Mouse Genome Informatics
hm1
    Vhltm1Wml/Vhltm1Wml
involves: 129S1/Sv * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype

Placental histopathology of normal and Vhltm1Wml/Vhltm1Wml embryos

mortality/aging
• death between E10.5 and E12.5, likely due to abnormal placental development

embryogenesis
• failed embryonic vasculogenesis, with hemorrhage evident by E11.5 to E12.5
• lacked embryonic endothelium and blood vessels
• evident between E9.5 and E10.5
• appeared normal until E9.5, but did not progress developmentally

cardiovascular system
• failed embryonic vasculogenesis, with hemorrhage evident by E11.5 to E12.5
• lacked embryonic endothelium and blood vessels
• hemorrhagic placenta


Mouse Genome Informatics
ht2
    Vhltm1Wml/Vhl+
B6;129
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• increased incidence of vascular neoplasms in the liver, uterus, ovary, spleen and heart in response to streptozotocin, compared to controls
• highest incidence and number found in liver
• lesions seen: angiectasia, hemangisarcoma, hemangioma
• no increase in renal lesions in response to streptozotocin, compared to controls

homeostasis/metabolism
• increased incidence of vascular neoplasms in the liver, uterus, ovary, spleen and heart in response to streptozotocin, compared to controls
• highest incidence and number found in liver
• lesions seen: angiectasia, hemangisarcoma, hemangioma
• no increase in renal lesions in response to streptozotocin, compared to controls

Mouse Models of Human Disease
OMIM IDRef(s)
Von Hippel-Lindau Syndrome; VHL 193300 J:42486 , J:88492