutation (0 available); any Cdkn2a mutation (49 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• starting between 6 and 24 weeks with metastasis
• adenocarcinomas in 9 of 9 invasive carcinomas in the pancreas

mortality/aging
• median survival 25.5 weeks

neoplasm
• starting between 6 and 24 weeks with metastasis
• adenocarcinomas in 9 of 9 invasive carcinomas in the pancreas
• adenocarcinomas in 9 of 9 invasive carcinomas in the pancreas

growth/size/body
• starting between 6 and 24 weeks
• increased girth starting between 6 and 24 weeks

liver/biliary system
• starting between 6 and 24 weeks

homeostasis/metabolism
• starting between 6 and 24 weeks




Genotype
MGI:6295996
cn22
Allelic
Composition
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Hmga2tm1.1Mmw/Hmga2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (3 available); any Gt(ROSA)26Sor mutation (493 available)
Hmga2tm1.1Mmw mutation (1 available); any Hmga2 mutation (5 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm2Tyj mutation (3 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice develop pancreatic ductal adenocarcinoma (PDAC)

neoplasm
• mice develop pancreatic ductal adenocarcinoma (PDAC)
• GFP+ PDAC cells form tumors form more metastases than GFP- PDAC cells when transplanted into recipient mice
• the highly metastatic PDAC subpopulation is enriched for hypoxia-induced genes

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:245611




Genotype
MGI:5502381
cn23
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (49 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• starting between 6 and 24 weeks with metastasis
• adenocarcinomas in 21 of 22 invasive carcinomas in the pancreas

mortality/aging
• median survival 15.5 weeks

neoplasm
• starting between 6 and 24 weeks with metastasis
• adenocarcinomas in 21 of 22 invasive carcinomas in the pancreas
• adenocarcinomas in 21 of 22 invasive carcinomas in the pancreas

growth/size/body
• starting between 6 and 24 weeks
• increased girth starting between 6 and 24 weeks

liver/biliary system
• starting between 6 and 24 weeks

homeostasis/metabolism
• starting between 6 and 24 weeks




Genotype
MGI:5438089
cn24
Allelic
Composition
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm1(sb13)Tuv/Gt(ROSA)26Sor+
Tg(Pdx1-cre)6Tuv/0
TgTn(sb-T2/Onc)#Dla/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(sb13)Tuv mutation (0 available); any Gt(ROSA)26Sor mutation (493 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
TgTn(sb-T2/Onc)#Dla mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• rapid progression, multi-focal and invasive
• pancreatic ductal adenocarcinoma or invasive cystic neoplasms with metastasis to the liver and lungs

mortality/aging
• mice succumb to invasive pancreatic neoplasms

neoplasm
• rapid progression, multi-focal and invasive
• pancreatic ductal adenocarcinoma or invasive cystic neoplasms with metastasis to the liver and lungs




Genotype
MGI:5494465
cn25
Allelic
Composition
Brca1tm1Thl/Brca1tm2.1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Thl mutation (0 available); any Brca1 mutation (87 available)
Brca1tm2.1Thl mutation (0 available); any Brca1 mutation (87 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 45 days compared with 68 days in Krastm4Tyj/Kras+ Tg(Ipf1-cre)6Tuv Trp53tm1Thl/Trp53tm1Thl
• however, latency is similar to in Brca1tm1Thl/Brca1tm1Thl Krastm4Tyj/Kras+ Tg(Ipf1-cre)6Tuv Trp53tm1Thl/Trp53tm1Thl




Genotype
MGI:4941336
cn26
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm2Tyj mutation (3 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• all but one mouse, develop large, firm, fibrotic head of the pancreas tumors
• metastatic foci spread to the surface of the liver, lungs, diaphragm, and adrenals with occasional metastasis to the peripancreatic, mesenteric, and retroperitoneal lymph nodes
• mice exhibit the full spectrum of preinvasive lesions
• some tumors are minor, poorly differentiated, or undifferentiated with anaplastic or sarcomatoid features

mortality/aging

neoplasm
• all but one mouse, develop large, firm, fibrotic head of the pancreas tumors
• metastatic foci spread to the surface of the liver, lungs, diaphragm, and adrenals with occasional metastasis to the peripancreatic, mesenteric, and retroperitoneal lymph nodes
• mice exhibit the full spectrum of preinvasive lesions
• some tumors are minor, poorly differentiated, or undifferentiated with anaplastic or sarcomatoid features
• some mice exhibit esophageal papillomas and hyperplasias or papillomatosis of the biliary tree unlike control mice

liver/biliary system

homeostasis/metabolism
• hemorrhagic

cellular
• in tumor cells

growth/size/body

digestive/alimentary system
• mice frequently exhibit small bowel obstructions unlike control mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:98936




