All Phenotypes Ptf1a<tm1.1(cre)Cvw> MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Ptf1a^{tm1.1(cre)Cvw}
targeted mutation 1.1, Christopher VE Wright
MGI:2387812

Summary

34 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a^{tm1.1(cre)Cvw}	involves: 129S1/Sv * 129X1/SvJ	MGI:3695166
cn2	Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	B6.129(Cg)-Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw}	MGI:3836557
cn3	Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(MUC1)79.24Gend/0	B6.Cg-Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} Tg(MUC1)79.24Gend	MGI:3836556
cn4	Cadps^tm1.1Tfr/Cadps^tm1.2Tfr Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	B6.Cg-Ptf1a^{tm1.1(cre)Cvw} Cadps^tm1.1Tfr Cadps^tm1.2Tfr	MGI:5562545
cn5	Pgbd5^tm1.2Aken/Pgbd5^tm1.2Aken Ptch1^tm1Bjw/Ptch1^tm1Bjw Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129 * C57BL/6J * C57BL/6NTac * FVB/N * SW	MGI:7616725
cn6	Pgbd5^tm1.1Aken/Pgbd5^tm1.2Aken Ptch1^tm1Bjw/Ptch1^tm1Bjw Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129 * C57BL/6J * C57BL/6NTac * FVB/N * SW	MGI:7616728
cn7	Cdkn2a^tm4Rdp/Cdkn2a⁺ Kras^tm4Tyj/Kras⁺ Smad4^tm1Rdp/Smad4^tm1Rdp Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129 * FVB/N	MGI:3695424
cn8	Cdkn2a^tm4Rdp/Cdkn2a^tm4Rdp Kras^tm4Tyj/Kras⁺ Smad4^tm1Rdp/Smad4^tm1Rdp Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129 * FVB/N	MGI:3695428
cn9	Kras^tm4Tyj/Kras⁺ Smad4^tm1Rdp/Smad4^tm1Rdp Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129 * FVB/N	MGI:3695421
cn10	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Smad4^tm1Rdp/Smad4^tm1Rdp	involves: 129 * FVB/N	MGI:3695420
cn11	Fat3^tm1.1Good/Fat3^tm1.2Good Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:5295430
cn12	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras*G12D)#Rdp/0 Trp53^tm1Brn/Trp53⁺	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N	MGI:5648533
cn13	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras*G12D)#Rdp/0 Trp53^tm1Brn/Trp53^tm1Brn	involves: 129P2/OlaHsd * 129S/Sv * 129X1/SvJ * C57BL/6 * FVB/N	MGI:5648534
cn14	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Robo3^tm1.1Ache/Robo3^tm1.1Ache	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ	MGI:4441338
cn15	Cdkn2a^tm4Rdp/Cdkn2a⁺ Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ	MGI:3695432
cn16	Cdkn2a^tm4Rdp/Cdkn2a^tm4Rdp Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ	MGI:3695431
cn17	Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ	MGI:3032576
cn18	Kras^tm4Tyj/Kras⁺ Tgfbr2^tm1.2Hlm/Tgfbr2⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2	MGI:3695569
cn19	Kras^tm4Tyj/Kras⁺ Tgfbr2^tm1.2Hlm/Tgfbr2^tm1.2Hlm Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2	MGI:3695567
cn20	Kras^tm4Tyj/Kras⁺ Tg(Erbb2*)#Maed/0 Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6J	MGI:6192639
cn21	Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor^tm1Sor Ptf1a^{tm1.1(cre)Cvw}/Ptf1a^{tm1.1(cre)Cvw}	involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * Black Swiss	MGI:3695168
cn22	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tgfbr2^tm1.2Hlm/Tgfbr2^tm1.2Hlm	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * DBA/2	MGI:3695570
cn23	Gad1^tm2Oba/Gad1^tm2Oba Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129X1/SvJ	MGI:3805734
cn24	Fat3^tm1.2Good/Fat3^tm1.2Good Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(CAG-Bgeo/GFP)21Lbe/0	involves: 129S1/Sv * 129X1/SvJ	MGI:5295428
cn25	Smad4^tm1.1Gsu/Smad4^tm1.1Gsu Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129X1/SvJ	MGI:5792846
cn26	Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2	MGI:3695568
cn27	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras*G12D)#Rdp/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N	MGI:5648532
cn28	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras2)12Hev/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N	MGI:5569002
cn29	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras2)12Hev/0 Trp53^tm1Tyj/Trp53⁺	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N	MGI:5569005
cn30	Chd7^{tm2c(EUCOMM)Wtsi}/Chd7^{tm2c(EUCOMM)Wtsi} Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S1/Sv * 129X1/SvJ * C57BL/6N	MGI:7493473
cn31	Smad4^tm1.1Gsu/Smad4^tm1.1Gsu Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(MtTGFA)Lmb/0	involves: 129S1/Sv * 129X1/SvJ * CD-1	MGI:5792847
cn32	Tg(Erbb2*)#Maed/0 Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺	involves: 129S/Sv * 129X1/SvJ * C57BL/6J	MGI:6192638
cn33	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Sec24c^{tm1c(EUCOMM)Wtsi}/Sec24c^{tm1c(EUCOMM)Wtsi}	involves: 129S/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:5896386
cx34	Ptf1a^{tm1.1(cre)Cvw}/Cbll^{Tg(Alb-KL)7-2Mhos}	involves: C57BL/6	MGI:3771566

