Improvement in Making ACI-rat Model of Hepatocellular Carcinoma in The Experiments of Interventional Therapy and Its Imaging Properties

PURPOSE To improve the preparation of August Copenhagen Irish(ACI)-rat model suitable for interventional therapy, and to investigate its 18F-2-fluoro-2-deoxy-D -glucose-Positron emission tomography(FDG-PET) and magnetic resonance imaging(MRI) features. METHODS Morris hepatoma 3924A tumors were implanted in the left lobe of the liver in 20 male ACI rats. FDG-PET and MRI scans were performed on day 14 after implantation. After that, all the rats were sacrificed and samples of tissues were fixed and used for various analyses. RESULTS FDG-PET scans showed increased uptake of 18F-FDG of tumor nodules, and no signs of wound and peritoneal cavity metastases. The average maximum standardized uptake value(SUVmax) in tumors was 4.85 ± 0.86(range, 3.58–6.6) and 0.79 ± 0.42(range, 0.27–1.63) in the surrounding normal liver tissues. Tumor nodules on MRI were shown to be hypointensity on T1-weighted images and hyperintensity on T2-weighted images. The average tumor volume was 106 ± 15 mm3. No intrahepatic metastasis or lung metastasis were found on day 14. CONCLUSION FDG-PET is useful in screening the earlier cases with implantation metastasis. MRI is useful in assessing this interventional model. The tumor model shows a well application for the interventional therapy experiment.

Tissue-Specific Actions of the Ept1, Ept2, Ept6, and Ept9 Genetic Determinants of Responsiveness to Estrogens in the Female Rat

Ept1, Ept2, Ept6, and Ept9 are quantitative trait loci mapped in crosses between the ACI and Copenhagen (COP) rat strains as genetic determinants of responsiveness of the pituitary gland to estrogens. We have developed four congenic rat strains, each of which carries, on the genetic background of the ACI rat strain, alleles from the COP rat strain that span one of these quantitative trait loci. Relative to the female ACI rats, female ACI.COP-Ept1 rats exhibited reduced responsiveness to 17β-estradiol (E2) in the pituitary gland, as evidenced by quantification of pituitary mass and circulating prolactin, and in the mammary gland, as evidenced by reduced susceptibility to E2-induced mammary cancer. The ACI.COP-Ept2 rat strain exhibited reduced responsiveness to E2 in the pituitary gland but did not differ from the ACI strain in regard to susceptibility to E2-induced mammary cancer. Interestingly, female Ept2 congenic rats exhibited increased responsiveness to E2 in the thymus, as evidenced by enhanced thymic atrophy. The ACI.COP-Ept6 rat strain exhibited increased responsiveness to E2 in the pituitary gland, which was associated with a qualitative phenotype suggestive of enhanced pituitary vascularization. The ACI.COP-Ept9 rat strain exhibited reduced responsiveness to E2 in the anterior pituitary gland, relative to the ACI rat strain. Neither Ept6 nor Ept9 impacted responsiveness to E2 in the mammary gland or thymus. These data indicate that each of these Ept genetic determinants of estrogen action is unique in regard to the tissues in which it exerts its effects and/or the direction of its effect on estrogen responsiveness.