Phenotypes associated with this allele

• Allele Symbol: Polr2a^{tm1(cre/ERT2)Bbd}
• Allele Name: targeted mutation 1, Mariano Barbacid
• Allele ID: MGI:3772332
• Summary: 31 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Mapk1^tm1.1Hed/Mapk1^tm1.1Hed Mapk3^tm1Gpg/Mapk3^tm1Gpg Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129	MGI:5508241
cn2	Mapk14^tm2Nbr/Mapk14^tm2Nbr Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	involves: 129 * C57BL/6 * CD-1 * SJL	MGI:3716853
cn3	Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd Raf1^tm2Bacc/Raf1^tm2Bacc	involves: 129P2/OlaHsd	MGI:5508348
cn4	Braf^tm1Sva/Braf^tm1Sva Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd Raf1^tm2Bacc/Raf1^tm2Bacc	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:5508350
cn5	Braf^tm1Sva/Braf^tm1Sva Kras^tm1Bbd/Kras^+ Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd Raf1^tm2Bacc/Raf1^tm2Bacc	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:5508357
cn6	Kras^tm1Bbd/Kras^+ Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd Raf1^tm2Bacc/Raf1^tm2Bacc	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:5508355
cn7	Braf^tm1Mmcm/Braf^+ Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	involves: 129P2/OlaHsd * C57BL/6 * SJL	MGI:3712024
cn8	Cdk6^tm1Bbd/Cdk6^tm1Bbd Kras^tm1Bbd/Kras^+ Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ	MGI:4844194
cn9	Braf^tm1Sva/Braf^tm1Sva Kras^tm1Bbd/Kras^+ Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ	MGI:5508351
cn10	Cdk2^tm1Sgo/Cdk2^tm1Sgo Kras^tm1Bbd/Kras^+ Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ	MGI:4844195
cn11	Cdk4^tm2.2Bbd/Cdk4^tm2.2Bbd Kras^tm1Bbd/Kras^tm1Bbd Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ	MGI:4844188
cn12	Cdk2^tm2Sgo/Cdk2^tm2Sgo Kras^tm1Bbd/Kras^tm2Bbd Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ	MGI:4844189
cn13	Kras^tm1Bbd/Kras^tm2Bbd Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ	MGI:4844190
cn14	Cdk4^tm2.1Bbd/Cdk4^tm2.1Bbd Kras^tm1Bbd/Kras^tm2Bbd Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ	MGI:4844191
cn15	Cdk4^tm2.2Bbd/Cdk4^tm2.1Bbd Kras^tm1Bbd/Kras^tm2Bbd Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ	MGI:4844192
cn16	Kras^tm1Bbd/Kras^+ Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ	MGI:4844193
cn17	Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+ Rnf2^tm1Mvi/Rnf2^tm1Mvi	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/10 * SJL	MGI:3772193
cn18	Fntb^tm1Bbd/Fntb^tm1Bbd Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL	MGI:3582819
cn19	Fntb^tm1Bbd/Fntb^tm1.1Bbd Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL	MGI:3582821
cn20	Fntb^tm1Bbd/Fntb^tm1Bbd Kras^tm1Bbd/Kras^+ Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL	MGI:3582832
cn21	Mapk14^tm1Nbr/Mapk14^tm2Nbr Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL	MGI:3716854
cn22	Kras^tm1Bbd/Kras^+ Mapk14^tm1Nbr/Mapk14^tm2Nbr Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL	MGI:3716855
cn23	Kras^tm1Bbd/Kras^+ Mapk14^tm2Nbr/Mapk14^+ Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL	MGI:3716857
cn24	Cdk2^tm2Sgo/Cdk2^tm2Sgo Cdk4^tm2.1Bbd/Cdk4^tm2.1Bbd Polr2a^tm1(cre/ERT2)Bbd/?	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:3759577
cn25	E4f1^tm1Pisc/E4f1^tm1.1Llca Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:4867861
cn26	Cdkn2a^tm1Rdp/Cdkn2a^tm1Rdp E4f1^tm1Pisc/E4f1^tm1.1Llca Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	involves: 129/Sv * 129S4/SvJae * C57BL/6 * SJL	MGI:4867863
cn27	Cdc20^tm1.1Mama/Cdc20^tm1.2Mama Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	involves: 129/Sv * BALB/cJ * C57BL/6 * CD-1 * SJL	MGI:4887575
cn28	Map2k1^tm1Chrn/Map2k1^tm1Chrn Map2k2^tm1Chrn/Map2k2^tm1Chrn Polr2a^tm1(cre/ERT2)Bbd/Polr2a^tm1(cre/ERT2)Bbd	involves: 129/Sv * C57BL/6J * SJL	MGI:5508246
cn29	Ebf1^tm1.1Rug/Ebf1^tm1.1Rug Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+ Tg(BCL2)#Wehi/0	involves: C57BL/6 * C57BL/6JWehi * SJL * SJL/JWehi	MGI:5316372
cn30	Ebf1^tm1.1Rug/Ebf1^tm1.1Rug Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	involves: C57BL/6 * SJL	MGI:5316370
cn31	Mastl^tm1.1Mama/Mastl^tm1.1Mama Polr2a^tm1(cre/ERT2)Bbd/Polr2a^+	Not Specified	MGI:5556128

Genotype
MGI:5508241

cn1

• Allelic Composition: Mapk1^tm1.1Hed/Mapk1^tm1.1Hed; Mapk3^tm1Gpg/Mapk3^tm1Gpg; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129

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

mortality/aging

premature death ( J:172200 )