Allelic Composition	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a^{tm1.1(cre)Cvw}
Genetic Background	involves: 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

neonatal lethality, complete penetrance ( J:130251 )

• mice die as neonates

vision/eye

abnormal eye development ( J:115271 )

• precursors normally fated to become amacrine and horizontal cells switch to ganglion cell fates

• although cells belonging to the outer neuroblastic layer are confined to the ventricular zone in wild-type, they tend to invade into the ganglion cell layer in mutant retinas

abnormal retina morphology ( J:115271 )

• retinal explants are significantly thinner after 2 weeks of culture compared to wild-type and often exhibit substantial focal perturbations in laminar organization and rosette-like structures, however exhibit normal generation of photoreceptor cells, bipolar cells, and glial cells

• retinas at E16.5 show abnormal laminar organization

absent amacrine cells ( J:115271 )

• lack of calbindin-positive and syntaxin-positive cells in cultured retinas indicates that amacrine cells, including the displaced amacrine cells in the ganglion cell layer, are profoundly missing

increased retina ganglion cell number ( J:115271 )

• increased number and expanded spatial localization of cells expressing the ganglion cell marker Brn3b in retinas indicating increased ganglion cell number

• precursors normally fated to become amacrine and horizontal cells switch to ganglion cell fates

absent retina horizontal cells ( J:115271 )

• calbindin-positive cells in the outer border of the inner nuclear layer are entirely absent in cultured retinas, indicating complete loss of horizontal cells

thick retina ganglion layer ( J:115271 )

• the ganglion cell layer is significantly thicker

absent retina inner plexiform layer ( J:115271 )

• by E18.5, the inner plexiform layer is absent

abnormal retina outer plexiform layer morphology ( J:200752 )

• reduced expression of horizontal cell (HC) marker Lim1 at age E14.5

nervous system

absent amacrine cells ( J:115271 )

• lack of calbindin-positive and syntaxin-positive cells in cultured retinas indicates that amacrine cells, including the displaced amacrine cells in the ganglion cell layer, are profoundly missing

increased retina ganglion cell number ( J:115271 )

• increased number and expanded spatial localization of cells expressing the ganglion cell marker Brn3b in retinas indicating increased ganglion cell number

• precursors normally fated to become amacrine and horizontal cells switch to ganglion cell fates

absent retina horizontal cells ( J:115271 )

• calbindin-positive cells in the outer border of the inner nuclear layer are entirely absent in cultured retinas, indicating complete loss of horizontal cells

endocrine/exocrine glands

absent pancreas ( J:130251 )

• neonates have no pancreas

Allelic Composition	Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	B6.129(Cg)-Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw}

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kras^tm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased pancreas tumor incidence ( J:138959 )

• pancreatic tumors exhibit higher proliferation rates than in Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} heterozygotes

increased pancreatic ductal adenocarcinoma incidence ( J:138959 )

• in 8 of 10 mice at 26 weeks

increased pancreatic intraepithelial neoplasia incidence ( J:138959 )

• at 6 weeks of age

increased metastatic potential ( 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 Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} heterozygotes

endocrine/exocrine glands

increased pancreas weight ( J:138959 )

• pancreatic weight is greater than in Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} heterozygotes

increased pancreas tumor incidence ( J:138959 )

• pancreatic tumors exhibit higher proliferation rates than in Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} heterozygotes

increased pancreatic ductal adenocarcinoma incidence ( J:138959 )

• in 8 of 10 mice at 26 weeks

increased pancreatic intraepithelial neoplasia incidence ( J:138959 )

• at 6 weeks of age

growth/size/body

increased pancreas weight ( J:138959 )

• pancreatic weight is greater than in Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} heterozygotes

Allelic Composition	Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(MUC1)79.24Gend/0
Genetic Background	B6.Cg-Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} Tg(MUC1)79.24Gend

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased pancreas tumor incidence ( J:138959 , J:234412 )

• pancreatic tumors exhibit lower proliferation rates than in Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} Tg(MUC1)79.24Gend heterozygotes (J:138959)

• mice exhibit carcinoma in situ in the pancreas (J:234412)

increased pancreatic ductal adenocarcinoma incidence ( J:138959 )

• in 1 of 10 mice at 26 weeks

increased pancreatic intraepithelial neoplasia incidence ( J:138959 , J:234412 )

• mice exhibit high-grade PanIN lesions and carcinoma in situ, associated with disorganized glandular epithelium (J:234412)

• mice treated with gemcitabine exhibit normal pancreatic glandular structure 26 weeks after the beginning of treatment (J:234412)

decreased metastatic potential ( 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 Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} Tg(MUC1)79.24Gend heterozygotes

endocrine/exocrine glands

increased pancreas tumor incidence ( J:138959 , J:234412 )

• pancreatic tumors exhibit lower proliferation rates than in Kras^tm4Tyj Ptf1a^{tm1.1(cre)Cvw} Tg(MUC1)79.24Gend heterozygotes (J:138959)

• mice exhibit carcinoma in situ in the pancreas (J:234412)

increased pancreatic ductal adenocarcinoma incidence ( J:138959 )

• in 1 of 10 mice at 26 weeks

increased pancreatic intraepithelial neoplasia incidence ( J:138959 , J:234412 )

• mice exhibit high-grade PanIN lesions and carcinoma in situ, associated with disorganized glandular epithelium (J:234412)

• mice treated with gemcitabine exhibit normal pancreatic glandular structure 26 weeks after the beginning of treatment (J:234412)

