Phenotypes associated with this allele

• Allele Symbol: Cdkn2a⁺
• Allele Name: wild type
• Allele ID: MGI:2433413
• Summary: 27 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
ht1	Cdkn2a^tm3(cre)Cjs/Cdkn2a^+	involves: 129S1/Sv * C57BL/6	MGI:3842676
ht2	Cdkn2a^tm2.1Rdp/Cdkn2a^+	involves: 129S6/SvEvTac * FVB/N	MGI:3814390
ht3	Cdkn2a^tm1Cjs/Cdkn2a^+	involves: 129X1/SvJ * C57BL/6 * NIH/OlaHsd	MGI:3774768
cn4	Cdkn2a^tm2.1Rdp/Cdkn2a^+ Kras^tm4Tyj/Kras^+ Trp53^tm1Brn/Trp53^tm1Brn Tg(Pdx1-cre)89.1Dam/0	involves: 129 * C57BL/6 * CBA * FVB/N	MGI:5308951
cn5	Cdkn2a^tm2.1Rdp/Cdkn2a^+ Kras^tm4Tyj/Kras^+ Trp53^tm1Brn/Trp53^+ Tg(Pdx1-cre)89.1Dam/0	involves: 129 * C57BL/6 * CBA * FVB/N	MGI:5308961
cn6	Cdkn2a^tm4Rdp/Cdkn2a^+ Kras^tm4Tyj/Kras^+ Smad4^tm1Rdp/Smad4^tm1Rdp Ptf1a^tm1.1(cre)Cvw/Ptf1a^+	involves: 129 * FVB/N	MGI:3695424
cn7	Cdkn2a^tm2Brn/Cdkn2a^+ Nf2^tm2Gth/Nf2^tm2Gth	involves: 129P2/OlaHsd	MGI:3850445
cn8	Cdkn2a^tm2.1Nesh/Cdkn2a^+ Kras^tm4Tyj/Kras^+ Trp53^tm1Brn/Trp53^+ Tg(Tyr-cre/ERT2)13Bos/0	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB	MGI:4835045
cn9	Cdkn2a^tm1.1Brn/Cdkn2a^+ Nf2^tm2Gth/Nf2^tm2Gth Trp53^tm1Brn/Trp53^tm1Brn	involves: 129P2/OlaHsd * 129S7/SvEvBrd	MGI:3850449
cn10	Cdkn2a^tm4Rdp/Cdkn2a^+ Kras^tm4Tyj/Kras^+ Ptf1a^tm1.1(cre)Cvw/Ptf1a^+	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ	MGI:3695432
cn11	Cdkn2a^tm4Rdp/Cdkn2a^+ Kras^tm4Tyj/Kras^+ Tg(Pdx1-cre)89.1Dam/0	involves: 129S4/SvJae * C57BL/6 * CBA	MGI:3695430
cn12	Cdkn2a^tm4Rdp/Cdkn2a^+ Kras^tm4Tyj/Kras^+ Tg(Pdx1-cre)89.1Dam/0	involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N	MGI:5308806
cn13	Cdkn2a^tm4Rdp/Cdkn2a^+ Kras^tm4Tyj/Kras^+ Smad4^tm1Rdp/Smad4^tm1Rdp Tg(Pdx1-cre)89.1Dam/0	involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N	MGI:3695426
cn14	Cdkn2a^tm4Rdp/Cdkn2a^+ Smad4^tm1Rdp/Smad4^tm1Rdp Tg(Pdx1-cre)89.1Dam/0	involves: 129S/SvEv * C57BL/6 * CBA * FVB/N	MGI:3695427
cn15	Cdkn2a^tm1Rdp/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
cx16	Cdkn2a^tm1Rdp/Cdkn2a^+ Tg(NES-TVA)J12Ech/0	involves: 129 * C57BL/6 * FVB/N * SJL	MGI:3835347
cx17	Cdkn2a^tm1Cjs/Cdkn2a^+ Ppm1d^tm1Lad/Ppm1d^tm1Lad Tg(IghMyc)22Bri/0	involves: 129 * C57BL * FVB/N * SJL	MGI:3710182
cx18	Cdkn2a^tm1Cjs/Cdkn2a^+ Tgfb2^tm1Doe/Tgfb2^tm1Doe	involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6	MGI:3848999
cx19	Cdkn2a^tm1Cjs/Cdkn2a^+ Kat5^tm1Jwl/Kat5^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:3814377
cx20	Cdkn2a^tm1Rdp/Cdkn2a^+ Nf1^tm1Tyj/Nf1^+	involves: 129S2/SvPas * 129S6/SvEvTac	MGI:3776070
cx21	Cdkn2a^tm1Sxs/Cdkn2a^+ Tgfb2^tm1Doe/Tgfb2^tm1Doe	involves: 129/Sv * 129P2/OlaHsd * C57BL/6	MGI:3848997
cx22	Cdkn2a^tm1Rdp/Cdkn2a^+ Lig4^tm1Fwa/Lig4^tm1Fwa	involves: 129/Sv * 129S6/SvEvTac * C57BL/6J * SJL	MGI:3656002
cx23	Cdkn2a^tm1Rdp/Cdkn2a^+ Tg(Tyr-NRAS*Q61K)1Bee/?	involves: 129/Sv * C57BL/6 * DBA/2 * SJL	MGI:3768653
cx24	Cdkn2a^tm1Rdp/Cdkn2a^+ X/Tg(Tyr-HRAS)60Lc	involves: 129/Sv * C57BL/6J * CBA/J * FVB/N * SJL	MGI:3815142
cx25	Cdkn2a^tm1Rdp/Cdkn2a^+ Tg(S100b-v-erbB)4496Waw/0	involves: 129/Sv * C57BL/6J * DBA/2J * FVB/N * SJL	MGI:3822321
cx26	Cdkn2a^tm1Rdp/Cdkn2a^+ Terc^tm1Rdp/Terc^tm1Rdp	involves: 129/Sv * C57BL/6J * SJL	MGI:3719054
cx27	Cdkn2a^tm1Cjs/Cdkn2a^+ Tg(CKMM-tTA)A3Rhvh/0 Tg(tetO-Hgf,-EGFP)24Tcre/0	involves: 129X1/SvJ * FVB	MGI:5882411