• mice fed a tamoxifen-containing diet show a deterioration of health and die within 3 weeks due to multiple organ failure

Genotype
MGI:3716853

cn2

• Allelic Composition: Mapk14^tm2Nbr/Mapk14^tm2Nbr; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: involves: 129 * C57BL/6 * CD-1 * SJL

respiratory system

abnormal lung morphology ( J:122397 )

• 2 weeks after 5-hydroxytamoxifen treatment, lungs show increased cellularity

abnormal lung epithelium morphology ( J:122397 )

• lungs show multicellular septa and reduction of the alveolar lumen as early as 2 weeks after 5-hydroxytamoxifen treatment, and is marked after 8 weeks, extending to 60% of the lungs

abnormal pulmonary alveolus epithelial cell morphology ( J:122397 )

• after 5-hydroxytamoxifen treatment, there is an increase in alveolar type II cells compared to controls

• when cultured, isolated progenitor and stem cells (SP-C+, CC-10+ cells) when put under differentiation conditions do not have the capacity to form single positive cells; overexpression of C/EBP alpha in these cells restores the capacity to form SP-C+ cells

cellular

abnormal cell cycle ( J:122397 )

increased cell proliferation ( J:122397 )

• 8 weeks after 5-hydroxytamoxifen treatment, lungs display hyperproliferation (~5-fold increased proliferation) compared to wild-type or heterozygous lungs

Genotype
MGI:5508348

cn3

• Allelic Composition: Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}; Raf1^tm2Bacc/Raf1^tm2Bacc
• Genetic Background: involves: 129P2/OlaHsd

normal phenotype

no abnormal phenotype detected ( J:172200 )

• 30 day old mice fed a tamoxifen diet for 3 months show normal weight and activity and no obvious anatomical defects

Genotype
MGI:5508350

cn4

• Allelic Composition: Braf^tm1Sva/Braf^tm1Sva; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}; Raf1^tm2Bacc/Raf1^tm2Bacc
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

normal phenotype

no abnormal phenotype detected ( J:172200 )

• 30 day old mice fed a tamoxifen diet for 3 months are healthy and show normal weight and activity and no obvious anatomical defects

Genotype
MGI:5508357

cn5

• Allelic Composition: Braf^tm1Sva/Braf^tm1Sva; Kras^tm1Bbd/Kras⁺; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}; Raf1^tm2Bacc/Raf1^tm2Bacc
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

cellular

decreased cell proliferation ( J:172200 )

• primary mouse embryonic fibroblasts exposed to 4OHT for 5 days to activate cre/ERT2 recombinase exhibit decreased proliferation that is similar to that in single Kras mutants without further additive effects

Genotype
MGI:5508355

cn6

• Allelic Composition: Kras^tm1Bbd/Kras⁺; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}; Raf1^tm2Bacc/Raf1^tm2Bacc
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

cellular

decreased cell proliferation ( J:172200 )

• primary mouse embryonic fibroblasts exposed to 4OHT for 5 days to activate cre/ERT2 recombinase exhibit decreased proliferation compared to single Kras heterozygotes

Genotype
MGI:3712024

cn7

• Allelic Composition: Braf^tm1Mmcm/Braf⁺; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * SJL

neoplasm

increased lung adenoma incidence ( J:121715 )

• with induction of Cre expression from the transgene, multiple adenomatous tumors form in mouse lungs

respiratory system

increased lung adenoma incidence ( J:121715 )

• with induction of Cre expression from the transgene, multiple adenomatous tumors form in mouse lungs

Genotype
MGI:4844194

cn8

• Allelic Composition: Cdk6^tm1Bbd/Cdk6^tm1Bbd; Kras^tm1Bbd/Kras⁺; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

premature death ( J:161780 )

• 50% of tamoxifen-treated mice survive at 40 weeks

neoplasm

increased adenoma incidence ( J:161780 )

• in mice treated with tamoxifen at weaning

increased lung non-small cell carcinoma incidence ( J:161780 )

• in mice treated with tamoxifen at weaning

respiratory system

increased lung non-small cell carcinoma incidence ( J:161780 )

• in mice treated with tamoxifen at weaning

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
lung cancer		DOID:1324	OMIM:211980 OMIM:608935 OMIM:612571 OMIM:612593 OMIM:614210	J:161780

Genotype
MGI:5508351

cn9

• Allelic Composition: Braf^tm1Sva/Braf^tm1Sva; Kras^tm1Bbd/Kras⁺; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

cellular

decreased cell proliferation ( J:172200 )

• primary mouse embryonic fibroblasts exposed to 4OHT for 5 days to activate cre/ERT2 recombinase exhibit decreased proliferation compared to single Kras heterozygotes

Genotype
MGI:4844195

cn10

• Allelic Composition: Cdk2^tm1Sgo/Cdk2^tm1Sgo; Kras^tm1Bbd/Kras⁺; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

premature death ( J:161780 )

• mice treated tamoxifen at weaning exhibit an increase in lifespan of 8 weeks (42 weeks) compared with similarly treated Kras^tm1Bbd/Kras⁺ Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} littermates (34 weeks)

neoplasm

decreased tumor incidence ( J:161780 )

• tamoxifen-treated mice exhibit reduced tumor burden compared with similarly treated Kras^tm1Bbd/Kras⁺ Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

Genotype
MGI:4844188

cn11

• Allelic Composition: Cdk4^tm2.2Bbd/Cdk4^tm2.2Bbd; Kras^tm1Bbd/Kras^tm1Bbd; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

neoplasm

decreased tumor incidence ( J:161780 )