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

Allelic Composition	Cadps^tm1.1Tfr/Cadps^tm1.2Tfr Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	B6.Cg-Ptf1a^{tm1.1(cre)Cvw} Cadps^tm1.1Tfr Cadps^tm1.2Tfr

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cadps^tm1.1Tfr mutation (1 available); any Cadps mutation (70 available)
Cadps^tm1.2Tfr mutation (0 available); any Cadps mutation (70 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

nervous system phenotype ( J:204664 )

N	• normal basic synaptic transmission, short-term plasticity, and climber-fiber-Purkinje innervation

abnormal cerebellar molecular layer ( J:204664 )

• decrease in the density of BDNF+ climbing fibers

• reduction of dense core vesicle density in the presynaptic area and a decrease in the number of synaptic vesicles per presynapse

abnormal synaptic bouton morphology ( J:204664 )

• reduction of dense core vesicle density in the presynaptic area

abnormal synaptic vesicle number ( J:204664 )

• reduction in the number of synaptic vesicles per presynapse

decreased excitatory postsynaptic current amplitude ( J:204664 )

• decrease in climbing fiber-EPSC amplitude

abnormal paired-pulse inhibition ( J:204664 )

• enhanced paired-pulse depression of climbing fiber EPSCs

Allelic Composition	Pgbd5^tm1.2Aken/Pgbd5^tm1.2Aken Ptch1^tm1Bjw/Ptch1^tm1Bjw Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129 * C57BL/6J * C57BL/6NTac * FVB/N * SW

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pgbd5^tm1.2Aken mutation (0 available); any Pgbd5 mutation (35 available)
Ptch1^tm1Bjw mutation (2 available); any Ptch1 mutation (115 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

increased tumor-free survival time ( J:346387 )

• increased survival compared to mutant mice wild-type for Pgbd5

neoplasm

decreased classified tumor incidence ( J:346387 )

• up to 70% of mice do not develop medulloblastomas at up to 1 year of life while 79% of mutant mice wild-type for Pgdb5 rapidly develop medulloblastomas

Allelic Composition	Pgbd5^tm1.1Aken/Pgbd5^tm1.2Aken Ptch1^tm1Bjw/Ptch1^tm1Bjw Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129 * C57BL/6J * C57BL/6NTac * FVB/N * SW

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pgbd5^tm1.1Aken mutation (1 available); any Pgbd5 mutation (35 available)
Pgbd5^tm1.2Aken mutation (0 available); any Pgbd5 mutation (35 available)
Ptch1^tm1Bjw mutation (2 available); any Ptch1 mutation (115 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased medulloblastoma incidence ( J:346387 )

• develop tumors with a similar latency to mice with one wild-type Pgbd5 allele, but most tumors retain an unrecombined floxed Pgbd5 allele

nervous system

increased medulloblastoma incidence ( J:346387 )

• develop tumors with a similar latency to mice with one wild-type Pgbd5 allele, but most tumors retain an unrecombined floxed Pgbd5 allele

Allelic Composition	Cdkn2a^tm4Rdp/Cdkn2a⁺ Kras^tm4Tyj/Kras⁺ Smad4^tm1Rdp/Smad4^tm1Rdp Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2a^tm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Kras^tm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Smad4^tm1Rdp mutation (0 available); any Smad4 mutation (48 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 12 of 13 mice develop pancreatic ductal adenocarcinoma

• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4

mortality/aging

decreased tumor-free survival time ( J:116130 )

• average tumor-free survival is 14 weeks

neoplasm

increased tumor incidence ( J:116130 )

• 5 of 13 mice develop intraductal papillary mucinous neoplasms

• tumor fibrosis is increased compared to mice wild-type for Smad4

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 12 of 13 mice develop pancreatic ductal adenocarcinoma

• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4

Allelic Composition	Cdkn2a^tm4Rdp/Cdkn2a^tm4Rdp Kras^tm4Tyj/Kras⁺ Smad4^tm1Rdp/Smad4^tm1Rdp Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129 * FVB/N

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 4 of 4 mice develop pancreatic ductal adenocarcinoma

• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4

• tumor fibrosis is increased compared to mice wild-type for Smad4

mortality/aging

decreased tumor-free survival time ( J:116130 )

• average tumor-free survival is 8.8 weeks

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 4 of 4 mice develop pancreatic ductal adenocarcinoma

• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4

• tumor fibrosis is increased compared to mice wild-type for Smad4

Allelic Composition	Kras^tm4Tyj/Kras⁺ Smad4^tm1Rdp/Smad4^tm1Rdp Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129 * FVB/N

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

pancreas cyst ( J:116130 )

• seen in all mice

mortality/aging

decreased tumor-free survival time ( J:116130 )

• mice die between 8 and 24 weeks of age

• average tumor-free survival is 15.7 weeks

neoplasm

increased tumor incidence ( J:116130 )

• 12 of 12 mice develop intraductal papillary mucinous neoplasms

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 2 of 12 mice develop pancreatic ductal adenocarcinoma

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 2 of 12 mice develop pancreatic ductal adenocarcinoma

pancreas cyst ( J:116130 )

• seen in all mice

Allelic Composition	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Smad4^tm1Rdp/Smad4^tm1Rdp
Genetic Background	involves: 129 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Smad4^tm1Rdp mutation (0 available); any Smad4 mutation (48 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:116130 )

N	• pancreatic development, morphology, and function are all similar to wild-type and no pancreatic neoplasms develop