Genotype
MGI:4941337
cn27
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• PanIN-1 and PanIN-2, but not PanIN-3 or pancreatic ductal adenocarcinoma, are seen at 22 weeks after birth (J:214846)

digestive/alimentary system
• mice develop a varying number of ductal cell proliferation foci in the pancreas from 9 weeks after birth

endocrine/exocrine glands
• mice develop a varying number of ductal cell proliferation foci in the pancreas from 9 weeks after birth
• PanIN-1 and PanIN-2, but not PanIN-3 or pancreatic ductal adenocarcinoma, are seen at 22 weeks after birth (J:214846)




Genotype
MGI:5494464
cn28
Allelic
Composition
Brca1tm1Thl/Brca1tm1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Thl mutation (0 available); any Brca1 mutation (87 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice succumb to pancreatic tumors with an average latency of 68 days




Genotype
MGI:5494462
cn29
Allelic
Composition
Brca1tm1Thl/Brca1tm3.1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Thl mutation (0 available); any Brca1 mutation (87 available)
Brca1tm3.1Thl mutation (0 available); any Brca1 mutation (87 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• as in Krastm4Tyj/Kras+ Tg(Ipf1-cre)6Tuv Trp53tm1Thl/Trp53tm1Thlmice succumb to pancreatic tumors with an average latency of 65 days




Genotype
MGI:4940098
cn30
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm3Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm3Tyj mutation (2 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 24 of 30 mutants develop pancreatic ductal adenocarcinomas

neoplasm
• 24 of 30 mutants develop pancreatic ductal adenocarcinomas

mortality/aging
• average survival time is 168 days, with a range of 60-254 days




Genotype
MGI:3032575
cn31
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/?
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• transitions of epithelium from cuboid to columnar as early as 2 weeks
• number and extent of lesions increases with age
• by 7-10 months occasional animals with invasive and metastatic adenocarcinomas
• lesions eventually found in liver diaphragm and lungs

endocrine/exocrine glands
• transitions of epithelium from cuboid to columnar as early as 2 weeks
• number and extent of lesions increases with age
• by 7-10 months occasional animals with invasive and metastatic adenocarcinomas
• lesions eventually found in liver diaphragm and lungs

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:87973




Genotype
MGI:5494463
cn32
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice succumb to pancreatic tumors with an average latency of 68 days




Genotype
MGI:5438091
cn33
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Usp9x+
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Usp9xtm1Tuv mutation (0 available); any Usp9x mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• within 3 months, mice develop pancreatic intraepithelial neoplasia and microinvasive neoplasms

digestive/alimentary system
• aggressive oral papillomas

mortality/aging
• due to local or metastatic pancreatic cancer or aggressive oral papillomas

neoplasm
• aggressive oral papillomas
• within 3 months, mice develop pancreatic intraepithelial neoplasia and microinvasive neoplasms
• in the face and urogenital area at 3 months

integument
• in the face and urogenital area at 3 months




Genotype
MGI:5438090
cn34
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Y
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Usp9xtm1Tuv mutation (0 available); any Usp9x mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• within 3 months, mice develop pancreatic intraepithelial neoplasia and microinvasive neoplasms

digestive/alimentary system
• aggressive oral papillomas

mortality/aging
• due to local or metastatic pancreatic cancer or aggressive oral papillomas

neoplasm
• aggressive oral papillomas
• within 3 months, mice develop pancreatic intraepithelial neoplasia and microinvasive neoplasms
• in the face and urogenital area at 3 months

integument
• in the face and urogenital area at 3 months




Genotype
MGI:6113915
cn35
Allelic
Composition
Krastm4Tyj/Kras+
Rab11fip1tm1.1Jicn/Rab11fip1tm1.1Jicn
Tg(Pdx1-cre)6Tuv/0
Trp53tm2.1Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Rab11fip1tm1.1Jicn mutation (0 available); any Rab11fip1 mutation (26 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm2.1Tyj mutation (2 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• phenotypes are relative to the control KPC (KrasG12D/+, p53R172H/+, Pdx1-Cre) PDAC (pancreatic adenocarcinoma) model mice
• size of PDAC primary tumors same as control
• significantly reduced number of detectable PDAC metastases to liver, lung and other tissues
• reduced migration of PDAC cells in vitro

mortality/aging
N
• survival same as control




Genotype
MGI:5502379
cn36
Allelic
Composition
Cdkn2atm1.1Gsu/Cdkn2atm1.1Gsu
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1.1Gsu mutation (0 available); any Cdkn2a mutation (49 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mice do not develop pancreatic neoplasms




