Protein Predicts Hepatocellular Carcinoma Recurrence After Transplantation
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Protein Predicts Hepatocellular Carcinoma Recurrence After Transplantation

HOBOKEN, NJ -- February 4, 2009 -- A study published in the February issue of Hepatology suggests that Capn4 is associated with hepatocellular carcinoma recurrence and metastasis after liver transplantation.

Patients with hepatocellular carcinoma often undergo liver transplantation in an attempt to rid their bodies of the disease. Unfortunately, the cancer recurs in some patients and even metastasises to other parts of the body, making their prognosis poor.

Jia Fan, MD, Liver Cancer Institute, Shanghai, China, and colleagues utilised proteomic technology to study liver cancer cells in search of proteins associated with recurrence of hepatocellular carcinoma after liver transplantation.

They identified 149 proteins, including 52 that had changes in expression. Additional tests focused their interest on Capn4. They examined it further to determine its association with clinical outcomes of liver cancer patients who undergo transplantation.

The findings showed that Capn4 is an important molecule associated with hepatocellular carcinoma metastasis and recurrence. "It was dramatically overexpressed in all metastatic tissues, while it was down-regulated in the nonmetastatic tissues," wrote the authors.
They found that Capn4 expression was significantly correlated with tumour number, maximal tumour size, tumour encapsulation, venous invasion, and pathological tumour-node-metastasis stage.

"Furthermore, patients with Capn4-positive tumours had an increasing risk of recurrence and significantly reduced overall post-transplant survival," the authors wrote.

"This is the first study that describes the up-regulation of Capn4 associated with tumour invasion and metastasis after liver transplantation for hepatocellular carcinoma."

They conclude that Capn4 has the potential to be used as a novel prognostic marker for liver cancer patients and as a target for therapy.

SOURCE: Wiley-Blackwell

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