Allelic Composition	Fat3^tm1.1Good/Fat3^tm1.2Good Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fat3^tm1.1Good mutation (1 available); any Fat3 mutation (241 available)
Fat3^tm1.2Good mutation (0 available); any Fat3 mutation (241 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

vision/eye

abnormal retina neuronal layer morphology ( J:176668 )

• amacrine cells form an additional plexiform layers (outer misplaced plexiform layers) compared with wild-type mice

• amacrine cells develop bipolar morphologies

• however, amacrine cell migration is normal and no inner misplaced plexiform layer is formed

Allelic Composition	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras*G12D)#Rdp/0 Trp53^tm1Brn/Trp53⁺
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy} mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Tg(tetO-Kras*G12D)#Rdp mutation (0 available)
Trp53^tm1Brn mutation (18 available); any Trp53 mutation (240 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:186194 )

• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age

• tumors exhibit features of human PDAC, including glandular tumor structures, exuberant stroma, local invasion into surrounding structures such as the duodenum, and distant metastases to the liver and lung

• mice show rapid tumor regression staring 48 hours and peaking at 72 hours following doxycycline withdrawal, with a reduction in tumor mass of about 50% after 1 week of doxycycline withdrawal; tumor regression is accompanied by decreased tumor cell proliferation and increased apoptosis

• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:186194 )

• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age

• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro

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

Allelic Composition	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras*G12D)#Rdp/0 Trp53^tm1Brn/Trp53^tm1Brn
Genetic Background	involves: 129P2/OlaHsd * 129S/Sv * 129X1/SvJ * C57BL/6 * FVB/N

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:186194 )

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

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:186194 )

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

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

Allelic Composition	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Robo3^tm1.1Ache/Robo3^tm1.1Ache
Genetic Background	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Robo3^tm1.1Ache mutation (0 available); any Robo3 mutation (76 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Ataxic gait in Robo3^tm1.1Ache/Robo3^tm1.1Ache Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ mice

nervous system

abnormal brain commissure morphology ( J:158918 )

• severe impairment of the interolivary commissure

abnormal innervation ( J:158918 )

• only about 1/3 of inferior olivary neurons project contralaterally compared to wild-type controls where all neurons project contralaterally

behavior/neurological

abnormal motor coordination/balance ( J:158918 )

• in an Erasmus ladder test step time and overall walking pattern are severely abnormal

• impairment is more severe than that of Grid2^Lc mice

ataxia ( J:158918 )

• severe

impaired coordination ( J:158918 )

• decrease in latency to fall of a rotarod

• impairment is more severe than that of Grid2^Lc mice

Allelic Composition	Cdkn2a^tm4Rdp/Cdkn2a⁺ Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

decreased tumor-free survival time ( J:116130 )

• average tumor-free survival is 38 weeks

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 6 of 10 mice develop pancreatic ductal adenocarcinoma

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 6 of 10 mice develop pancreatic ductal adenocarcinoma

Allelic Composition	Cdkn2a^tm4Rdp/Cdkn2a^tm4Rdp Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

decreased tumor-free survival time ( J:116130 )

• average tumor-free survival is 8.6 weeks

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 6 of 6 mice develop pancreatic ductal adenocarcinoma

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 6 of 6 mice develop pancreatic ductal adenocarcinoma

Allelic Composition	Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased tumor incidence ( J:87973 )

increased pancreatic ductal adenocarcinoma incidence ( J:87973 , J:116130 )

• 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)

increased pancreatic intraepithelial neoplasia incidence ( J:262746 )

• pancreatic intraepithelial neoplasia (PanIN)-1 lesions are distributed widely throughout the pancreas, whereas PanIN-2 or -3 lesions are rarely seen

digestive/alimentary system

abnormal pancreatic acinar cell morphology ( J:262746 )

• 6 month old mice exhibit mild acinar cell loss

endocrine/exocrine glands

abnormal pancreatic acinar cell morphology ( J:262746 )

• 6 month old mice exhibit mild acinar cell loss

enlarged pancreas ( J:87973 )

increased pancreatic ductal adenocarcinoma incidence ( J:87973 , J:116130 )

• 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)

increased pancreatic intraepithelial neoplasia incidence ( J:262746 )

• pancreatic intraepithelial neoplasia (PanIN)-1 lesions are distributed widely throughout the pancreas, whereas PanIN-2 or -3 lesions are rarely seen

growth/size/body

enlarged pancreas ( J:87973 )

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

Allelic Composition	Kras^tm4Tyj/Kras⁺ Tgfbr2^tm1.2Hlm/Tgfbr2⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:116129 )

• exhibit reduced survival than controls after 200 days of age, with a median survival of 347 days

neoplasm

increased pancreas tumor incidence ( J:116129 )

• pancreatic tumors examined demonstrate a dominant sarcomatoid histology (50% or more) as well as the ductal adenocarcinoma

increased pancreatic ductal adenocarcinoma incidence ( J:116129 )

• at 200 days of age or later, show well-differentiated ductal adenocarcinoma in the pancreas head region

increased pancreatic intraepithelial neoplasia incidence ( J:116129 )

• develop pancreatic intraepithelial neoplasia (mPanIN) lesions predominantly in the pancreas tail region

increased metastatic potential ( J:116129 )

• tumors frequently show gross metastasis to the liver and lung, direct invasion to the duodenum, and also peritoneal dissemination