Genotype
MGI:3842676

ht1

• Allelic Composition: Cdkn2a^tm3(cre)Cjs/Cdkn2a⁺
• Genetic Background: involves: 129S1/Sv * C57BL/6

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

reproductive system

male infertility ( J:147752 )

♂ • males are infertile whereas female mutants are fertile

Genotype
MGI:3814390

ht2

• Allelic Composition: Cdkn2a^tm2.1Rdp/Cdkn2a⁺
• Genetic Background: involves: 129S6/SvEvTac * FVB/N

neoplasm

increased tumor incidence ( J:71394 )

• between 28 and 58 weeks, 4 out of 60 mice develop tumors unlike wild-type mice

Genotype
MGI:3774768

ht3

• Allelic Composition: Cdkn2a^tm1Cjs/Cdkn2a⁺
• Genetic Background: involves: 129X1/SvJ * C57BL/6 * NIH/OlaHsd

neoplasm

increased incidence of tumors by chemical induction ( J:93298 )

• by 20 weeks after a single dose of DMBA and twice weekly application of TPA for 15 weeks, mutants show an increase in papilloma number and size compared to wild-type

• tumors of heterozygous mice show loss of heterozygosity during benign to malignant conversion

increased carcinoma incidence ( J:93298 )

• by 28 weeks, 60% of DMBA/TPA treated heterozygotes develop carcinomas compared to 25% of wild-type

increased papilloma incidence ( J:93298 )

• mutants have an average of 2.6 more papillomas than wild-type after DMBA/TPA treatment

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:93298 )

• by 20 weeks after a single dose of DMBA and twice weekly application of TPA for 15 weeks, mutants show an increase in papilloma number and size compared to wild-type

• tumors of heterozygous mice show loss of heterozygosity during benign to malignant conversion

Genotype
MGI:5308951

cn4

• Allelic Composition: Cdkn2a^tm2.1Rdp/Cdkn2a⁺; Kras^tm4Tyj/Kras⁺; Trp53^tm1Brn/Trp53^tm1Brn; Tg(Pdx1-cre)89.1Dam/0
• Genetic Background: involves: 129 * C57BL/6 * CBA * FVB/N

neoplasm

increased pancreas tumor incidence ( J:108298 )

• mutants develop pancreatic tumors with an average latency of 6.5 weeks

• 20% of tumors exhibit anaplastic carcinoma histology

increased pancreatic ductal adenocarcinoma incidence ( J:108298 )

• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology

endocrine/exocrine glands

increased pancreas tumor incidence ( J:108298 )

• mutants develop pancreatic tumors with an average latency of 6.5 weeks

• 20% of tumors exhibit anaplastic carcinoma histology

increased pancreatic ductal adenocarcinoma incidence ( J:108298 )

• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology

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

Genotype
MGI:5308961

cn5

• Allelic Composition: Cdkn2a^tm2.1Rdp/Cdkn2a⁺; Kras^tm4Tyj/Kras⁺; Trp53^tm1Brn/Trp53⁺; Tg(Pdx1-cre)89.1Dam/0
• Genetic Background: involves: 129 * C57BL/6 * CBA * FVB/N

neoplasm

increased pancreas tumor incidence ( J:108298 )

• mutants develop pancreatic tumors with an average latency of 14.7 weeks

• 19% of tumors exhibit sarcomatoid differentiation

increased pancreatic ductal adenocarcinoma incidence ( J:108298 )

• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology

increased metastatic potential ( J:108298 )

• 25% of tumors exhibit metastasis

endocrine/exocrine glands

increased pancreas tumor incidence ( J:108298 )

• mutants develop pancreatic tumors with an average latency of 14.7 weeks

• 19% of tumors exhibit sarcomatoid differentiation

increased pancreatic ductal adenocarcinoma incidence ( J:108298 )

• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology

Genotype
MGI:3695424

cn6

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

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

Genotype
MGI:3850445

cn7

• Allelic Composition: Cdkn2a^tm2Brn/Cdkn2a⁺; Nf2^tm2Gth/Nf2^tm2Gth
• Genetic Background: involves: 129P2/OlaHsd

mortality/aging

premature death ( J:132943 )

• following adenoviral cre treatment, median survival time is 495 days

neoplasm

increased tumor incidence ( J:132943 )

• following adenoviral cre treatment, 35% of mice develop thoracic tumors (including malignant mesotheliomas, 18 of 52) with a longer latency than in mice homozygous for all alleles

• following adenoviral cre treatment, mice develop hepatomegaly either due to oval cell hyperplasia, cholangio-carcinomas and/or hepatomas, and leiomyomas of the uterus

• following adenoviral cre treatment, 19% of mice develop aspecific tumors not induced by adeno-cre treatment

increased uterus leiomyoma incidence ( J:132943 )

♀ • in 16% of mice following adenoviral cre treatment

increased leukemia incidence ( J:132943 )

• following adenoviral cre treatment, 16% of mice develop monocytic myeloid leukemias

liver/biliary system

enlarged liver ( J:132943 )

• following adenoviral cre treatment, mice develop hepatomegaly either due to oval cell hyperplasia, cholangio-carcinomas and/or hepatomas, and leiomyomas of the uterus

muscle

increased uterus leiomyoma incidence ( J:132943 )

♀ • in 16% of mice following adenoviral cre treatment

growth/size/body

enlarged liver ( J:132943 )

• following adenoviral cre treatment, mice develop hepatomegaly either due to oval cell hyperplasia, cholangio-carcinomas and/or hepatomas, and leiomyomas of the uterus

reproductive system

increased uterus leiomyoma incidence ( J:132943 )

♀ • in 16% of mice following adenoviral cre treatment

Genotype
MGI:4835045

cn8

• Allelic Composition: Cdkn2a^tm2.1Nesh/Cdkn2a⁺; Kras^tm4Tyj/Kras⁺; Trp53^tm1Brn/Trp53⁺; Tg(Tyr-cre/ERT2)13Bos/0
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB

neoplasm

increased spindle cell carcinoma incidence ( J:164588 )

• tamoxifen-treated mice develop melanomas with spindle-like morphology

increased melanoma incidence ( J:164588 )

• 3 of 7 (43%) mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology at a median latency greater than 52 weeks compared with Cdkn2a^tm2.1Nesh/Cdkn2a^tm2.1Nesh Kras^tm4Tyj/Kras⁺ Trp53^tm1Brn/Trp53^tm1Brn Tg(Tyr-cre/ERT2)13Bos mice whose median latency is 14 weeks

pigmentation

abnormal melanocyte morphology ( J:164588 )

• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice

hyperpigmentation ( J:164588 )

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

Genotype
MGI:3850449

cn9

• Allelic Composition: Cdkn2a^tm1.1Brn/Cdkn2a⁺; Nf2^tm2Gth/Nf2^tm2Gth; Trp53^tm1Brn/Trp53^tm1Brn
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd

neoplasm

increased metastatic potential ( J:132943 )