• tamoxifen-treated mice exhibit reduced tumor burden and tumor grade compared with similarly treated Kras^tm1Bbd/Kras⁺ Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

Genotype
MGI:4844189

cn12

• Allelic Composition: Cdk2^tm2Sgo/Cdk2^tm2Sgo; Kras^tm1Bbd/Kras^tm2Bbd; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

premature death ( J:161780 )

• tamoxifen-treated mice exhibit an increase in lifespan compared with similarly treated Kras^tm1Bbd/Kras⁺ Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} littermates

neoplasm

decreased tumor incidence ( J:161780 )

• tamoxifen-treated mice exhibit reduced tumor burden and tumor grade compared with similarly treated Kras^tm1Bbd/Kras⁺ Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

Genotype
MGI:4844190

cn13

• Allelic Composition: Kras^tm1Bbd/Kras^tm2Bbd; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

premature death ( J:161780 )

• 50% survival for tamoxifen-treated mice is 25 weeks compared with 42 weeks for similarly treated Kras^tm1Bbd/Kras⁺ Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} littermates

neoplasm

increased lung tumor incidence ( J:161780 )

• lung tumors in tamoxifen-treated mice are more aggressive than in similarly treated Kras^tm1Bbd/Kras⁺ Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

• however, treatment with the Cdk4 inhibitor PD0332991 reduces tumor formation

increased lung non-small cell carcinoma incidence ( J:161780 )

• in mice treated with tamoxifen

cellular

increased cell proliferation ( J:161780 )

• proliferation of lung cells in tamoxifen-treated mice exhibit 8- to 10-fold greater proliferation than in Cdk4^tm2.1Bbd/Cdk4^tm2.1Bbd Kras^tm1Bbd/Kras^tm2Bbd Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

respiratory system

increased lung tumor incidence ( J:161780 )

• lung tumors in tamoxifen-treated mice are more aggressive than in similarly treated Kras^tm1Bbd/Kras⁺ Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

• however, treatment with the Cdk4 inhibitor PD0332991 reduces tumor formation

increased lung non-small cell carcinoma incidence ( J:161780 )

• in mice treated with tamoxifen

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
lung cancer		DOID:1324	OMIM:211980 OMIM:608935 OMIM:612571 OMIM:612593 OMIM:614210	J:161780

Genotype
MGI:4844191

cn14

• Allelic Composition: Cdk4^tm2.1Bbd/Cdk4^tm2.1Bbd; Kras^tm1Bbd/Kras^tm2Bbd; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

neoplasm

decreased tumor growth/size ( J:161780 )

• lung cells in tamoxifen-treated mice exhibit 8- to 10-fold reduction in proliferation and early senescence compared to in similarly treated Kras^tm1Bbd/Kras^tm2Bbd Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

increased adenocarcinoma incidence ( J:161780 )

• tamoxifen-treated mice exhibit adenocarcinomas that are not as severe as in Kras^tm1Bbd/Kras^tm2Bbd Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

cellular

decreased cell proliferation ( J:161780 )

• proliferation of lung cells in tamoxifen-treated mice exhibit 8- to 10-fold less proliferation than in similarly treated Kras^tm1Bbd/Kras^tm2Bbd Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

early cellular replicative senescence ( J:161780 )

• tamoxifen-treated mice exhibit increased cell replicative senescence in the lungs compared to in similarly treated Kras^tm1Bbd/Kras^tm2Bbd Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

Genotype
MGI:4844192

cn15

• Allelic Composition: Cdk4^tm2.2Bbd/Cdk4^tm2.1Bbd; Kras^tm1Bbd/Kras^tm2Bbd; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

neoplasm

decreased tumor growth/size ( J:161780 )

• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit decreased proliferation and early senescence of tumor cells compared with tamoxifen and infected with GFP-expressing adenovirus

decreased tumor incidence ( J:161780 )

• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit reduced lesions compared to in mice treated with tamoxifen and infected with GFP-expressing adenovirus

increased tumor incidence ( J:161780 )

• in tamoxifen-treated mice as in similarly treated Kras^tm1Bbd/Kras^tm2Bbd Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd} mice

cellular

decreased cell proliferation ( J:161780 )

• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit early senescence of tumor cells compared with tamoxifen and infected with GFP-expressing adenovirus

early cellular replicative senescence ( J:161780 )

• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit decreased proliferation of tumor cells compared with tamoxifen and infected with GFP-expressing adenovirus

Genotype
MGI:4844193

cn16

• Allelic Composition: Kras^tm1Bbd/Kras⁺; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ

mortality/aging

premature death ( J:161780 )

• the mean lifespan of mice treated tamoxifen is 34-42 weeks

neoplasm

increased adenoma incidence ( J:161780 )

• in mice treated with tamoxifen at weaning

increased lung non-small cell carcinoma incidence ( J:161780 )

• in mice treated with tamoxifen at weaning

respiratory system

increased lung non-small cell carcinoma incidence ( J:161780 )

• in mice treated with tamoxifen at weaning

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
lung cancer		DOID:1324	OMIM:211980 OMIM:608935 OMIM:612571 OMIM:612593 OMIM:614210	J:161780

Genotype
MGI:3772193

cn17

• Allelic Composition: Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺; Rnf2^tm1Mvi/Rnf2^tm1Mvi
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/10 * SJL

hematopoietic system

abnormal bone marrow cell morphology/development ( J:130397 )