Genotype
MGI:5544101
cn37
Allelic
Composition
Nkx2-2tm5.1Suss/Nkx2-2tm5.1Suss
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * FVB/N * NTac:NIHBS * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nkx2-2tm5.1Suss mutation (0 available); any Nkx2-2 mutation (9 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die within the first week after birth

homeostasis/metabolism
• severe

endocrine/exocrine glands




Genotype
MGI:4356152
cn38
Allelic
Composition
Sox17tm1Jaw/Sox17tm1Jaw
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S6/SvEvTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sox17tm1Jaw mutation (1 available); any Sox17 mutation (15 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• at E10.5, the biliary primordium is reduced compared to in control mice

liver/biliary system
• at E10.5, the biliary primordium is reduced compared to in control mice




Genotype
MGI:4940100
cn39
Allelic
Composition
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Cam mutation (0 available); any Brca2 mutation (33 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 12 of 40 mutants develop pancreatic ductal adenocarcinomas

neoplasm
• 12 of 40 mutants develop pancreatic ductal adenocarcinomas

mortality/aging
• reduction in pancreatic ductal adenocarcinoma-free survival




Genotype
MGI:4940099
cn40
Allelic
Composition
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Cam mutation (0 available); any Brca2 mutation (33 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm3Tyj mutation (2 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 26 of 30 mutants develop pancreatic ductal adenocarcinomas

neoplasm
• 26 of 30 mutants develop pancreatic ductal adenocarcinomas

mortality/aging
• average survival time is 143 days, with a range of 91-191 days




Genotype
MGI:5569766
cn41
Allelic
Composition
Grb10tm1.1Fliu/Grb10tm1.1Fliu
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Grb10tm1.1Fliu mutation (0 available); any Grb10 mutation (30 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• mice fed standard chow or a high fat diet exhibit normal insulin tolerance
• in a hyperglycemic clamp study, mice fed standard chow exhibit a higher glucose infusion rate compared with wild-type mice
• mice exhibit reduced STZ-induced hyperglycemic effect compared with wild-type mice
• in mice fed standard chow during the hyperglycemic clamp studies
• in STZ-treated mice
• slightly in fasting mice fed standard chow
• in mice fed a high fat diet
• in mice fed standard chow or a high fat diet

growth/size/body
• mice exhibit are protected from STZ-induced weight loss compared with wild-type mice

cellular
• in mice fed standard chow

endocrine/exocrine glands
• beta cells contain increased insulin granules
• however, beta cell size is normal
• in mice fed standard chow
• in mice fed standard chow
• in STZ-treated mice
• mice are protected from STZ-induced beta cell loss via apoptosis compared with wild-type mice
• in mice fed standard chow
• in mice fed standard chow during the hyperglycemic clamp studies
• in STZ-treated mice




Genotype
MGI:4838406
cn42
Allelic
Composition
Wlstm1.1Lan/Wlstm1.1Lan
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S/SvEv * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Pdx1-cre)6Tuv mutation (2 available)
Wlstm1.1Lan mutation (1 available); any Wls mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands




Genotype
MGI:5898453
cn43
Allelic
Composition
Apctm2Rak/Apc+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Rak mutation (1 available); any Apc mutation (59 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• survival is shorter than either single conditional mutant; mice can survive up to 32 weeks but most have to be euthanized at 24-26 weeks of age

