Analysis Tools
mortality/aging
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• mice fed a tamoxifen-containing diet show a deterioration of health and die within 3 weeks due to multiple organ failure
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice fed a tamoxifen-containing diet show a deterioration of health and die within 3 weeks due to multiple organ failure
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 2 weeks after 5-hydroxytamoxifen treatment, lungs show increased cellularity
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• 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
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• 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
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• 8 weeks after 5-hydroxytamoxifen treatment, lungs display hyperproliferation (~5-fold increased proliferation) compared to wild-type or heterozygous lungs
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 30 day old mice fed a tamoxifen diet for 3 months show normal weight and activity and no obvious anatomical defects
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 30 day old mice fed a tamoxifen diet for 3 months are healthy and show normal weight and activity and no obvious anatomical defects
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• primary mouse embryonic fibroblasts exposed to 4OHT for 5 days to activate cre/ERT2 recombinase exhibit decreased proliferation compared to single Kras heterozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• with induction of Cre expression from the transgene, multiple adenomatous tumors form in mouse lungs
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• with induction of Cre expression from the transgene, multiple adenomatous tumors form in mouse lungs
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 50% of tamoxifen-treated mice survive at 40 weeks
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• in mice treated with tamoxifen at weaning
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• in mice treated with tamoxifen at weaning
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• in mice treated with tamoxifen at weaning
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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 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• primary mouse embryonic fibroblasts exposed to 4OHT for 5 days to activate cre/ERT2 recombinase exhibit decreased proliferation compared to single Kras heterozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice treated tamoxifen at weaning exhibit an increase in lifespan of 8 weeks (42 weeks) compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd littermates (34 weeks)
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• tamoxifen-treated mice exhibit reduced tumor burden compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice exhibit reduced tumor burden and tumor grade compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice exhibit an increase in lifespan compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd littermates
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• tamoxifen-treated mice exhibit reduced tumor burden and tumor grade compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 50% survival for tamoxifen-treated mice is 25 weeks compared with 42 weeks for similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd littermates
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• lung tumors in tamoxifen-treated mice are more aggressive than in similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
• however, treatment with the Cdk4 inhibitor PD0332991 reduces tumor formation
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• in mice treated with tamoxifen
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• proliferation of lung cells in tamoxifen-treated mice exhibit 8- to 10-fold greater proliferation than in Cdk4tm2.1Bbd/Cdk4tm2.1Bbd Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• lung tumors in tamoxifen-treated mice are more aggressive than in similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
• however, treatment with the Cdk4 inhibitor PD0332991 reduces tumor formation
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• in mice treated with tamoxifen
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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 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• lung cells in tamoxifen-treated mice exhibit 8- to 10-fold reduction in proliferation and early senescence compared to in similarly treated Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• tamoxifen-treated mice exhibit adenocarcinomas that are not as severe as in Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• proliferation of lung cells in tamoxifen-treated mice exhibit 8- to 10-fold less proliferation than in similarly treated Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• tamoxifen-treated mice exhibit increased cell replicative senescence in the lungs compared to in similarly treated Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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
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• 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
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• in tamoxifen-treated mice as in similarly treated Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit early senescence of tumor cells compared with tamoxifen and infected with GFP-expressing adenovirus
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• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit decreased proliferation of tumor cells compared with tamoxifen and infected with GFP-expressing adenovirus
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the mean lifespan of mice treated tamoxifen is 34-42 weeks
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• in mice treated with tamoxifen at weaning
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• in mice treated with tamoxifen at weaning
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• in mice treated with tamoxifen at weaning
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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 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• when cells are exposed to tamoxifen ex vivo, the progenitor compartment is increased compared to unexposed cells
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• 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
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• when cells are exposed to tamoxifen ex vivo, fewer pre-B cells are present compared to unexposed cells
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• when cells are exposed to tamoxifen ex vivo, fewer pre-B cells are present compared to unexposed cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• double homozygous MEFs treated with 4-hydroxy-tamoxifen to induce Cre mediated recombination proliferate less efficiently compared to untreated double homozygous MEFs
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• 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
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• 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
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• 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
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• 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
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• 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
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• 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)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• double homozygous MEFs treated with 4-hydroxy-tamoxifen to induce Cre mediated recombination proliferate less efficiently compared to untreated double homozygous MEFs
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• 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
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• 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
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• 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
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• 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
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• 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
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• 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)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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
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• 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
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• 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
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die before week 32 due to increased lung cancer progression
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• 20 weeks after treatment, lungs are increased in size
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• 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
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• 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, Mapk14tm2Nbr/+ control mice
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• adenocarcinomas are detected at 15 weeks but not in controls
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• lung differentiation is abnormal with increased SP-C-positive cells
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• 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
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• 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
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• 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, Mapk14tm2Nbr/+ control mice
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• adenocarcinomas are detected at 15 weeks but not in controls
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• 20 weeks after treatment, lungs are increased in size
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die before week 32 due to increased lung cancer progression
