Current estimates indicate that in the WHO European Region, 14 million people live with chronic hepatitis B, while approximately 9 million people are infected with the hepatitis C virus. Up to 90% of hepatitis patients are unaware of their infections.

ELPA conducted a survey to gauge the political commitment to combat hepatitis in Europe. The survey will be launched today at a conference on “Fighting Hepatitis to Tackle Liver Cancer” in the European Parliament hosted by Alojz Peterle MEP (EPP-ED, Slovenia).

Key findings include:

- In Austria, only 9% of newly diagnosed Hepatitis C patients were aware of the disease and only 3% realised that they were at risk once they had been diagnosed

- Only France, Spain and United Kingdom have conducted hepatitis awareness campaigns.

- France, the Netherlands, the UK and Sweden are the only countries to have developed a comprehensive national plan to fight hepatitis.

In light of this national inertia, ELPA calls for action at EU level. ELPA President Nadine Piorkowsky explains: “If Member States don’t act, the EU has to guide them in the development of targeted screening campaigns for Hepatitis risk groups. Countries like France have proven that investment in the fight against Hepatitis pays off. There is no reason why this should not be replicated by other Member States.”

Alojz Peterle MEP adds: “Hepatitis represents one of the major challenges for public health in Europe. If policy makers want to lower tomorrow’s mortality and morbidity rates, they have to act today.”

The consequences of inaction will be terrible. People infected with the virus and treated too late frequently experience severe liver damage such as liver scarring, liver cancer, or liver failure. Since the vast majority of those who carry the hepatitis virus are unaware of their infection, the number of patients with such follow-on diseases will rise dramatically.

Dr. Heiner Wedemeyer, Vice-Secretary of the European Association for the Study of the Liver (EASL), concludes: “Liver cancer is very frequently fatal and the incidence has already doubled in the past 20 years. Since there is a strong relationship between Hepatitis and liver cancer, concrete efforts have to be made to find those hepatitis carriers, so they can become patients and receive treatment before cancer can set in.

The event will take place today at the European Parliament in Brussels, Members’ Salon from 18.30h to 20.00h.

About ELPA

ELPA emerged from a desire amongst European liver patient groups to share their experiences of the often very different approaches adopted in different countries. ELPA was formally launched in Paris on April 14th 2005 during the annual conference of the European Association for the Study of the Liver (EASL) and now has 21 members from 17 countries.

ELPA’s aim is to promote the interests of people with liver disease by furthering awareness and prevention among healthcare professionals, policymakers and the public at large; by addressing the low profile of liver disease compared to other disease areas; by sharing experience of successful case examples as regards the management of the disease; by working with professional bodies such as EASL to ensure that treatment and care are aligned across Europe to the highest standards. Find out more about ELPA at: http://www.elpa-info.org/.

Cancer of the liver, also known as hepatocellular carcinoma, is the fifth most common type of cancer in the world. It is increasing in incidence, largely due to the spread of hepatitis C. Its growing prevalence may also be related to the rise of obesity and type-2 diabetes, which are associated with non-alcoholic fatty liver disease (NAFLD). However, liver cancers associated with NAFLD have been poorly described.

Researchers, led by Valerie Paradis of Beaujon hospital in Paris, decided to analyze a series of liver cancers which arose in patients whose only risk factor for chronic liver disease was metabolic syndrome. They compared their findings to the characteristics of hepatocellular carcinomas that developed in the setting of other chronic liver diseases.

Their retrospective analysis included 128 patients in their hospital who had undergone surgery to remove a liver tumor between 1995 and 2007. Of these, 81 patients had an overt cause of chronic liver disease (CLD), like hepatitis B or hepatitis C. Thirty-one patients had features of the metabolic syndrome (MS) as their only risk factor. And sixteen patients had no identifiable risk factors.

“Most hepatocellular carcinoma associated with features of metabolic syndrome as the only risk factor for chronic liver disease develop in non-fibrotic liver,” the authors report. They found that just over 35 percent of liver tumors in these patients occurred in bridging fibrosis or cirrhosis, compared to 75 percent in the patients with chronic liver disease.

“Our results suggest that well-recognized multistep progression, i.e. fibrosis-cirrhosis-HCC, may not be the main carcinogenic pathway in the context of metabolic syndrome,” they write. They suggest that the metabolic syndrome itself could have a direct cancer-causing effect, perhaps through the effects of insulin, lipid peroxidation or free radical oxidative stress.