neoplasm
• all mice develop pancreatic neoplasms between 16 and 24 weeks
• 100% of mice exhibit large cystic pancreata which are mucinous cystadenomas, characterized by the presence of unilocular megacystic lesions with mucoid/watery cyst content, and nodules or peripheral calcification on the cyst wall resembling human mucinous cystic neoplasm
• mucinous cystic neoplasms become malignant pancreatic cancer with nuclear anaplastic features, and show stomach, duodenal or intestinal invasion or liver or lung metastasis, consistent with aggressive pancreatic cystic adenocarcinoma
• 6 week old mice treated with the Wnt inhibitor IWP-2 for 12 weeks show a reduction of or absence of hypertrophic pancreas with cysts
• tumors exhibit a high incidence of metastasis and invasion
• 100% of mice exhibit large cystic pancreata which are mucinous cystadenomas

endocrine/exocrine glands
• all mice develop pancreatic neoplasms between 16 and 24 weeks
• 100% of mice exhibit large cystic pancreata which are mucinous cystadenomas, characterized by the presence of unilocular megacystic lesions with mucoid/watery cyst content, and nodules or peripheral calcification on the cyst wall resembling human mucinous cystic neoplasm
• mucinous cystic neoplasms become malignant pancreatic cancer with nuclear anaplastic features, and show stomach, duodenal or intestinal invasion or liver or lung metastasis, consistent with aggressive pancreatic cystic adenocarcinoma
• 6 week old mice treated with the Wnt inhibitor IWP-2 for 12 weeks show a reduction of or absence of hypertrophic pancreas with cysts

homeostasis/metabolism
• cystic fluid of the pancreata shows the induction of the following cytokines: FasL, soluble tumor necrosis factor receptor 1, IL-1beta, IL-6, macrophage inflammatory protein 1gamma, keratinocyte chemoattractant and monocyte chemoattractant protein 1

immune system
• cystic fluid of the pancreata shows the induction of the following cytokines: FasL, soluble tumor necrosis factor receptor 1, IL-1beta, IL-6, macrophage inflammatory protein 1gamma, keratinocyte chemoattractant and monocyte chemoattractant protein 1

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic mucinous cystadenoma DOID:7235 J:234310




Genotype
MGI:5521487
cn44
Allelic
Composition
Cdkn2atm1Rdp/Cdkn2a+
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw/0
Tg(Pdx1-cre)6Tuv/0
Tg(tetO-MYC)36Bop/0
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Rdp mutation (5 available); any Cdkn2a mutation (49 available)
Tg(CAG-Bgeo,-tTA,-EGFP)2A11Kuw mutation (1 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Tg(tetO-MYC)36Bop mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mutants develop pancreatic tumors with a similar tumor latency as in mutants with wild-type Cdkn2a, however mice show an increase in the occurrence of more aggressive primary pancreatic ductal adenocarcinomas (PDACs) that quickly metastasized to the liver
• mutants show an increase in the occurrence of more aggressive primary pancreatic ductal adenocarcinomas
• 77% of mice show invasive PDAC and 85% show poorly differentiated adenocarcinoma

neoplasm
• mutants develop pancreatic tumors with a similar tumor latency as in mutants with wild-type Cdkn2a, however mice show an increase in the occurrence of more aggressive primary pancreatic ductal adenocarcinomas (PDACs) that quickly metastasized to the liver
• mutants show an increase in the occurrence of more aggressive primary pancreatic ductal adenocarcinomas
• 77% of mice show invasive PDAC and 85% show poorly differentiated adenocarcinoma
• primary pancreatic ductal adenocarcinomas quickly metastasize to the liver
• 67% incidence of metastases to the liver, 18% incidence to the lung, and 15% incidence to the thymus

mortality/aging
• due to pancreatic tumors




Genotype
MGI:5898452
cn45
Allelic
Composition
Apctm2Rak/Apctm2Rak
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129/Sv * C57BL/6J * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Rak mutation (1 available); any Apc mutation (59 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

endocrine/exocrine glands
• maturation of the prenatal pancreas is disrupted

digestive/alimentary system
• altered gastrointestinal development




Genotype
MGI:4356154
cn46
Allelic
Composition
Smotm1Amc/Smotm1Amc
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smotm1Amc mutation (1 available); any Smo mutation (9 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• ventral pancreas and gall bladder development is normal at E10.5




Genotype
MGI:5883577
cn47
Allelic
Composition
Senp1tm1.1Eyeh/Senp1+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Senp1tm1.1Eyeh mutation (0 available); any Senp1 mutation (51 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• male mice show an intermediate phenotype of glucose intolerance following an oral glucose challenge




