Scientists identify specific markers that trigger aggressiveness of liver cancer

	Tweet

Hepatocellular carcinoma (HCC) or primary liver cancer forms in the epithelial tissue of the liver and is most commonly caused by the hepatitis B virus (HBV) or hepatitis C virus (HCV). In the U.S., the National Cancer Institute (NCI) estimates that 15,000 men and 6,000 women are diagnosed with HCC each year. Worldwide, HCC accounts for 632,000 cases with the highest regions being Western Pacific and Africa according to a 2004 World Health Organization (WHO) report.

Researchers from Taipei Veterans General Hospital investigated the molecular mechanisms of HCC, one of the most common tumors found in Taiwan and largely caused by the high prevalence (15%-20%) of HBV in the country. The study, funded in part by a grant from the National Science Council, is the first to provide a comprehensive profile of multiple Epithelial-Mesenchymal Transition (EMT) markers and to demonstrate that Snail and Twist, but not Slug, are the major inducers of EMT in HCC. Results of the study are published in the November issue of Hepatology, a journal of the American Association for the Study of Liver Diseases.

EMT is critical in the development of invasiveness and metastatic potential of human cancers, and described as process where epithelial cells no longer adhere to one another, taking on fibroblastic properties. The EMT process is initiated by suppression of E-cadherin function through the major EMT regulators (Snail, Slug, and Twist). E-cadherin (calcium dependent adhesion molecules) is a type of protein found in the epithelial cells that ensure tissue cells bind together. When E-cadherin function is lost, cancer is able to progress and metastasize.

Professor Jaw-Ching Wu and colleagues obtained samples of primary HCC with adjacent non-tumorous liver tissues from 123 patients who had hepatic resection surgery between 1990 and 2002 at Taipei Veterans General Hospital. Reduced E-cadherin function was observed in 60.2% of patients. “We found a significant decrease in cancer-free intervals and overall survival for those patients who had a reduction in E-cadherin function,” explained Dr. Wu. A downregulated expression of E-cadherin was also associated with large tumor size and multi-nodular tumors.

Results show that co-expression Snail and Twist (transcription factors or proteins that control when genes are switched on or off) indicates the worst prognosis for HCC patients. “Our research is the first to prove that the two proteins (Snail and Twist) work independently, but together promote EMT,” noted Dr. Wu.

According to the study, overexpression of Twist is correlated with HCV-related HCC, partially explaining the highly invasive behavior and poor prognosis for patients with this form of liver cancer. Dr Wu added, “Our results provide essential information for determining HCC prognosis in patients and identifies possible new treatments for future HCC management.”

###

Article: “A Comprehensive Analysis of the Independent Effect of Twist and Snail in Promoting Metastasis of Hepatocellular Carcinoma,” Muh-Hwa Yang, Chi-Li Chen, Gar-Yang Chau, Shih-Hwa Chiou, Chien-Wei Su, Teh-Ying Chou, Wei-Li Peng, and Jaw-Ching Wu. Hepatology; Published Online: August 10, 2009 (DOI: 10.1002/hep.23221); Print Issue Date: November 2009. http://www3.interscience.wiley.com/journal/122542499/abstract

Editorial: “The Epithelial Mesenchymal Transition: fact or fiction in cancer?” Gianluigi Giannelli. Hepatology; Published Online: October 29, 2009 (DOI: 10.1002/hep.23329); Print Issue Date: November 2009.

Media Advisory

What: The 60th Annual Meeting of the American Association for the Study of Liver Diseases (AASLD)

Founded in 1950, AASLD is the leading organization of scientists and healthcare professionals committed to preventing and curing liver disease. AASLD has grown into an international society responsible for all aspects of hepatology, and the annual meeting attracts 7,500 physicians, surgeons, researchers, and allied health professionals from around the world.

The Liver Meeting® is the premier meeting in the science and practice of hepatology, including the latest findings on new drugs, novel treatments, and the results from pilot and multicenter studies.

When: October 31 – November 3, 2009

Where : Hynes Convention Center
900 Boylston Street
Boston, Massachusetts

Contact: Please contact Ann Tracy at 703-299-9766 or to obtain a press pass for this event.

Contact: Dawn Peters

781-388-8408
Wiley-Blackwell

RELATED STORIES:
Eating mandarins reduces the risk of liver disease, hardened arteries and insulin resistance   The ignored virus that causes liver cancer   Metformin May Protect Against Liver Cancer   A promising molecular target for liver cancer therapy   The relationship between body mass index and age at hepatocellular carcinoma onset   Statins may cut liver cancer risk in diabetics   More evidence coffee may cut risk of liver cancer   Studies of patients with cirrhosis uncover limitations in liver cancer screening   Liver cancer is likely caused by cycles of liver cell death and renewal   More Reliable Biomarkers Needed for Liver Cancer Detection   Racial disparities evident in early-stage liver cancer survival   Researchers Find That Targeted Therapy Combination Overcomes Treatment Resistance in Liver Cancer   Hepatitis C ups liver cancer risk, study confirms   Liver cancer in cirrhotic patients effectively treated with radiofrequency ablation   Blacks with Liver Cancer More Likely to Die   Experts find rogue stem cells in liver cancer   Wilmot Researchers Create New Way to Study Liver Cancer   A diagnostic marker in hepatocellular carcinoma   Study shows skin rash in patients treated for liver cancer determines survival   Personalized treatment may help some liver cancer patients   Saffron shows promise in preventing liver cancer   Proton beams control liver tumors

Comments

[ + Post Your Own ]

Now you're in the public comment zone. What follows is not Armenian Medical Network's stuff; it comes from other people and we don't vouch for it. A reminder: By using this Web site you agree to accept our Terms of Service. Click here to read the Rules of Engagement.

There are no comments for this entry yet. [ + Comment here + ]