• frequency of metastasis or invasion is much higher (about 50%) than in similar mutants with homozygous, instead of heterozygous, loss of Tgfbr2

endocrine/exocrine glands

increased pancreas tumor incidence ( J:116129 )

• pancreatic tumors examined demonstrate a dominant sarcomatoid histology (50% or more) as well as the ductal adenocarcinoma

increased pancreatic ductal adenocarcinoma incidence ( J:116129 )

• at 200 days of age or later, show well-differentiated ductal adenocarcinoma in the pancreas head region

increased pancreatic intraepithelial neoplasia incidence ( J:116129 )

• develop pancreatic intraepithelial neoplasia (mPanIN) lesions predominantly in the pancreas tail region

Allelic Composition	Kras^tm4Tyj/Kras⁺ Tgfbr2^tm1.2Hlm/Tgfbr2^tm1.2Hlm Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:116129 )

• some die suddenly with a median survival of 59 days

growth/size/body

weight loss ( J:116129 )

distended abdomen ( J:116129 )

• begin to demonstrate abdominal distension at around 6-7 weeks of age due to pancreatic tumor

enlarged spleen ( J:116129 )

• seen frequently

neoplasm

increased pancreas tumor incidence ( J:116129 )

• 100% penetrance of pancreatic tumors

increased pancreatic ductal adenocarcinoma incidence ( J:116129 )

• progressive development of pancreatic ductal adenocarcinoma; tumor uniformly occupies the whole pancreas and is irregularly shaped and results in almost complete loss of normal pancreatic tissue

• carcinoma cells frequently show nuclear atypia and invasion beyond the basement membrane

• stromal expansion starts in the early tumorigenesis stages and tumors do not show sarcomatoid architecture

• 100% penetrance and tumors are always accompanied by a whole panel of pancreatic intraepithelial neoplasia (mPanIN) lesions and acinar-ductal metaplasia lesions

increased pancreatic intraepithelial neoplasia incidence ( J:116129 )

• tumors are always accompanied by a whole panel of pancreatic intraepithelial neoplasia (mPanIN) lesions and acinar-ductal metaplasia lesions

increased metastatic potential ( J:116129 )

• although no distant metastasis is seen at 7-10 weeks of age, the few mutants that survive up to 24-27 weeks, show prominent desmoplasia and liver metastasis, lung metastasis, diaphragmatic and duodenal invasion and peritoneal dissemination

liver/biliary system

dilated gallbladder ( J:116129 )

• duodenum loop is compressed by the tumor, resulting in duodenal and gallbladder dilatation

hepatic necrosis ( J:116129 )

• at late-stage tumor burden, exhibit multiple necrotic areas in the distal liver parenchyma

jaundice ( J:116129 )

• observed sometimes

homeostasis/metabolism

abnormal hepatic portal vein thrombosis ( J:116129 )

• at late-stage tumor burden (7-10 weeks of age), 32% exhibit portal vein thrombosis; the main trunk of the portal vein is completely obstructed with thrombus

hemorrhagic ascites ( J:116129 )

• frequently display bloody ascites

hematopoietic system

enlarged spleen ( J:116129 )

• seen frequently

immune system

enlarged spleen ( J:116129 )

• seen frequently

behavior/neurological

paralysis ( J:116129 )

• a few mutants exhibit paraplegia, most likely because of circulation failure due to oppression of large vessels by the growing tumor

digestive/alimentary system

abnormal duodenum morphology ( J:116129 )

• duodenum loop is compressed by the tumor, resulting in duodenal and gallbladder dilatation

endocrine/exocrine glands

dilated gallbladder ( J:116129 )

• duodenum loop is compressed by the tumor, resulting in duodenal and gallbladder dilatation

increased pancreas tumor incidence ( J:116129 )

• 100% penetrance of pancreatic tumors

increased pancreatic ductal adenocarcinoma incidence ( J:116129 )

• progressive development of pancreatic ductal adenocarcinoma; tumor uniformly occupies the whole pancreas and is irregularly shaped and results in almost complete loss of normal pancreatic tissue

• carcinoma cells frequently show nuclear atypia and invasion beyond the basement membrane

• stromal expansion starts in the early tumorigenesis stages and tumors do not show sarcomatoid architecture

• 100% penetrance and tumors are always accompanied by a whole panel of pancreatic intraepithelial neoplasia (mPanIN) lesions and acinar-ductal metaplasia lesions

increased pancreatic intraepithelial neoplasia incidence ( J:116129 )

• tumors are always accompanied by a whole panel of pancreatic intraepithelial neoplasia (mPanIN) lesions and acinar-ductal metaplasia lesions

cardiovascular system

abnormal hepatic portal vein morphology ( J:116129 )

• at late-stage tumor burden (7-10 weeks of age), 32% exhibit portal vein thrombosis; the main trunk of the portal vein is completely obstructed with thrombus

Allelic Composition	Kras^tm4Tyj/Kras⁺ Tg(Erbb2*)#Maed/0 Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6J

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

abnormal pancreatic acinar cell morphology ( J:262746 )

• 6 month old mice exhibit severe acinar cell loss

endocrine/exocrine glands

abnormal pancreatic acinar cell morphology ( J:262746 )

• 6 month old mice exhibit severe acinar cell loss

increased pancreatic intraepithelial neoplasia incidence ( J:262746 )