Genotype
MGI:5883576
cn48
Allelic
Composition
Senp1tm1.1Eyeh/Senp1tm1.1Eyeh
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Senp1tm1.1Eyeh mutation (0 available); any Senp1 mutation (51 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in vitro, islets isolated from male mice exhibit an impaired secretory response to glucose (16.7 mM) and KCl (30 mM) in a perifusion assay; the area under the curve (AUC) of the responses to glucose and KCl is reduced
• when KATP channels are held open with diazoxide (100 uM), isolated islets show a blunted secretory response to KCl (30 mM) at 16.7 mM glucose
• impaired insulin secretion is likely due to impaired glucose-dependent amplification of exocytosis
• however, the insulin content of mutant islets is unchanged
• male mice show a significant reduction in the plasma insulin response to oral glucose relative to control littermates
• however, islet morphology and alpha and beta cell mass is normal at 14 weeks of age
• male mice are glucose intolerant following an oral glucose challenge at 6 and 12 weeks of age
• however, insulin tolerance is similar to that in control littermates

endocrine/exocrine glands
• pancreatic beta cells exhibit loss of the glucose-dependent amplification of insulin exocytosis and fail to respond to NADPH and glutathione (GSH), unlike control beta cells
• impaired glucose-dependent amplification of exocytosis can be rescued by reintroduction of the SENP1 catalytic domain (cSENP1) via the patch pipette
• action potential firing is only modestly altered in beta cells, although islet intracellular Ca2+ responses remain largely normal
• in vitro, islets isolated from male mice exhibit an impaired secretory response to glucose (16.7 mM) and KCl (30 mM) in a perifusion assay; the area under the curve (AUC) of the responses to glucose and KCl is reduced
• when KATP channels are held open with diazoxide (100 uM), isolated islets show a blunted secretory response to KCl (30 mM) at 16.7 mM glucose
• impaired insulin secretion is likely due to impaired glucose-dependent amplification of exocytosis
• however, the insulin content of mutant islets is unchanged

nervous system
• action potential firing is only modestly affected in pancreatic beta cells, as shown by a small but significant reduction in action potential height with no significant differences in inter-spike membrane potential
• however, islet intracellular Ca2+ responses remain largely normal

growth/size/body
N
• male mice exhibit normal body weight between 6 and 14 weeks of age




Genotype
MGI:5704414
cn49
Allelic
Composition
Hmgb1tm1.1Dltg/Hmgb1tm1.1Dltg
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hmgb1tm1.1Dltg mutation (0 available); any Hmgb1 mutation (9 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• following induction of injection of L-arginine or cerulein

homeostasis/metabolism
• following induction of injection of L-arginine or cerulein
• following induction of injection of L-arginine or cerulein
• following induction of injection of L-arginine or cerulein
• following induction of injection of L-arginine or cerulein

endocrine/exocrine glands
N
• mice exhibit normal pancreatic development
• following induction of injection of L-arginine or cerulein
• with elevated serum amylase, exaggerated acinar cell death, leukocyte infiltration, interstitial edema, worsened acute lung injury, and increased serum TNF and IL6 following induction of injection of L-arginine or cerulean
• however, administration of N-acetyl-L-cysteine or neutralization of extracellular Histone and HMGB1 protects mice

immune system
• with elevated serum amylase, exaggerated acinar cell death, leukocyte infiltration, interstitial edema, worsened acute lung injury, and increased serum TNF and IL6 following induction of injection of L-arginine or cerulean
• however, administration of N-acetyl-L-cysteine or neutralization of extracellular Histone and HMGB1 protects mice
• following induction of injection of L-arginine or cerulein
• following induction of injection of L-arginine or cerulein




Genotype
MGI:6113916
cx50
Allelic
Composition
Epha2tm1Jrui/Epha2tm1Jrui
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2.1Tyj/Trp53+
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Epha2tm1Jrui mutation (2 available); any Epha2 mutation (32 available)
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Tg(Pdx1-cre)6Tuv mutation (2 available)
Trp53tm2.1Tyj mutation (2 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• phenotypes are relative to the control KPC (KrasG12D/+, p53R172H/+, Pdx1-Cre) PDAC (pancreatic adenocarcinoma) model mice
• size of PDAC primary tumors same as control
• significantly reduced number of detectable PDAC metastases to liver, lung and other tissues
• reduced migration of PDAC cells in vitro

mortality/aging
• survival reduced compared to control





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last database update
07/09/2019
MGI 6.14
The Jackson Laboratory