• when cells are exposed to tamoxifen ex vivo, the progenitor compartment is increased compared to unexposed cells

abnormal common myeloid progenitor cell morphology ( J:130397 )

• when cells are exposed to tamoxifen ex vivo, the number of myeloid colony forming units is increased compared to unexposed cells

• when cells are exposed to tamoxifen ex vivo, the proliferation of myeloid precursor cells is increased compared to unexposed cells

• however, myeloid cell apoptosis rates and differentiation are normal

decreased B cell number ( J:130397 )

• when cells are exposed to tamoxifen ex vivo, fewer pre-B cells are present compared to unexposed cells

immune system

decreased B cell number ( J:130397 )

• when cells are exposed to tamoxifen ex vivo, fewer pre-B cells are present compared to unexposed cells

Genotype
MGI:3582819

cn18

• Allelic Composition: Fntb^tm1Bbd/Fntb^tm1Bbd; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL

cellular

decreased cell proliferation ( J:98944 )

• double homozygous MEFs treated with 4-hydroxy-tamoxifen to induce Cre mediated recombination proliferate less efficiently compared to untreated double homozygous MEFs

hematopoietic system

small spleen ( J:98944 )

• about a 20% decrease in spleen size is seen in 6 month old double homozygous treated with 4-hydroxy-tamoxifen at 10 days of age

abnormal hematopoietic system physiology ( J:98944 )

• removal of 0.8 ml of blood from 6 month old double homozygous treated with 4-hydroxy-tamoxifen at 10 days of age resulted in a smaller increase in spleen size and in the splenic erythroid compartment compared to controls

immune system

small spleen ( J:98944 )

• about a 20% decrease in spleen size is seen in 6 month old double homozygous treated with 4-hydroxy-tamoxifen at 10 days of age

neoplasm

decreased incidence of tumors by chemical induction ( J:98944 )

• treatment with 4-hydroxy-tamoxifen 2 weeks after treatment with 7,12 dimethyl-benzanthracene (DMBA) and 12-o-tetradecanoylphorbol-13-acetate (TPA) results in fewer and smaller papillomas compared to mice that were mot treated with 4-hydroxy-tamoxifen

• however, treatment with 4-hydroxy-tamoxifen for 20 weeks before treatment with DMBA and TPA had no effect on tumor incidence, size, or pathological appearance compared to mice that were not treated with 4-hydroxy-tamoxifen

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:98944 )

• treatment with 4-hydroxy-tamoxifen 2 weeks after treatment with 7,12 dimethyl-benzanthracene (DMBA) and 12-o-tetradecanoylphorbol-13-acetate (TPA) results in fewer and smaller papillomas compared to mice that were mot treated with 4-hydroxy-tamoxifen

• however, treatment with 4-hydroxy-tamoxifen for 20 weeks before treatment with DMBA and TPA had no effect on tumor incidence, size, or pathological appearance compared to mice that were not treated with 4-hydroxy-tamoxifen

delayed wound healing ( J:98944 )

• 6 month old double homozygous treated with 4-hydroxy-tamoxifen at 10 days of age take 12 days to fully heal compared to 9 days for control mice; however at 10 weeks of age no difference was seen in wound healing or liver regeneration after partial hepatectomy (not done in 6 month old mice)

Genotype
MGI:3582821

cn19

• Allelic Composition: Fntb^tm1Bbd/Fntb^tm1.1Bbd; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL

cellular

decreased cell proliferation ( J:98944 )

• double homozygous MEFs treated with 4-hydroxy-tamoxifen to induce Cre mediated recombination proliferate less efficiently compared to untreated double homozygous MEFs

hematopoietic system

small spleen ( J:98944 )

• about a 20% decrease in spleen size is seen in 6 month old double homozygous treated with 4-hydroxy-tamoxifen at 10 days of age

abnormal hematopoietic system physiology ( J:98944 )

• removal of 0.8 ml of blood from 6 month old double homozygous treated with 4-hydroxy-tamoxifen at 10 days of age resulted in a smaller increase in spleen size and in the splenic erythroid compartment compared to controls

immune system

small spleen ( J:98944 )

• about a 20% decrease in spleen size is seen in 6 month old double homozygous treated with 4-hydroxy-tamoxifen at 10 days of age

neoplasm

decreased incidence of tumors by chemical induction ( J:98944 )

• treatment with 4-hydroxy-tamoxifen 2 weeks after treatment with 7,12 dimethyl-benzanthracene (DMBA) and 12-o-tetradecanoylphorbol-13-acetate (TPA) results in fewer and smaller papillomas compared to mice that were mot treated with 4-hydroxy-tamoxifen

• however, treatment with 4-hydroxy-tamoxifen for 20 weeks before treatment with DMBA and TPA had no effect on tumor incidence, size, or pathological appearance compared to mice that were not treated with 4-hydroxy-tamoxifen

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:98944 )

• treatment with 4-hydroxy-tamoxifen 2 weeks after treatment with 7,12 dimethyl-benzanthracene (DMBA) and 12-o-tetradecanoylphorbol-13-acetate (TPA) results in fewer and smaller papillomas compared to mice that were mot treated with 4-hydroxy-tamoxifen

• however, treatment with 4-hydroxy-tamoxifen for 20 weeks before treatment with DMBA and TPA had no effect on tumor incidence, size, or pathological appearance compared to mice that were not treated with 4-hydroxy-tamoxifen

delayed wound healing ( J:98944 )