• mice show accelerated pancreatic intraepithelial neoplasia (PanIN) lesions with severe acinar cell loss, with majority of lesions being PanIN-1 but having some PanIN-2 and -3 lesions

neoplasm

increased pancreatic intraepithelial neoplasia incidence ( J:262746 )

• mice show accelerated pancreatic intraepithelial neoplasia (PanIN) lesions with severe acinar cell loss, with majority of lesions being PanIN-1 but having some PanIN-2 and -3 lesions

Allelic Composition	Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor^tm1Sor Ptf1a^{tm1.1(cre)Cvw}/Ptf1a^{tm1.1(cre)Cvw}
Genetic Background	involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * Black Swiss

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^tm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

vision/eye

increased retina ganglion cell number ( J:115271 )

• precursors normally fated to become amacrine and horizontal cells switch to ganglion cell fates, resulting in an increase in ganglion cells

nervous system

increased retina ganglion cell number ( J:115271 )

• precursors normally fated to become amacrine and horizontal cells switch to ganglion cell fates, resulting in an increase in ganglion cells

digestive/alimentary system

abnormal digestive system development ( J:78710 )

• exhibit a switch of pancreatic progenitors such that their progeny proliferate in and adopt the normal fates of duodenal epithelium, including its stem-cell compartment

absent pancreatic acini ( J:78710 )

• at E10.5, E12.5, E14.5, E16.5, and E18.5, exocrine acini are completely absent

endocrine/exocrine glands

absent pancreatic acini ( J:78710 )

• at E10.5, E12.5, E14.5, E16.5, and E18.5, exocrine acini are completely absent

abnormal pancreas development ( J:78710 )

• conversion of pancreatic precursors into duodenal fates; form rudimentary pancreatic tissue that contains ductal and endocrine cell types

Allelic Composition	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tgfbr2^tm1.2Hlm/Tgfbr2^tm1.2Hlm
Genetic Background	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * DBA/2

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Tgfbr2^tm1.2Hlm mutation (0 available); any Tgfbr2 mutation (40 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

endocrine/exocrine glands

abnormal pancreas development ( J:116129 )

• somatostatin-positive cells are more frequently observed at 1 day of age and at 7 weeks of age, however this difference disappears by 12 weeks of age and the pancreas appears very normal, indicating only subtle effects on pancreas development

Allelic Composition	Gad1^tm2Oba/Gad1^tm2Oba Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gad1^tm2Oba mutation (0 available); any Gad1 mutation (65 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

impaired coordination ( J:134497 )

• at 6 weeks, rotarod performance is impaired compared to wild-type; mutants fall from rod more quickly than controls

abnormal gait ( J:134497 )

• gait is similar with almost equivalent stride length, but slightly larger stride width at 6 weeks of age

nervous system

abnormal nervous system morphology ( J:134497 )

• GABA level in mutant cerebellum is >44% of controls; largest reduction is observed at P7-P8 (reduced to 16%)

abnormal inhibitory postsynaptic currents ( J:134497 )

• frequency and amplitudes of spontaneous IPSCs in Purkinje cells are reduced compared to controls

• frequency and amplitudes of miniature IPSCs in Purkinje cells are significantly reduced compared to controls

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:134497 )

N	• Langerhans islets are not affected in number or size

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:134497 )

N	• at 6 weeks of age, blood insulin and glucose levels are not different from controls

craniofacial

craniofacial phenotype ( J:134497 )

N	• mice do not develop cleft palate like Gad1 germline-null mice

Allelic Composition	Fat3^tm1.2Good/Fat3^tm1.2Good Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(CAG-Bgeo/GFP)21Lbe/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fat3^tm1.2Good mutation (0 available); any Fat3 mutation (241 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Tg(CAG-Bgeo/GFP)21Lbe mutation (2 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal amacrine cell morphology ( J:176668 )

• amacrine cells retain two processes after reaching the inner plexiform layer unlike unipolar wild-type cells

• amacrine cells fail to retract trailing processes upon reaching the inner plexiform layer

• amacrine cells develop a second arbor that extends to the outer misplaced plexiform layer

vision/eye

abnormal amacrine cell morphology ( J:176668 )

• amacrine cells retain two processes after reaching the inner plexiform layer unlike unipolar wild-type cells

• amacrine cells fail to retract trailing processes upon reaching the inner plexiform layer

• amacrine cells develop a second arbor that extends to the outer misplaced plexiform layer

abnormal retina neuronal layer morphology ( J:176668 )

• amacrine cells form two additional plexiform layers (inner and outer misplaced plexiform layers) compared with wild-type mice

Allelic Composition	Smad4^tm1.1Gsu/Smad4^tm1.1Gsu Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Smad4^tm1.1Gsu mutation (0 available); any Smad4 mutation (48 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Pancreatic fibrosis and acinar-to-ductal metaplasia in Tg(MtTGFA)Lmb/0 (MT-TGFalpha) and Smad4^tm1.1Gsu/Smad4^tm1.1Gsu Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(MtTGFA)Lmb/0 (STP) mice

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:229184 )

N	• mice exhibit no pancreatic abnormalities

Allelic Composition	Kras^tm4Tyj/Kras⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased pancreatic intraepithelial neoplasia incidence ( J:116129 )

• develop pancreatic intraepithelial neoplasia (mPanIN) lesions within a large amount of normal pancreas

endocrine/exocrine glands

increased pancreatic intraepithelial neoplasia incidence ( J:116129 )

• develop pancreatic intraepithelial neoplasia (mPanIN) lesions within a large amount of normal pancreas