They noted that most tumors arising in the context of the metabolic syndrome were well differentiated – nearly 65 percent compared to 28 percent in the patients with chronic liver disease. These tumors were more similar to those in patients with tumors from unknown causes, which also had better differentiation and a low prevalence of significant fibrosis.

Interestingly, the researchers found that among the patients with metabolic syndrome, five cases of liver cancer were associated with liver cell adenoma (a benign liver tumor).

“Our results suggest that a significant percentage of hepatocellular carcinoma that developed in the context of metabolic syndrome without significant fibrosis arose from malignant transformation of liver cell adenoma,” they report.

Also Included In: Cancer / Oncology; Obesity / Weight Loss / Fitness; Diabetes

“If these results are confirmed, this EGF variation could be used to determine which cirrhotic patients should be screened more intensively for tumor development,” says Kenneth Tanabe, MD, chief of Surgical Oncology at the MGH Cancer Center, the study’s lead author. “In addition, the molecular pathway controlled by EGF and its receptor EGFR – which is known to be important in several types of cancer – appears to be an excellent target for chemoprevention studies. This is a deadly cancer and so progress in prevention and early detection is critically important.”

HCC is the sixth most common solid tumor worldwide and most commonly develops in individuals with cirrhosis, which may be caused by infection with the hepatitis B or C viruses. There are currently no effective treatments for most HCC patients, so there is considerable interest in strategies that may prevent development of the tumor.

EGF’s normal function is to stimulate tissue growth. Animal studies have shown that elevated levels of this protein in the liver lead to tumor development and that blocking the protein’s receptor can prevent development of liver cancer. The current study was designed to determine whether cirrhotic patients with higher EGF levels are at greater risk for liver cancer and to determine the influence of a particular inherited gene on EGF levels in cirrhotic patients.

The researchers focused on a known variation in the EGF gene – the presence of the nucleotide guanine (G) instead of the more common adenine (A) in a particular location – which has been shown to increase EGF secretion in blood cells and raise the risk for malignant melanoma. Individuals inherit one copy of the gene from each parent and therefore have this gene with either two copies of A (A/A), two copies of G (G/G), or one copy of each (A/G). Genetic analysis of liver tumor cell lines showed that messenger RNA transcribed from DNA strands with the G allele was more stable that that transcribed from the A version, which could explain why cells with two G copies tend to secrete higher levels of EGF.

The researchers then studied tissue samples from all patients in the MGH Cancer Center Tumor Bank who had cirrhosis. Among the 207 patients with cirrhosis, most of whom were infected with the hepatitis C virus, 59 also had HCC. Patients with at least one copy of the G nucleotide had a significantly higher risk of developing HCC than did A/A patients – ranging from a more than twofold increase for those with one G to an over fourfold increase for those with two G alleles. In all three genotypes, tissue analysis showed that EGF levels were highest in the G/G patients, as was activation of the EGFR receptor. In addition, blood levels of EGF were highest in those with two copies of the G allele.

To confirm these finding in a different patient population, the MGH team worked with colleagues from the Paul Brousse Hospital in Paris. Samples from this group, all of whom had alcoholic cirrhosis, also showed that patients with the G/G version of the EGF gene had a significantly greater risk of developing the liver tumor than did the A/A patients, in this instance an almost threefold risk increase.

In both the MGH and French study groups, controlling for factors such as age and gender did not change the increased risk associated with the G allele. While both groups primarily consisted of Caucasian patients, in the MGH group, it was noted that the G allele was more common among Asian patients; and it is well known that more than half the cases of HCC worldwide occur in China.

“We now need to prospectively study EGF levels in cirrhotic patients, to see if elevated levels will correlate with a greater risk of developing HCC, and look at factors such as diet, drugs or ethnicity that may modulate EGF levels,” Tanabe says. “I think this is a terrific opportunity to see if targeting a specific pathway will prevent HCC in this group of patients, who are at risk for liver cancer because of their cirrhosis.” Tanabe is an associate professor of Surgery at Harvard Medical School.