• 6 month old double homozygous treated with 4-hydroxy-tamoxifen at 10 days of age take 12 days to fully heal compared to 9 days for control mice; however at 10 weeks of age no difference was seen in wound healing or liver regeneration after partial hepatectomy (not done in 6 month old mice)

Genotype
MGI:3582832

cn20

• Allelic Composition: Fntb^tm1Bbd/Fntb^tm1Bbd; Kras^tm1Bbd/Kras⁺; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL

neoplasm

increased lung adenoma incidence ( J:98944 )

• after treatment with 4-hydroxy-tamoxifen for 24 weeks multiple lung adenomas develop by 7 months of age; however no difference in the latency, number, or size of tumors was seen compared to double mutants wild-type for Fntb

increased lung adenocarcinoma incidence ( J:98944 )

• after treatment with 4-hydroxy-tamoxifen for 24 weeks multiple lung adenocarcinomas develop by 7 months of age; however no difference in the latency, number, or size of tumors was seen compared to double mutants wild-type for Fntb

respiratory system

increased lung adenoma incidence ( J:98944 )

• after treatment with 4-hydroxy-tamoxifen for 24 weeks multiple lung adenomas develop by 7 months of age; however no difference in the latency, number, or size of tumors was seen compared to double mutants wild-type for Fntb

increased lung adenocarcinoma incidence ( J:98944 )

• after treatment with 4-hydroxy-tamoxifen for 24 weeks multiple lung adenocarcinomas develop by 7 months of age; however no difference in the latency, number, or size of tumors was seen compared to double mutants wild-type for Fntb

Genotype
MGI:3716854

cn21

• Allelic Composition: Mapk14^tm1Nbr/Mapk14^tm2Nbr; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL

mortality/aging

premature death ( J:122397 )

• mice die before week 32 due to increased lung cancer progression

respiratory system

enlarged lung ( J:122397 )

• 20 weeks after treatment, lungs are increased in size

increased lung tumor incidence ( J:122397 )

• 2 weeks after 5-hydroxytamoxifen treatment, small tumors are found in the lungs

• 20 weeks after treatment, lungs are oversized with 2-3 times as many tumors, many often >2mm in diameter, while lungs of Kras, Mapk14 heterozygotes have normal lungs with fewer, smaller tumors; tumors in Mapk14 homozygotes are more poorly differentiated and have higher mitotic indices

• at 26 weeks, total tumor number is slightly higher than in controls with much higher numbers of tumors larger than 2 mm in diameter and a higher ratio of lung mass to total mass

increased lung adenoma incidence ( J:122397 )

• tumors are detected 2 weeks after 5-hydroxytamoxifen treatment and after 4 weeks, clear signs of adenomas are present in most lungs compared to only a few small adenomas in lungs of treated Kras, Mapk14^tm2Nbr/+ control mice

increased lung adenocarcinoma incidence ( J:122397 )

• adenocarcinomas are detected at 15 weeks but not in controls

abnormal lung development ( J:122397 )

• lung differentiation is abnormal with increased SP-C-positive cells

neoplasm

abnormal tumor incidence ( J:122397 )

• mice also have tumors in the thymus and organs such as kidney and liver by 24 weeks after treatment whereas controls only have tumors in lungs and thymus

increased lung tumor incidence ( J:122397 )

• 2 weeks after 5-hydroxytamoxifen treatment, small tumors are found in the lungs

• 20 weeks after treatment, lungs are oversized with 2-3 times as many tumors, many often >2mm in diameter, while lungs of Kras, Mapk14 heterozygotes have normal lungs with fewer, smaller tumors; tumors in Mapk14 homozygotes are more poorly differentiated and have higher mitotic indices

• at 26 weeks, total tumor number is slightly higher than in controls with much higher numbers of tumors larger than 2 mm in diameter and a higher ratio of lung mass to total mass

increased lung adenoma incidence ( J:122397 )

• tumors are detected 2 weeks after 5-hydroxytamoxifen treatment and after 4 weeks, clear signs of adenomas are present in most lungs compared to only a few small adenomas in lungs of treated Kras, Mapk14^tm2Nbr/+ control mice

increased lung adenocarcinoma incidence ( J:122397 )

• adenocarcinomas are detected at 15 weeks but not in controls

growth/size/body

enlarged lung ( J:122397 )

• 20 weeks after treatment, lungs are increased in size

Genotype
MGI:3716855

cn22

• Allelic Composition: Kras^tm1Bbd/Kras⁺; Mapk14^tm1Nbr/Mapk14^tm2Nbr; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL

mortality/aging

premature death ( J:122397 )

• mice die before week 32 due to increased lung cancer progression

respiratory system

enlarged lung ( J:122397 )

• 20 weeks after treatment, lungs are increased in size

increased lung tumor incidence ( J:122397 )

• 2 weeks after 5-hydroxytamoxifen treatment, small tumors are found in the lungs

• 20 weeks after treatment, lungs are oversized with 2-3 times as many tumors, many often >2mm in diameter, while lungs of Kras, Mapk14 heterozygotes have normal lungs with fewer, smaller tumors; tumors in Mapk14 homozygotes are more poorly differentiated and have higher mitotic indices

• at 26 weeks, total tumor number is slightly higher than in controls with much higher numbers of tumors larger than 2 mm in diameter and a higher ratio of lung mass to total mass

increased lung adenoma incidence ( J:122397 )

