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 22 November 2017

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News

5-Fluorouracil cytotoxicity may be compromised in GI cancer patients

A team from London, England, has shown for the first time that the cytotoxicity of 5-Fluorouracil could be compromised in patients with gastrointestinal cancer

News image

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The researchers investigated whether the cytotoxicity of 5-Fluorouracil (5-FU) is compromised in patients with gastrointestinal cancer.

They reported their findings in the latest issue of Cancer Research.

Tumor and normal tissue pharmacokinetics of 5-FU in patients can be determined with positron emission tomography scanning. However, the data obtained are of limited value because of the inability to distinguish catabolites (inactive species) from parent 5-FU and anabolites (cytotoxic species).

The researchers blocked 5-FU catabolism with eniluracil, an inactivator of dihydropyrimidine dehydrogenase, in one arm of a paired study. This enabled catabolite correction and calculation of tissue pharmacokinetic parameters to be achieved.

The team found that net clearance of 5-[18F]FU from plasma into the tumors (liver metastases and pancreatic tumor) of patients was low (KI = 0.0033 ml plasma/ml tissue/min).

Hepatic catabolism reduces systemic availability of 5-FU.
Cancer Research

In contrast, the initial clearance through catabolism in the liver was found to be high (KI = 0.7313 ml plasma/ml tissue/min).

In the absence of eniluracil, catabolites in tumors accounted for 83% of total tumor exposure, whereas catabolites in liver accounted for 96% of total liver exposure.

Eric O. Aboagye, of Imperial College School of Medicine, London, concluded on behalf of his colleagues, "This study provides definitive evidence that, in patients with gastrointestinal cancer, the cytotoxicity of 5-FU could be compromised.

"This is due to its intrinsically low uptake by tumors, as well as decreased systemic availability through hepatic catabolism."

Cancer Res 2001; 61 (13): 4937-41
03 July 2001

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