Analysis Tools
neoplasm
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• mutants exhibit accelerated development of HBV-induced premalignant lesions compared to hemizygous Tg(Alb1HBV)44Bri mice
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Allele Symbol Allele Name Allele ID |
Tg(Alb1HBV)44Bri transgene insertion 44, Ralph L Brinster MGI:2678809 |
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| Summary |
3 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutants exhibit accelerated development of HBV-induced premalignant lesions compared to hemizygous Tg(Alb1HBV)44Bri mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice injected with the hepatotoxin AFB1 develop nodules at 6 months after treatment; more nodules are seen in mice treated with AFB1 than in untreated mice and most nodules are large
• abundance and size of liver lesions in adults exposed to AFB1 increase over time after treatment and AFB1 treatment accelerates the liver lesions in older mice
• male neonates exposed to AFB1 show a tendency to develop lesions earlier than females, however, by 15 months, females have an about equal frequency of liver lesions as males
• mice injected with AFB1 at day 7 develop regenerative foci, adenoma, and carcinoma as do mice injected with AFB1 in adulthood but much more frequently
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• mice develop nodules in the liver at 9 months of age; nodules are mostly small although some large ones develop
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• end-stage liver tumors are molecularly similar and resemble hepatocellular carcinoma
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• mice develop only regenerative foci or adenomas at 15 months of age
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• mice injected with the hepatotoxin AFB1 develop nodules at 6 months after treatment; more nodules are seen in mice treated with AFB1 than in untreated mice and most nodules are large
• abundance and size of liver lesions in adults exposed to AFB1 increase over time after treatment and AFB1 treatment accelerates the liver lesions in older mice
• male neonates exposed to AFB1 show a tendency to develop lesions earlier than females, however, by 15 months, females have an about equal frequency of liver lesions as males
• mice injected with AFB1 at day 7 develop regenerative foci, adenoma, and carcinoma as do mice injected with AFB1 in adulthood but much more frequently
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• mice develop overt liver lesions (hepatitis) beginning from 9-12 months of age
• mice injected with the hepatotoxin AFB1 develop a large number of liver lesions that are obvious from 9 months after treatment
• mice injected with AFB1 at adulthood show an increase in liver lesions compared with untreated mice
• males are more susceptible to liver lesions much earlier than females when adults are injected with AFB1 at 6 months, although by 5 months, similar incidence rates are seen for both genders
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• mice develop overt liver lesions (hepatitis) beginning from 9-12 months of age
• mice injected with the hepatotoxin AFB1 develop a large number of liver lesions that are obvious from 9 months after treatment
• mice injected with AFB1 at adulthood show an increase in liver lesions compared with untreated mice
• males are more susceptible to liver lesions much earlier than females when adults are injected with AFB1 at 6 months, although by 5 months, similar incidence rates are seen for both genders
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• mice develop nodules in the liver at 9 months of age; nodules are mostly small although some large ones develop
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• end-stage liver tumors are molecularly similar and resemble hepatocellular carcinoma
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• mice develop only regenerative foci or adenomas at 15 months of age
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| hepatocellular carcinoma | DOID:684 |
OMIM:114550 |
J:223921 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 9-12 months after the onset of hepatocellular injury, mutants develop liver tumors, with all mice developing hepatocellular neoplasms by 18-21 months of age
• multiple tumors of various sizes are present in the same liver and tumors are highly vascularized
• Background Sensitivity: liver tumors develop more rapidly in mice derived from transgenic by nontransgenic (C57BL/6J x SJL/J) matings than in mice derived by repeated backcrossing against C57BL/6J mice
• in mutants backcrossed against C57BL/6J, males develop liver tumors more rapidly than females
• younger males tend to harbor adenomas, while carcinomas are more common in older males
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• hepatocellular adenomas
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• mutants develop hepatocellular injury at around 2-3 months of age, followed by hyperplasia and neoplasia
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• 9-12 months after the onset of hepatocellular injury, mutants develop liver tumors, with all mice developing hepatocellular neoplasms by 18-21 months of age
• multiple tumors of various sizes are present in the same liver and tumors are highly vascularized
• Background Sensitivity: liver tumors develop more rapidly in mice derived from transgenic by nontransgenic (C57BL/6J x SJL/J) matings than in mice derived by repeated backcrossing against C57BL/6J mice
• in mutants backcrossed against C57BL/6J, males develop liver tumors more rapidly than females
• younger males tend to harbor adenomas, while carcinomas are more common in older males
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• hepatocellular adenomas
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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 04/16/2024 MGI 6.23 |
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