Allelic Composition	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras*G12D)#Rdp/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:186194 )

• infrequently, mice exhibit occurrence of invasive pancreatic ductal adenocarcinoma after long latency (35-70 weeks) following doxycline treatment

increased pancreatic intraepithelial neoplasia incidence ( J:186194 )

• mice develop PanIN lesions within 2 weeks of doxycycline induction

pancreatic acinar-to-ductal metaplasia ( J:186194 )

• mice develop acinar-to-ductal metaplasia within 2 weeks of doxycycline induction

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:186194 )

• infrequently, mice exhibit occurrence of invasive pancreatic ductal adenocarcinoma after long latency (35-70 weeks) following doxycline treatment

increased pancreatic intraepithelial neoplasia incidence ( J:186194 )

• mice develop PanIN lesions within 2 weeks of doxycycline induction

Allelic Composition	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras2)12Hev/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased pancreas tumor incidence ( J:184378 )

• 1 of 2 mice treated with doxycycline (dox) at 4-6 weeks of age show frank adenocarcinoma by 23 weeks on dox

• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction

increased pancreatic intraepithelial neoplasia incidence ( J:184378 )

• mice treated with doxycycline (dox) at 4-6 weeks of age to induce Kras2 expression begin to show low-grade pancreatic intraepithelial neoplasia (PanIN) beginning at 3 weeks after dox treatment

• mice treated with dox at 4-6 weeks of age show PanIN, surrounded by areas of fibrosis and embedded in the acinar parenchyma after 18 weeks on dox and by 23 weeks, large areas of the pancreatic parenchyma are substituted with PanIN lesions of different grade, with frank adenocarcinoma seen in 1 of 2 mice

• mice kept on dox for 23 weeks show reversion of PanINs when dox is removed for 2 weeks

• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein, to induce acute pancreatitis, develop low- and high-grade PanIN lesions at 5 weeks after induction

• mice treated with dox 72 hours prior to induction of pancreatitis also show reversion of PanINs when dox is removed for 2 weeks

homeostasis/metabolism

increased susceptibility to injury ( J:184378 )

• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show impaired recovery from pancreatitis, showing acinar-ductal metaplasia with progressive accumulation of fibrotic stroma at 1 week after induction, replacement of the whole pancreatic parenchyma with ductal structures and signs of PanINs at 3 weeks after induction, and low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction compared to adult mice without dox which show completely resolved damage

• mice kept on dox for 5 weeks prior to induction of pancreatitis and then dox removal for 2 weeks show incomplete repair process resulting in a small, fibrotic pancreas with fewer acini; after 5 weeks of dox removal, no PanINs are observed however, the pancreas appears fibrotic and is small

endocrine/exocrine glands

small pancreas ( J:184378 )

• mice kept on dox for 5 weeks following pancreatitis induction show an increase in apoptotic cells and small pancreas size upon removal of dox

increased pancreas tumor incidence ( J:184378 )

• 1 of 2 mice treated with doxycycline (dox) at 4-6 weeks of age show frank adenocarcinoma by 23 weeks on dox

increased pancreatic intraepithelial neoplasia incidence ( J:184378 )

• mice treated with doxycycline (dox) at 4-6 weeks of age to induce Kras2 expression begin to show low-grade pancreatic intraepithelial neoplasia (PanIN) beginning at 3 weeks after dox treatment

• mice kept on dox for 23 weeks show reversion of PanINs when dox is removed for 2 weeks

• mice treated with dox 72 hours prior to induction of pancreatitis also show reversion of PanINs when dox is removed for 2 weeks

pancreatic acinar-to-ductal metaplasia ( J:184378 )

• mice treated with dox at 4-6 weeks of age begin to show acinar-ductal metaplasia beginning at 3 weeks after dox treatment

Allelic Composition	Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy}/Gt(ROSA)26Sor⁺ Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(tetO-Kras2)12Hev/0 Trp53^tm1Tyj/Trp53⁺
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm1(rtTA,EGFP)Nagy} mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
Trp53^tm1Tyj mutation (12 available); any Trp53 mutation (240 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:184378 )

• mice die between 8 and 18 weeks after doxycycline (dox) treatment to induce Kras2 expression due to pancreatic ductal adenocarinoma

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:184378 )

• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion

• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant

increased pancreatic intraepithelial neoplasia incidence ( J:184378 )

• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma

homeostasis/metabolism

increased susceptibility to injury ( J:184378 )

• adult mice treated with dox for 5 weeks prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis exhibit a small, translucent remnant of pancreatic tissue, without fibrosis or PanIN lesions

• when dox is removed after pancreatitis induction, mice show show normal acini interspersed with dilated ducts and acinar-ductal metaplasia, fibrosis and occasional lipomatosis, but with minimal inflammatory infiltrate, and reduced proliferation

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:184378 )

• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant

increased pancreatic intraepithelial neoplasia incidence ( J:184378 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
pancreatic carcinoma		DOID:4905	OMIM:260350	J:184378

Allelic Composition	Chd7^{tm2c(EUCOMM)Wtsi}/Chd7^{tm2c(EUCOMM)Wtsi} Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chd7^{tm2c(EUCOMM)Wtsi} mutation (0 available); any Chd7 mutation (138 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

nervous system phenotype ( J:243947 )

N	• no defects in Purkinje cells

Allelic Composition	Smad4^tm1.1Gsu/Smad4^tm1.1Gsu Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(MtTGFA)Lmb/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * CD-1