• following adenoviral cre treatment, the parietal pleura often shows invasion with concomitant pleural effusion

increased tumor incidence ( J:132943 )

• following adenoviral cre treatment, 94% of mice develop aggressive thoracic tumors (including malignant mesotheliomas, 15 of 51; and rhabdomyosarcomas, 1 of 51) with the parietal pleura often showing invasion with concomitant pleural effusion

• following adenoviral cre treatment, 1% of mice develop aspecific tumors not induced by adeno-cre treatment

increased rhabdomyosarcoma incidence ( J:132943 )

increased mesothelioma incidence ( J:132943 )

homeostasis/metabolism

pleural effusion ( J:132943 )

• following adenoviral cre treatment, the parietal pleura often shows invasion with concomitant pleural effusion

respiratory system

pleural effusion ( J:132943 )

• following adenoviral cre treatment, the parietal pleura often shows invasion with concomitant pleural effusion

muscle

increased rhabdomyosarcoma incidence ( J:132943 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malignant mesothelioma		DOID:1790	OMIM:156240	J:132943

Genotype
MGI:3695432

cn10

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

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

Genotype
MGI:3695430

cn11

• Allelic Composition: Cdkn2a^tm4Rdp/Cdkn2a⁺; Kras^tm4Tyj/Kras⁺; Tg(Pdx1-cre)89.1Dam/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * CBA

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

Genotype
MGI:5308806

cn12

• Allelic Composition: Cdkn2a^tm4Rdp/Cdkn2a⁺; Kras^tm4Tyj/Kras⁺; Tg(Pdx1-cre)89.1Dam/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N

neoplasm

increased pancreas tumor incidence ( J:108298 )

• mutants develop pancreatic tumors with an average latency of 34.2 weeks

• 43% of tumors exhibit sarcomatoid differentiation

increased pancreatic ductal adenocarcinoma incidence ( J:108298 )

• 57% of tumors exhibit well differentiated ductal adenocarcinoma histology

increased metastatic potential ( J:108298 )

• 69% of tumors exhibit metastasis

endocrine/exocrine glands

increased pancreas tumor incidence ( J:108298 )

• mutants develop pancreatic tumors with an average latency of 34.2 weeks

• 43% of tumors exhibit sarcomatoid differentiation

increased pancreatic ductal adenocarcinoma incidence ( J:108298 )

• 57% of tumors exhibit well differentiated ductal adenocarcinoma histology

Genotype
MGI:3695426

cn13

• Allelic Composition: Cdkn2a^tm4Rdp/Cdkn2a⁺; Kras^tm4Tyj/Kras⁺; Smad4^tm1Rdp/Smad4^tm1Rdp; Tg(Pdx1-cre)89.1Dam/0
• Genetic Background: involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N

mortality/aging

decreased tumor-free survival time ( J:116130 )

• average tumor-free survival is 12.6 weeks

neoplasm

increased tumor incidence ( J:116130 )

• 4 of 12 mice develop intraductal papillary mucinous neoplasms

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

increased stomach tumor incidence ( J:116130 )

• 8 of 12 mice develop gastric cancer

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 4 of 12 mice develop pancreatic ductal adenocarcinoma

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

digestive/alimentary system

increased stomach tumor incidence ( J:116130 )

• 8 of 12 mice develop gastric cancer

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:116130 )

• 4 of 12 mice develop pancreatic ductal adenocarcinoma

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

Genotype
MGI:3695427

cn14

• Allelic Composition: Cdkn2a^tm4Rdp/Cdkn2a⁺; Smad4^tm1Rdp/Smad4^tm1Rdp; Tg(Pdx1-cre)89.1Dam/0
• Genetic Background: involves: 129S/SvEv * C57BL/6 * CBA * FVB/N

neoplasm

neoplasm ( J:116130 )

N • tumor-free survival is greater than 52 weeks and only 1 of 10 mice developed an intraductal papillary mucinous neoplasm

Genotype
MGI:5521487

cn15

• Allelic Composition: Cdkn2a^tm1Rdp/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

neoplasm

increased pancreas tumor incidence ( J:197052 )

• 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

increased pancreatic ductal adenocarcinoma incidence ( J:197052 )

• 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

increased metastatic potential ( J:197052 )

• 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

endocrine/exocrine glands

increased pancreas tumor incidence ( J:197052 )