• tumors are detected 2 weeks after 5-hydroxytamoxifen treatment and after 4 weeks, clear signs of adenomas are present in most lungs compared to only a few small adenomas in lungs of treated Kras, Mapk14^tm2Nbr/+ control mice

increased lung adenocarcinoma incidence ( J:122397 )

• adenocarcinomas are detected at 15 weeks but not in controls

abnormal lung development ( J:122397 )

• lung differentiation is abnormal with increased SP-C-positive cells

neoplasm

abnormal tumor incidence ( J:122397 )

• mice also have tumors in the thymus and organs such as kidney and liver by 24 weeks after treatment whereas controls only have tumors in lungs and thymus

increased lung tumor incidence ( J:122397 )

• 2 weeks after 5-hydroxytamoxifen treatment, small tumors are found in the lungs

• 20 weeks after treatment, lungs are oversized with 2-3 times as many tumors, many often >2mm in diameter, while lungs of Kras, Mapk14 heterozygotes have normal lungs with fewer, smaller tumors; tumors in Mapk14 homozygotes are more poorly differentiated and have higher mitotic indices

• at 26 weeks, total tumor number is slightly higher than in controls with much higher numbers of tumors larger than 2 mm in diameter and a higher ratio of lung mass to total mass

increased lung adenoma incidence ( J:122397 )

• tumors are detected 2 weeks after 5-hydroxytamoxifen treatment and after 4 weeks, clear signs of adenomas are present in most lungs compared to only a few small adenomas in lungs of treated Kras, Mapk14^tm2Nbr/+ control mice

increased lung adenocarcinoma incidence ( J:122397 )

• adenocarcinomas are detected at 15 weeks but not in controls

growth/size/body

enlarged lung ( J:122397 )

• 20 weeks after treatment, lungs are increased in size

Genotype
MGI:3716857

cn23

• Allelic Composition: Kras^tm1Bbd/Kras⁺; Mapk14^tm2Nbr/Mapk14⁺; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL

mortality/aging

premature death ( J:122397 )

• mice live up to 40 weeks

neoplasm

increased hemolymphoid system tumor incidence ( J:122397 )

• by 24 weeks, mice develop tumors in the thymus

increased lung tumor incidence ( J:122397 )

• by 24 weeks, mice develop tumors in lungs

increased lung adenoma incidence ( J:122397 )

• at 4 weeks after 5-hydroxytamoxifen treatment, a few small adenomas are observed in some animals

respiratory system

increased lung tumor incidence ( J:122397 )

• by 24 weeks, mice develop tumors in lungs

increased lung adenoma incidence ( J:122397 )

• at 4 weeks after 5-hydroxytamoxifen treatment, a few small adenomas are observed in some animals

Genotype
MGI:3759577

cn24

• Allelic Composition: Cdk2^tm2Sgo/Cdk2^tm2Sgo; Cdk4^tm2.1Bbd/Cdk4^tm2.1Bbd; Polr2a^{tm1(cre/ERT2)Bbd}/?
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

growth/size/body

decreased body size ( J:125217 )

• when 5 month old mice were treated with tamoxifen they exhibit reduced body size associated with the loss of the Cdk4 function

immune system

increased susceptibility to autoimmune diabetes ( J:125217 )

• when 5 month old mice were treated with tamoxifen they exhibit diabetes associated with the loss of the Cdk4 function

hematopoietic system

hematopoietic system phenotype ( J:125217 )

N • adult hematopoiesis is normal following tamoxifen treatment at 5 months of age

liver/biliary system

liver/biliary system phenotype ( J:125217 )

N • liver regeneration is normal following tamoxifen treatment at 5 months of age

Genotype
MGI:4867861

cn25

• Allelic Composition: E4f1^tm1Pisc/E4f1^tm1.1Llca; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * SJL

homeostasis/metabolism

impaired wound healing ( J:167157 )

• after topical application of 4-hydroxytamoxifen

integument

alopecia ( J:167157 )

• topical application of 4-hydroxytamoxifen to the unshaved tail results in complete alopecia by 6 weeks after application

abnormal hair follicle bulge morphology ( J:167157 )

• fewer hair follicle bulges are detected 4 - 6 weeks after topical application of 4-hydroxytamoxifen

• at 2 - 3 weeks after topical application of 4-hydroxytamoxifen the long term retaining cell region is expanded but by 6 weeks after application long term retaining cells appear to be lost

abnormal skin morphology ( J:167157 )

• broad disorganization of the interfollicular epithelium develops by 3 - 4 weeks after topical application of 4-hydroxytamoxifen

• hyperkeratosis is associated with loss of cellularity in the interfollicular epithelium

hyperkeratosis ( J:167157 )

• develops by 3 - 4 weeks after topical application of 4-hydroxytamoxifen

absent epidermis stratum granulosum ( J:167157 )

• after topical application of 4-hydroxytamoxifen

absent suprabasal layer ( J:167157 )

• after topical application of 4-hydroxytamoxifen

epidermal hyperplasia ( J:167157 )

• massive hyperplasia with increased cellularity in the interfollicular epithelium and the infundibulum in the first few weeks after topical application of 4-hydroxytamoxifen

• no abnormal cell death is seen in these lesions

spontaneous skin ulceration ( J:167157 )

• by 2 - 4 weeks after topical application of 4-hydroxytamoxifen, severe skin ulcerative lesions develop

abnormal skin condition ( J:167157 )