Six years ago, the UC San Diego School of Medicine research team discovered the cause of the excess fibrous tissue growth that leads to liver fibrosis and cirrhosis, and developed a way to block excess scar tissue in mice. At that time, the best hope seemed to be future development of a therapy that would prevent or stop damage in patients suffering from the excessive scarring related to liver or lung disease or severe burns.

In their current study, Martina Buck, Ph.D., assistant professor of medicine at UCSD and the Veterans Affairs San Diego Healthcare System, and Mario Chojkier, M.D., UCSD professor of medicine and liver specialist at the VA, show that by blocking a protein linked to overproduction of scar tissue, they can not only stop the progression of fibrosis in mice, but reverse some of the cell damage that already occurred.

In response to liver injury for example, cirrhosis caused by alcohol hepatic stellate cell (HSC) activated by oxidative stress results in large amounts of collagen. Collagen is necessary to heal wounds, but excessive collagen causes scars in tissues. In this paper, the researchers showed that activation of a protein called RSK results in HSC activation and is critical for the progression of liver fibrosis. They theorized that the RSK pathway would be a potential therapeutic target, and developed an RSK inhibitory peptide to block activation of RSK.

The scientists used mice with severe liver fibrosis similar to the condition in humans with cirrhosis of the liver that was induced by chronic treatment with a liver toxin known to cause liver damage. The animals, which continued on the liver toxin, were given the RSK-inhibitory peptide. The peptide inhibited RSK activation, which stopped the HSC from proliferating. The peptide also directly activated the caspase or “executioner” protein, which killed the cells producing liver cirrhosis but not the normal cells.

“All control mice had severe liver fibrosis, while all mice that received the RSK-inhibitory peptide had minimal or no liver fibrosis,” said Buck.

Buck explained that the excessive collagen response is blocked by the RSK-inhibitory peptide, but isn’t harmful to the liver. “The cells continue to do their normal, healing work but their excess proliferation is controlled,” Buck said. “Remarkably, the death of HSC may also allow recovery from liver injury and reversal of liver fibrosis.”

The researchers found a similar activation of RSK in activated HSC in humans with severe liver fibrosis but not in control livers, suggesting that this pathway is also relevant in human liver fibrosis. Liver biopsies from patients with liver fibrosis also showed activated RSK.

The study expands on work reported in 2001 in the journal Molecular Cell announcing that a team led by Buck had found that a small piece of an important regulatory protein called C/EBP beta was responsible for fibrous tissue growth, or excessive scar tissue following injury or illness. When normal scarring goes awry, excessive build-up of fibrous tissue can produce disfiguring scars or clog vital internal organs and lead to serious complications. Buck and colleagues developed a mutated protein that stopped this excessive fibrous tissue growth.

“Six years ago, we showed a way to prevent or stop the excessive scarring in animal models,” said Buck. “Our latest finding proves that we can actually reverse the damage.”

Worldwide, almost 800,000 people die from liver cirrhosis each year, and there is currently no treatment for it. Excessive tissue repair in chronic liver disease induced by viral, toxic, immunologic and metabolic disorders all result in excessive scar tissue, and could benefit from therapy developed from the UCSD researchers’ findings.

The research was supported by grants from the National Institutes of Health, the Department of Veterans Affairs and UCSD’s Medical Research Foundation. Buck is the recipient of a Howard Temin Award from the National Cancer Institute.

University of California – San Diego

http://www.ucsd.edu

For patients infected with genotype 2 or 3, a 24 week course of treatment with flat dose RBV + PEG-IFN was as effective as the standard 48-week course, with better tolerability, and in the overall study population flat dosing of ribavirin was as effective as weight-based ribavirin. However, within the flat-dose cohort of patients with genotypes 2 and 3, sustained response rates showed a slight decline in the higher weight patients given flat-dosed ribavirin.

“These findings help define optimal therapy for U.S. hepatitis C patients,” says the study’s principal investigator, Dr. Ira M. Jacobson, the Vincent Astor Professor of Clinical Medicine at Weill Cornell Medical College and chief of the Division of Gastroenterology and Hepatology at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. “Our findings underscore that weight-based-dosed combination therapy is significantly more effective than the flat-dosed RBV regimen, especially in more difficult-to-treat patient groups, such as patients with genotype 1 and African-American patients. Patients being treated for hepatitis C should talk to their doctors to be sure they are receiving the most effective therapy.”