• 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

increased pancreatic ductal adenocarcinoma incidence ( J:197052 )

• 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

mortality/aging

decreased tumor-free survival time ( J:197052 )

• due to pancreatic tumors

Genotype
MGI:3835347

cx16

• Allelic Composition: Cdkn2a^tm1Rdp/Cdkn2a⁺; Tg(NES-TVA)J12Ech/0
• Genetic Background: involves: 129 * C57BL/6 * FVB/N * SJL

neoplasm

increased glioma incidence ( J:52161 )

• 13 of 25 mice transfected with replication-competent ALV splice acceptor viral vector expressing a constitutively active EGFR develop gliomas unlike similarly treated wild-type mice

nervous system

increased glioma incidence ( J:52161 )

• 13 of 25 mice transfected with replication-competent ALV splice acceptor viral vector expressing a constitutively active EGFR develop gliomas unlike similarly treated wild-type mice

Genotype
MGI:3710182

cx17

• Allelic Composition: Cdkn2a^tm1Cjs/Cdkn2a⁺; Ppm1d^tm1Lad/Ppm1d^tm1Lad; Tg(IghMyc)22Bri/0
• Genetic Background: involves: 129 * C57BL * FVB/N * SJL

mortality/aging

premature death ( J:120284 )

• the median lifespan of >130 days

neoplasm

decreased tumor incidence ( J:120284 )

• similar to mice carrying double Ppm1d^tm1Lad allele without Cdkn2a^tm1Cjs allele, based on increased median survival time, mice carrying single Cdkn2a^tm1Cjs allele were considerably more resistant to tumor formation induced by myc than mice with homozygous wild-type Ppm1d⁺ allele

Genotype
MGI:3848999

cx18

• Allelic Composition: Cdkn2a^tm1Cjs/Cdkn2a⁺; Tgfb2^tm1Doe/Tgfb2^tm1Doe
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6

vision/eye

primary vitreous hyperplasia ( J:149526 )

Genotype
MGI:3814377

cx19

• Allelic Composition: Cdkn2a^tm1Cjs/Cdkn2a⁺; Kat5^tm1Jwl/Kat5⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6

neoplasm

decreased tumor latency ( J:125164 )

• mice exhibit the same early tumor onset as in Cdkn2a^tm1Cjs homozygotes

Genotype
MGI:3776070

cx20

• Allelic Composition: Cdkn2a^tm1Rdp/Cdkn2a⁺; Nf1^tm1Tyj/Nf1⁺
• Genetic Background: involves: 129S2/SvPas * 129S6/SvEvTac

neoplasm

increased neurofibrosarcoma incidence ( J:131914 )

• seen at lower frequencies and greater age (over 1 year) compared to mice heterozygous for Nf1^tm1Tyj and homozygous for Cdkn2a^tm2Rdp

nervous system

increased neurofibrosarcoma incidence ( J:131914 )

• seen at lower frequencies and greater age (over 1 year) compared to mice heterozygous for Nf1^tm1Tyj and homozygous for Cdkn2a^tm2Rdp

Genotype
MGI:3848997

cx21

• Allelic Composition: Cdkn2a^tm1Sxs/Cdkn2a⁺; Tgfb2^tm1Doe/Tgfb2^tm1Doe
• Genetic Background: involves: 129/Sv * 129P2/OlaHsd * C57BL/6

vision/eye

primary vitreous hyperplasia ( J:149526 )

• seen at E13.5

Genotype
MGI:3656002

cx22

• Allelic Composition: Cdkn2a^tm1Rdp/Cdkn2a⁺; Lig4^tm1Fwa/Lig4^tm1Fwa
• Genetic Background: involves: 129/Sv * 129S6/SvEvTac * C57BL/6J * SJL

mortality/aging

prenatal lethality, complete penetrance ( J:63078 )

• no doubly-deficient offspring are observed (0/170)

• numbers of double heterozygotes observed are similar to expected numbers

cellular

increased cellular sensitivity to ionizing radiation ( J:63078 )

• cells are highly sensitive to ionizing radiation compared to wild-type or Cdkn2a-deficient MEFs

increased neuron apoptosis ( J:63078 )

• high levels of pyknotic cells are observed in doubly-deficient embryos

decreased cell proliferation ( J:63078 )

• MEFs show premature growth arrest compared to wild-type MEFs

nervous system

increased neuron apoptosis ( J:63078 )