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• 20 weeks after treatment, lungs are increased in size
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• 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
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• 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, Mapk14tm2Nbr/+ control mice
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• adenocarcinomas are detected at 15 weeks but not in controls
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• lung differentiation is abnormal with increased SP-C-positive cells
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• 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
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• 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
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• 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, Mapk14tm2Nbr/+ control mice
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• adenocarcinomas are detected at 15 weeks but not in controls
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• 20 weeks after treatment, lungs are increased in size
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice live up to 40 weeks
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• by 24 weeks, mice develop tumors in the thymus
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• by 24 weeks, mice develop tumors in lungs
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• at 4 weeks after 5-hydroxytamoxifen treatment, a few small adenomas are observed in some animals
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• by 24 weeks, mice develop tumors in lungs
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• at 4 weeks after 5-hydroxytamoxifen treatment, a few small adenomas are observed in some animals
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• when 5 month old mice were treated with tamoxifen they exhibit reduced body size associated with the loss of the Cdk4 function
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• when 5 month old mice were treated with tamoxifen they exhibit diabetes associated with the loss of the Cdk4 function
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| N |
• adult hematopoiesis is normal following tamoxifen treatment at 5 months of age
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| N |
• liver regeneration is normal following tamoxifen treatment at 5 months of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after topical application of 4-hydroxytamoxifen
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• topical application of 4-hydroxytamoxifen to the unshaved tail results in complete alopecia by 6 weeks after application
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• 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
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• 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
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• develops by 3 - 4 weeks after topical application of 4-hydroxytamoxifen
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• after topical application of 4-hydroxytamoxifen
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• after topical application of 4-hydroxytamoxifen
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• 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
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• by 2 - 4 weeks after topical application of 4-hydroxytamoxifen, severe skin ulcerative lesions develop
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• between 1 - 2 weeks after topical application of 4-hydroxytamoxifen, back skin is ruffled and wrinkled
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• between 1 - 2 weeks after topical application of 4-hydroxytamoxifen, back skin is thickened
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• increase in the proportion of proliferating epidermal cells in the first few weeks after topical application of 4-hydroxytamoxifen
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• 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)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• development of hyperkeratosis following 4-hydroxytamoxifen treatment is reduced and delayed compared to mutant mice wild-type for Cdkn2a
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• development of hyperplasia following 4-hydroxytamoxifen treatment is reduced and delayed compared to mutant mice wild-type for Cdkn2a
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• partial restoration in long term outgrowth of 4-hydroxytamoxifen exposed keratinocytes in culture compared to mutant mice wild-type for Cdkn2a
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after 8 to 10 days on a tamoxifen diet
• however, survival is increased when older mice (1 year old) are treated with tamoxifen
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• 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
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• tamoxifen-treated mice exhibit reduced proliferation in the testis and spleen compared with control mice
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• in a two-stage carcinogenesis protocol, tamoxifen-treated mice exhibit tumor arrest unlike similarly treated control mice
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• in tamoxifen-treated mice
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• following topical application of tamoxifen, depilated mice exhibit impaired hair regeneration compared with similarly treated control mice
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• topical treatment results in metaphase figures in the basal layer compared to in similarly treated control mice
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• tamoxifen-treated mice exhibit loss of intestinal epithelium unlike in control mice
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• in tamoxifen-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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
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• mice fed a tamoxifen diet exhibit severe alterations in the structure of intestinal and colonic tissue
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• severe shortening of crypts in the colon of tamoxifen fed mice
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• severe shortening of crypts in the colon of tamoxifen fed mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• fewer CD25-kappa+ immature B cells in tamoxifen-treated mice
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• fewer CD25+kappa- pre-B cells in tamoxifen-treated mice
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• fewer CD25-kappa+ immature B cells in tamoxifen-treated mice
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• fewer CD25+kappa- pre-B cells in tamoxifen-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• tamoxifen-treated mice exhibit normal somatic hypermutation
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• 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
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• 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
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• of pre-B cells from tamoxifen-treated mice in vitro
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• in tamoxifen-treated mice, less severe 12 days after immunization
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• in tamoxifen-treated mice
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• reduced frequency of B220intCD43- pre-B cells in tamoxifen-treated mice
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• increased number of recirculating B220hiCD43- B cells in tamoxifen-treated mice
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• in immunized tamoxifen-treated mice
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• tamoxifen-treated mice exhibit impaired germinal center formation and germinal center B cell proliferation compared with control mice
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• by a factor of 5 in tamoxifen treated mice
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• by a factor of 3 in tamoxifen treated mice
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• 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
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• 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
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• 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
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• 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
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• of pre-B cells from tamoxifen-treated mice in vitro
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• in tamoxifen-treated mice, less severe 12 days after immunization
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• in tamoxifen-treated mice
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• reduced frequency of B220intCD43- pre-B cells in tamoxifen-treated mice
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• increased number of recirculating B220hiCD43- B cells in tamoxifen-treated mice
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• in immunized tamoxifen-treated mice
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• tamoxifen-treated mice exhibit impaired germinal center formation and germinal center B cell proliferation compared with control mice
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• by a factor of 5 in tamoxifen treated mice
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• by a factor of 3 in tamoxifen treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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
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• following treatment with tamoxifen at E12.5, at E14.5 an increase in mitotic figures is seen in the neuroepithelium
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• following treatment with tamoxifen at E12.5, at E14.5 an increase in mitotic figures is seen in the neuroepithelium
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 05/07/2024 MGI 6.23 |
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