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The assumption that high normal liver counts in close neighborhood of tumor regions might originate from the activity at the tumor is demonstrated in Pat2.
The presence of high normal liver uptake impairs complete assessment of liver lesions and urinary excretion interferes with imaging near the bladder.
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A reason may be that 18-F accumulation is high in normal liver tissue because of FLT glucuronidation in the hepatocytes [18, 19].
Hepatic adenoma and focal nodular hyperplasia (FNH) has a portal venous phase enhancement that is equal to or slightly higher than normal liver tissue.
The high accumulation in normal liver is likely due to high expression of FCR on liver sinusoidal endothelial cell [25].
Interpretation of 18F-FDGal PET/CT images is challenged by the very high uptake in normal liver tissue and heterogeneous uptake in cirrhotic patients.
To enhance the selective cytotoxicity of dT-QX, viral overexpression of TK1 in cells clearly was not an effective strategy on cancer cells due to a concurring high cytotoxicity in normal liver HL-7702 cells.
A comparison of CV levels between the tables shows a higher CV for normal liver parenchyma at some distance from the tumour, compared to adjacent to the tumour, consistent with differing mean activity concentrations.
In this study there was high accumulation in the normal liver.
Interestingly, metastases in the liver have been identified as regions of deficit uptake, because of the high background activity in normal liver tissue.
To further explore the Hedgehog-Gli signaling pathway to discriminate between groups A and B, we tested the expression of six additional genes involved in this pathway (DHH, SHH, GLI1, GLI2, GLI3, and GLI4) in three high IHH-expressing percutaneous normal liver samples and three low IHH-overexpressing surgical nontumoral liver samples.
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