• high levels of pyknotic cells are observed in doubly-deficient embryos

Genotype
MGI:3768653

cx23

• Allelic Composition: Cdkn2a^tm1Rdp/Cdkn2a⁺; Tg(Tyr-NRAS*Q61K)1Bee/?
• Genetic Background: involves: 129/Sv * C57BL/6 * DBA/2 * SJL

neoplasm

increased cutaneous melanoma incidence ( J:98545 )

• 15 of 18 mice develop cutaneous melanomas within 12 months of birth

integument

increased cutaneous melanoma incidence ( J:98545 )

• 15 of 18 mice develop cutaneous melanomas within 12 months of birth

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
skin melanoma		DOID:8923	OMIM:608035 OMIM:612263	J:98545

Genotype
MGI:3815142

cx24

• Allelic Composition: Cdkn2a^tm1Rdp/Cdkn2a⁺; X/Tg(Tyr-HRAS)60Lc
• Genetic Background: involves: 129/Sv * C57BL/6J * CBA/J * FVB/N * SJL

neoplasm

increased intraocular melanoma incidence ( J:140820 )

♂ • following exposure to UVA and UVB, 2 of 46 mice exhibit uveal melanoma

increased incidence of tumors by UV-induction ( J:140820 )

♂ • following exposure to UVA and UVB, 2 of 46 mice exhibit uveal melanoma

vision/eye

increased intraocular melanoma incidence ( J:140820 )

♂ • following exposure to UVA and UVB, 2 of 46 mice exhibit uveal melanoma

cataract ( J:140820 )

♂ • following exposure to UVA and UVB, only one mouse developed cataracts unlike Cdkn2a^tm1Rdp/Cdkn2a^tm1Rdp Tg(Tyr-HRAS)60Lc mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
uveal melanoma		DOID:6039	OMIM:155720 OMIM:606660 OMIM:606661	J:140820

Genotype
MGI:3822321

cx25

• Allelic Composition: Cdkn2a^tm1Rdp/Cdkn2a⁺; Tg(S100b-v-erbB)4496Waw/0
• Genetic Background: involves: 129/Sv * C57BL/6J * DBA/2J * FVB/N * SJL

neoplasm

increased glioma incidence ( J:82649 )

• mice develop gliomas as in Cdkn2a^tm1Rdp/Cdkn2a^tm1Rdp Tg(S100b-v-erbB)4496Waw mice with loss of function of the wild-type Cdkn2a allele

nervous system

increased glioma incidence ( J:82649 )

• mice develop gliomas as in Cdkn2a^tm1Rdp/Cdkn2a^tm1Rdp Tg(S100b-v-erbB)4496Waw mice with loss of function of the wild-type Cdkn2a allele

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
oligodendroglioma		DOID:3181		J:82649

Genotype
MGI:3719054

cx26

• Allelic Composition: Cdkn2a^tm1Rdp/Cdkn2a⁺; Terc^tm1Rdp/Terc^tm1Rdp
• Genetic Background: involves: 129/Sv * C57BL/6J * SJL

neoplasm

increased tumor incidence ( J:120065 )

• 84% of early generation mutants succumb to tumors with a median tumor-free latency of 71.6 weeks

• late generation mutants show a decrease in percent tumor death and an increase in tumor-free latency, from 84% to 20% and 71.6-104.9 weeks

increased lymphoma incidence ( J:120065 )

• 19% and 23% of early generation and late generation mutants, respectively, develop lymphomas

increased sarcoma incidence ( J:120065 )

• 35% and 39% of early generation and late generation mutants, respectively, develop histocytic sarcomas

• 20% and 23% of early generation and late generation mutants, respectively, develop soft tissue sarcomas

Genotype
MGI:5882411

cx27

• Allelic Composition: Cdkn2a^tm1Cjs/Cdkn2a⁺; Tg(CKMM-tTA)A3Rhvh/0; Tg(tetO-Hgf,-EGFP)24Tcre/0
• Genetic Background: involves: 129X1/SvJ * FVB

muscle

increased rhabdomyosarcoma incidence ( J:237183 )

• mice develop multi-step embryonal rhabdomyosarcoma with a latency of 6 months

• majority of tumors lose the wild-type allele

neoplasm

increased rhabdomyosarcoma incidence ( J:237183 )

• mice develop multi-step embryonal rhabdomyosarcoma with a latency of 6 months

• majority of tumors lose the wild-type allele