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Pancreatic fibrosis and acinar-to-ductal metaplasia in Tg(MtTGFA)Lmb/0 (MT-TGFalpha) and Smad4^tm1.1Gsu/Smad4^tm1.1Gsu Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Tg(MtTGFA)Lmb/0 (STP) mice

endocrine/exocrine glands

abnormal pancreas morphology ( J:229184 )

• activated pancreatic fibroblasts or stellate cells (PSCs) are seen in areas surrounding the ductal lesions in mice treated with zinc sulfate

abnormal pancreatic acinar cell morphology ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit progressive dilatation of the acinar lumen due to acinar-to-ductal metaplasia

• mice treated with zinc sulfate water for 8 months show a decrease in height of acinar cells

abnormal pancreatic duct morphology ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit increased ductal proliferation

dilated pancreatic duct ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit pancreatic duct dilation

abnormal pancreatic islet morphology ( J:229184 )

• disruption of islet cells due to ductal proliferation and increased fibrosis is seen in mice provided with zinc sulfate

enlarged pancreas ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit enlarged fibrotic pancreata

increased pancreatic intraepithelial neoplasia incidence ( J:229184 )

• mice treated with zinc sulfate water show increased numbers of ductal structures (both metaplastic ducts and/or PanIN-1 and -2)

• the number of PanIN-1 and -2 lesions is higher than in single Tg(MtTGFA)Lmb hemizygotes

• however, mice treated with zinc sulfate water do no develop malignant pancreatic tumors

pancreas cyst ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit frequent cystic formation in the pancreas due to duct dilation

pancreas fibrosis ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit pronounced interlobular fibrosis and progressive accumulation of fibrotic stroma and fibroblasts

pancreatic acinar-to-ductal metaplasia ( J:229184 )

• mice provided with zinc sulfate in water for 8 months to induce TGFA expression exhibit acinar-to-ductal metaplasia

• proliferation within the metaplastic ductal epithelia is increased compared to single Tg(MtTGFA)Lmb hemizygotes

chronic pancreas inflammation ( J:229184 )

• marker analysis shows increased upregulation of markers associated with chronic pancreatitis and desmoplasia in mice treated with zinc sulfate

immune system

chronic pancreas inflammation ( J:229184 )

• marker analysis shows increased upregulation of markers associated with chronic pancreatitis and desmoplasia in mice treated with zinc sulfate

neoplasm

increased pancreatic intraepithelial neoplasia incidence ( J:229184 )

• mice treated with zinc sulfate water show increased numbers of ductal structures (both metaplastic ducts and/or PanIN-1 and -2)

• the number of PanIN-1 and -2 lesions is higher than in single Tg(MtTGFA)Lmb hemizygotes

• however, mice treated with zinc sulfate water do no develop malignant pancreatic tumors

digestive/alimentary system

abnormal pancreatic acinar cell morphology ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit progressive dilatation of the acinar lumen due to acinar-to-ductal metaplasia

• mice treated with zinc sulfate water for 8 months show a decrease in height of acinar cells

abnormal pancreatic duct morphology ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit increased ductal proliferation

dilated pancreatic duct ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit pancreatic duct dilation

growth/size/body

enlarged pancreas ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit enlarged fibrotic pancreata

pancreas cyst ( J:229184 )

• mice treated with zinc sulfate water for 8 months exhibit frequent cystic formation in the pancreas due to duct dilation

Allelic Composition	Tg(Erbb2*)#Maed/0 Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺
Genetic Background	involves: 129S/Sv * 129X1/SvJ * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Tg(Erbb2*)#Maed mutation (0 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:262746 )

N	• mice show almost no phenotypes in pancreas at 6 months of age

Allelic Composition	Ptf1a^{tm1.1(cre)Cvw}/Ptf1a⁺ Sec24c^{tm1c(EUCOMM)Wtsi}/Sec24c^{tm1c(EUCOMM)Wtsi}
Genetic Background	involves: 129S/Sv * 129X1/SvJ * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)
Sec24c^{tm1c(EUCOMM)Wtsi} mutation (1 available); any Sec24c mutation (39 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:232065 )

N	• no defects in pancreas morphology are detected

growth/size/body

growth/size/body region phenotype ( J:232065 )

N	• no abnormalities in growth or weight gain are detected on either a normal chow or high fat diet compared to diet-matched controls

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:232065 )

N	• no differences in plasma cholesterol, triglyceride or insulin levels

Allelic Composition	Ptf1a^{tm1.1(cre)Cvw}/Cbll^{Tg(Alb-KL)7-2Mhos}
Genetic Background	involves: C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cbll^{Tg(Alb-KL)7-2Mhos} mutation (0 available); any Cbll mutation (0 available)
Ptf1a^{tm1.1(cre)Cvw} mutation (1 available); any Ptf1a mutation (31 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal Purkinje cell differentiation ( J:100997 )

• purkinje cells fail to develop similar to Cbll^{Tg(Alb-KL)7-2Mhos} homozygotes

abnormal GABAergic neuron morphology ( J:100997 )

• failure of GABA neurons to develop by 4 days after birth is similar to Cbll^{Tg(Alb-KL)7-2Mhos} homozygotes

cellular

abnormal Purkinje cell differentiation ( J:100997 )

• purkinje cells fail to develop similar to Cbll^{Tg(Alb-KL)7-2Mhos} homozygotes

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