• between 1 - 2 weeks after topical application of 4-hydroxytamoxifen, back skin is ruffled and wrinkled

thick skin ( J:167157 )

• between 1 - 2 weeks after topical application of 4-hydroxytamoxifen, back skin is thickened

abnormal skin physiology ( J:167157 )

• increase in the proportion of proliferating epidermal cells in the first few weeks after topical application of 4-hydroxytamoxifen

abnormal keratinocyte physiology ( J:167157 )

• after 10 - 15 days in culture keratinocytes from 4-hydroxytamoxifen treated skin fail to develop typical holoclones (corresponding to long term clonal outgrowth of epidermal stem cells)

Genotype
MGI:4867863

cn26

• Allelic Composition: Cdkn2a^tm1Rdp/Cdkn2a^tm1Rdp; E4f1^tm1Pisc/E4f1^tm1.1Llca; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: involves: 129/Sv * 129S4/SvJae * C57BL/6 * SJL

integument

hyperkeratosis ( J:167157 )

• development of hyperkeratosis following 4-hydroxytamoxifen treatment is reduced and delayed compared to mutant mice wild-type for Cdkn2a

epidermal hyperplasia ( J:167157 )

• development of hyperplasia following 4-hydroxytamoxifen treatment is reduced and delayed compared to mutant mice wild-type for Cdkn2a

abnormal keratinocyte physiology ( J:167157 )

• partial restoration in long term outgrowth of 4-hydroxytamoxifen exposed keratinocytes in culture compared to mutant mice wild-type for Cdkn2a

Genotype
MGI:4887575

cn27

• Allelic Composition: Cdc20^tm1.1Mama/Cdc20^tm1.2Mama; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: involves: 129/Sv * BALB/cJ * C57BL/6 * CD-1 * SJL

mortality/aging

premature death ( J:167609 )

• after 8 to 10 days on a tamoxifen diet

• however, survival is increased when older mice (1 year old) are treated with tamoxifen

cellular

abnormal mitosis ( J:167609 )

• tamoxifen-treated mice exhibit widespread metaphase arrest in proliferative areas of the intestine and testis unlike in control mice

• topical treatment results in metaphase figures in the basal layer and in the hair follicle cells in depilated mice compared to in similarly treated control mice

decreased cell proliferation ( J:167609 )

• tamoxifen-treated mice exhibit reduced proliferation in the testis and spleen compared with control mice

neoplasm

decreased tumor growth/size ( J:167609 )

• in a two-stage carcinogenesis protocol, tamoxifen-treated mice exhibit tumor arrest unlike similarly treated control mice

tumor regression ( J:167609 )

• in tamoxifen-treated mice

integument

delayed hair regrowth ( J:167609 )

• following topical application of tamoxifen, depilated mice exhibit impaired hair regeneration compared with similarly treated control mice

abnormal epidermis stratum basale morphology ( J:167609 )

• topical treatment results in metaphase figures in the basal layer compared to in similarly treated control mice

digestive/alimentary system

abnormal intestinal epithelium morphology ( J:167609 )

• tamoxifen-treated mice exhibit loss of intestinal epithelium unlike in control mice

growth/size/body

weight loss ( J:167609 )

• in tamoxifen-treated mice

Genotype
MGI:5508246

cn28

• Allelic Composition: Map2k1^tm1Chrn/Map2k1^tm1Chrn; Map2k2^tm1Chrn/Map2k2^tm1Chrn; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a^{tm1(cre/ERT2)Bbd}
• Genetic Background: involves: 129/Sv * C57BL/6J * SJL

mortality/aging

premature death ( J:172200 )

• mice fed a tamoxifen diet at 30 days of age show rapid deterioration of their health and die 2 weeks after starting the tamoxifen diet

digestive/alimentary system

abnormal intestine morphology ( J:172200 )

• mice fed a tamoxifen diet exhibit severe alterations in the structure of intestinal and colonic tissue

abnormal crypts of Lieberkuhn morphology ( J:172200 )

• severe shortening of crypts in the colon of tamoxifen fed mice

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:172200 )

• severe shortening of crypts in the colon of tamoxifen fed mice

Genotype
MGI:5316372

cn29

• Allelic Composition: Ebf1^tm1.1Rug/Ebf1^tm1.1Rug; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺; Tg(BCL2)#Wehi/0
• Genetic Background: involves: C57BL/6 * C57BL/6JWehi * SJL * SJL/JWehi

immune system

decreased immature B cell number ( J:182210 )

• fewer CD25-kappa+ immature B cells in tamoxifen-treated mice

decreased pre-B cell number ( J:182210 )

• fewer CD25+kappa- pre-B cells in tamoxifen-treated mice

hematopoietic system

decreased immature B cell number ( J:182210 )

• fewer CD25-kappa+ immature B cells in tamoxifen-treated mice

decreased pre-B cell number ( J:182210 )

• fewer CD25+kappa- pre-B cells in tamoxifen-treated mice

Genotype
MGI:5316370

cn30

• Allelic Composition: Ebf1^tm1.1Rug/Ebf1^tm1.1Rug; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: involves: C57BL/6 * SJL

immune system

immune system phenotype ( J:182210 )

N • tamoxifen-treated mice exhibit normal somatic hypermutation

increased B cell apoptosis ( J:182210 )

• tamoxifen-treated pro-B cells exhibit reduced survival compared with wild-type mice that cannot be rescued by expression of Bcl2 or Foxo1 or transformation with A-MuLV

