Hacking Into A Cancer Network

Liver cancer initiation molecular network identified

/ Author:  / Reviewed by: Joseph V. Madia, MD

(RxWiki News) Some cancers tend to reappear after treatment. Liver cancer is one of them, and at this point, there’s no way to prevent this from happening. An early study has discovered a network of molecules that could be hacked into to keep liver cancer from developing.

Spanish researchers have identified genes that work together to get liver cancer started.

This network of molecules could become targets for new drugs which may be able to prevent this cancer from ever forming.

This is very early research, and it could take years before such a medication is available.

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Liver cancer takes about a half a million people around the world every year. In this country, almost 27,000 people are diagnosed with the disease, and 20,500 don’t beat hepatocellular carcinoma (HCC) – the most common form of liver cancer.

Chronic hepatitis virus B and C infections and cirrhosis of the liver are major risk factors for HCC. And patients who’ve had surgery to remove liver tumors often see the cancer return.

A study, led by Erwin Wagner, the Director of the BBVA Foundation-CNIO Cancer Cell Biology Programme at the Spanish National Cancer Research Centre (CNIO), sought to understand what gets liver cancer started.

If the initiation process is understood, then ways to interrupt that process could lead to preventive therapies. Scientists might also have biomarkers that could be used for diagnosing the cancer.

Researchers learned that a gene regulator known as AP-1 is key to keeping alive cells that cause liver tumors to begin to form.

AP-1 controls the levels of another molecule called SIRT6 that works to block a protein known as survivin – which is involved in programmed cell death.

When these proteins were altered in mice models, liver cancer development was severely impaired.

After testing 150 human tissue samples, the researchers concluded that these proteins were involved in liver cancer initiation.

"Our study provides not only novel implications for the development of preventive therapies for high risk cirrhotic or post-resection [after surgery] patients, but also a new paradigm how one can molecularly dissect cancer initiation using mouse models in combination with the appropriate human samples", study author, Latifa Bakiri, said in a press release.

Study results were published in the October issue of Nature Cell Biology.

Reviewed by: 
Review Date: 
October 8, 2012
Last Updated:
October 11, 2012