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New biomarker may be the keystone of chemotherapy resistance in pancreatic cancer

15 May 2012

Researchers at the University of California, San Diego School of Medicine, and Moores Cancer Centre, have identified a new pancreatic cancer biomarker that may hold the key to chemotherapy resistance.

Biomarkers are molecules produced by cancer cells that can help to detect cancer earlier and guide decisions on treatment, such as whether or not a patient should receive chemotherapy. Unfortunately, identifying biomarkers that can easily be used as therapeutic targets has proved difficult.

In a study, published in Cancer Research, the US team discovered that an enzyme called PEAK1 is ‘switched on’ in the most common form of pancreatic cancer, pancreatic ductal adenocarcinoma (PDAC). As PDAC progresses the amount of PEAK1 in the cancer cells increases. PEAK1, which acts as an ‘on/off switch’ for many cell signalling pathways, was found to be activated during the early development of PDAC.

Lead researcher, Dr Jonathan Kelber, said: "This enzyme was clearly detected in biopsies of malignant tumours from human patients as well as in mouse models." Since PEAK1 is a critical signalling hub in cancer cells, it is an ideal candidate biomarker and potential therapeutic target.

When the researchers ‘switched off’ PEAK1 in mouse models of PDAC, they found that the tumours formed were significantly smaller and that they did not metastasise efficiently. Switching off PEAK1 also increased the effectiveness of chemotherapy treatment. The team revealed that a signalling network involving both PEAK1 and another enzyme, Kras, contributes to chemotherapy resistance in PDAC.

Co-investigator, Dr Michael Bouvet, said: "Since current therapies are often ineffective, our hope is that the findings from this research will open up a new line of investigation to bring a PEAK1 inhibitor to the clinic."


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