• stimulated B cells from tamoxifen-treated mice exhibit reduced survival compared with control cells

• however, expression of Myb or BAFF rescues B cell survival and expression of Bcl2l1 partially rescues B survival

decreased B cell proliferation ( J:182210 )

• with cell cycle defects in tamoxifen-treated mice

• of B cells from tamoxifen-treated mice stimulated with LPS, CpG or anti-IgM

• tamoxifen-treated mice exhibit impaired germinal center formation and germinal center B cell proliferation compared with control mice

• however, B cell proliferation is rescued by transformation with A-MuLV

decreased immature B cell number ( J:182210 )

• in tamoxifen-treated mice

decreased transitional stage B cell number ( J:182210 )

• in tamoxifen-treated mice

arrested B cell differentiation ( J:182210 )

• of pre-B cells from tamoxifen-treated mice in vitro

decreased germinal center B cell number ( J:182210 )

• in tamoxifen-treated mice, less severe 12 days after immunization

decreased marginal zone B cell number ( J:182210 )

• in tamoxifen-treated mice

decreased pre-B cell number ( J:182210 )

• reduced frequency of B220^intCD43- pre-B cells in tamoxifen-treated mice

increased B cell number ( J:182210 )

• increased number of recirculating B220^hiCD43- B cells in tamoxifen-treated mice

decreased spleen germinal center number ( J:182210 )

• in immunized tamoxifen-treated mice

abnormal germinal center B cell physiology ( J:182210 )

• tamoxifen-treated mice exhibit impaired germinal center formation and germinal center B cell proliferation compared with control mice

decreased IgG1 level ( J:182210 )

• by a factor of 5 in tamoxifen treated mice

decreased IgG3 level ( J:182210 )

• by a factor of 3 in tamoxifen treated mice

cellular

increased B cell apoptosis ( J:182210 )

• tamoxifen-treated pro-B cells exhibit reduced survival compared with wild-type mice that cannot be rescued by expression of Bcl2 or Foxo1 or transformation with A-MuLV

• stimulated B cells from tamoxifen-treated mice exhibit reduced survival compared with control cells

• however, expression of Myb or BAFF rescues B cell survival and expression of Bcl2l1 partially rescues B survival

decreased B cell proliferation ( J:182210 )

• with cell cycle defects in tamoxifen-treated mice

• of B cells from tamoxifen-treated mice stimulated with LPS, CpG or anti-IgM

• tamoxifen-treated mice exhibit impaired germinal center formation and germinal center B cell proliferation compared with control mice

• however, B cell proliferation is rescued by transformation with A-MuLV

hematopoietic system

increased B cell apoptosis ( J:182210 )

• tamoxifen-treated pro-B cells exhibit reduced survival compared with wild-type mice that cannot be rescued by expression of Bcl2 or Foxo1 or transformation with A-MuLV

• stimulated B cells from tamoxifen-treated mice exhibit reduced survival compared with control cells

• however, expression of Myb or BAFF rescues B cell survival and expression of Bcl2l1 partially rescues B survival

decreased B cell proliferation ( J:182210 )

• with cell cycle defects in tamoxifen-treated mice

• of B cells from tamoxifen-treated mice stimulated with LPS, CpG or anti-IgM

• tamoxifen-treated mice exhibit impaired germinal center formation and germinal center B cell proliferation compared with control mice

• however, B cell proliferation is rescued by transformation with A-MuLV

decreased immature B cell number ( J:182210 )

• in tamoxifen-treated mice

decreased transitional stage B cell number ( J:182210 )

• in tamoxifen-treated mice

arrested B cell differentiation ( J:182210 )

• of pre-B cells from tamoxifen-treated mice in vitro

decreased germinal center B cell number ( J:182210 )

• in tamoxifen-treated mice, less severe 12 days after immunization

decreased marginal zone B cell number ( J:182210 )

• in tamoxifen-treated mice

decreased pre-B cell number ( J:182210 )

• reduced frequency of B220^intCD43- pre-B cells in tamoxifen-treated mice

increased B cell number ( J:182210 )

• increased number of recirculating B220^hiCD43- B cells in tamoxifen-treated mice

decreased spleen germinal center number ( J:182210 )

• in immunized tamoxifen-treated mice

abnormal germinal center B cell physiology ( J:182210 )

• tamoxifen-treated mice exhibit impaired germinal center formation and germinal center B cell proliferation compared with control mice

decreased IgG1 level ( J:182210 )

• by a factor of 5 in tamoxifen treated mice

decreased IgG3 level ( J:182210 )

• by a factor of 3 in tamoxifen treated mice

Genotype
MGI:5556128

cn31

• Allelic Composition: Mastl^tm1.1Mama/Mastl^tm1.1Mama; Polr2a^{tm1(cre/ERT2)Bbd}/Polr2a⁺
• Genetic Background: Not Specified

cellular

abnormal mitosis ( J:201971 )

• following treatment with tamoxifen at E12.5, at E14.5 an increase in mitotic figures is seen in the neuroepithelium

• mitotic figures display an accumulation of prometaphases/metaphases

embryo

abnormal embryonic neuroepithelium morphology ( J:201971 )

• following treatment with tamoxifen at E12.5, at E14.5 an increase in mitotic figures is seen in the neuroepithelium

nervous system

abnormal embryonic neuroepithelium morphology ( J:201971 )

• following treatment with tamoxifen at E12.5, at E14.5 an increase in mitotic figures is seen in the neuroepithelium