Phenotypes Associated with This Genotype

Genotype
MGI:5314251

• Allelic Composition: Foxa1^tm1Khk/Foxa1^tm1Khk; Foxa2^tm1Khk/Foxa2^tm1Khk; Tg(Alb1-cre)1Khk/0
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

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

neoplasm

decreased incidence of tumors by chemical induction ( J:181296 )

• male mutants injected with DEN followed by TCPOBOP (carcinogen treatment) show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma

increased incidence of tumors by chemical induction ( J:181296 )

• female mutants injected with DEN followed by TCPOBOP (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development

• in females treated with fulverstrant to block estrogen signaling, DEN-induced liver injury is significantly attenuated

• estrogen treatment of male mutants enhances liver injury in DEN-treated males while in DEN-treated controls estrogen treatment prevents liver injury and carcinogenesis

increased hepatocellular carcinoma incidence ( J:181296 )

• female mutants injected with N,N-diethylnitrosamine (DEN) followed by TCPOBOP two-step strategy (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development

• male mutants injected with DEN followed by TCPOBOP show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:181296 )

• male mutants injected with DEN followed by TCPOBOP (carcinogen treatment) show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma

increased incidence of tumors by chemical induction ( J:181296 )

• female mutants injected with DEN followed by TCPOBOP (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development

• in females treated with fulverstrant to block estrogen signaling, DEN-induced liver injury is significantly attenuated

• estrogen treatment of male mutants enhances liver injury in DEN-treated males while in DEN-treated controls estrogen treatment prevents liver injury and carcinogenesis

liver/biliary system

increased hepatocellular carcinoma incidence ( J:181296 )

• female mutants injected with N,N-diethylnitrosamine (DEN) followed by TCPOBOP two-step strategy (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development

• male mutants injected with DEN followed by TCPOBOP show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma