@entity7007 -thymidine kinase-luciferase knockin XXXX : a novel model for dual modality longitudinal imaging of tumorigenesis in liver.

@entity108 @entity96 @entity5 @entity19 @entity1313 @entity5748 @entity7007 @entity157
BACKGROUND _ AIMS: @entity157 ( @entity157 ) is frequently a lethal disease and one of the few @entity5 that is still increasing in incidence around the world. Better animal models are highly desired to investigate the molecular basis of @entity157 and to develop novel therapeutic strategies. @entity7007 ( @entity7007 ) gene is expressed in fetal liver, silenced soon after birth, and highly re-expressed in @entity157 ( @entity157 ). We aimed to take advantage of the dramatic re-expression of the @entity7007 gene in @entity157 to develop a hepatocarcinogenesis reporter (HCR) @entity19 model for @entity5748 , longitudinal in vivo imaging of @entity96 development, and progression. METHODS: Knock in @entity19 were established by placing a thymidinekinase (tk)-luciferase (luc) reporter gene cassette under the transcriptional control of the endogenous @entity7007 promoter. @entity108 , a liver carcinogen, was used to induce @entity96 , which was monitored by both luc-based bioluminescent (BL) and tk-based positron emission tomography (PET) imaging. RESULTS: The expression profile of luc was identical to that of the endogenous @entity7007 gene during development. As early as 2 months after the exposure to @entity108 , BLI revealed multifocal signals in the liver, long before the appearance of histologically apparent @entity1313 . By 6 months, BL and PET dual imaging showed strong signals in malignant @entity157 . By serendipity, a strong BL signal was also detected in adult testes, a previously unknown site of @entity7007 expression. CONCLUSIONS: The HCR model enables longitudinal monitoring of @entity96 development and progression, providing a powerful tool in developing chemoprevention and therapeutic strategies for @entity157 .