Reported in the same journal is a subanalysis of the WIN-R data that evaluates the efficacy of weight-based dosing among African-American participants with genotype 1 infection. Twice as many of these patients cleared the virus when treated with the weight-based RBV regimen vs. the flat dose (21% vs. 10%); a lower rate was shown in the general study population with genotype 1 HCV, 34% vs. 28.9%. (However, the fact that over 300 patients with an end of treatment response missed their 24-week, post-treatment follow-up appointment accounts for some treatment failures under a strict intent-to-treat analysis.)

“These results are particularly significant for African-Americans, a group with known lower rates of response to HCV therapy than reported in other ethnic groups. Weight-based dosing vs. flat dosing clearly showed the greatest therapeutic impact in this group,” says Dr. Jacobson.

“The study data strongly suggest adopting a 1400 mg/dose for patients who weigh more than 105 kg. In my opinion, the larger dose provides an opportunity for very heavy patients to have the same chance of cure as lighter patients without compromising safety,” says Dr. Jacobson.

Overall safety with weight-based dosing was similar to that of the flat 800 mg dose. There was no difference in the occurrence of serious adverse events in the entire group, as well as in the African-American group.

Researchers at NewYork-Presbyterian/Weill Cornell are at the forefront of developing more effective prescription therapy for patients with HCV genotype 1 and are testing many drugs in various stages of development.

Collaborating with the study’s principal investigator Dr. Jacobson was Dr. Robert S. Brown Jr., co-principal investigator of the study and associate professor of clinical medicine at Columbia University College of Physicians and Surgeons; and chief of clinical hepatology and medical director of the Center of Liver Disease and Transplantation at NewYork-Presbyterian Hospital/Columbia University Medical Center.

Dr. Jacobson is also medical director of the Center for the Study of Hepatitis C in New York City, a unique interdisciplinary Center established jointly by The Rockefeller University, New York-Presbyterian Hospital, and Weill Cornell Medical College. He serves as a consultant, investigator and speaker for Schering-Plough.

WIN-R Study

WIN-R (Weight-Based Dosing of PEG-INTRON and REBETOL) is a community-based access trial involving more than 5,000 patients at 225 centers across the U.S.

The uniquely large database of the WIN-R study allowed investigators to address other questions of interest, which have been presented at international meetings, including analyses of the response to HCV therapy based on age, baseline viral load, degree of liver fibrosis (scarring), and the study site at which the medication was delivered.

WIN-R is an investigator-initiated clinical study supported by Schering-Plough Corporation and monitored by Schering-Plough Research Institute as part of a post-marketing commitment to the U.S. Food and Drug Administration (FDA). PEG-INTRON and REBETOL are registered trademarks of Schering-Plough.

Hepatitis C

Hepatitis C is the most common blood-borne infection in America. It affects approximately 4 million people, or about one in every 50 adults, including a disproportionately high percentage of African-Americans. Chronic hepatitis C can cause cirrhosis, liver failure and liver cancer. It has been estimated that at least 20 percent of patients with chronic hepatitis C develop cirrhosis, and a smaller percentage of patients with chronic disease develop liver cancer. Patients with chronic hepatitis C and related cirrhosis are 100 times more likely to develop liver cancer than uninfected persons. About half of all cases of primary liver cancer in the developed world are caused by hepatitis C, and hepatitis C-related liver disease is now the leading cause for liver transplants.

NewYork-Presbyterian Hospital/Weill Cornell Medical Center

NewYork-Presbyterian Hospital/Weill Cornell Medical Center, located in New York City, is one of the leading academic medical centers in the world, comprising the teaching hospital NewYork-Presbyterian and Weill Cornell Medical College, the medical school of Cornell University. NewYork-Presbyterian/Weill Cornell provides state-of-the-art inpatient, ambulatory and preventive care in all areas of medicine, and is committed to excellence in patient care, education, research and community service. Weill Cornell physician-scientists have been responsible for many medical advances — from the development of the Pap test for cervical cancer to the synthesis of penicillin, the first successful embryo-biopsy pregnancy and birth in the U.S., the first clinical trial for gene therapy for Parkinson’s disease, the first indication of bone marrow’s critical role in tumor growth, and, most recently, the world’s first successful use of deep brain stimulation to treat a minimally-conscious brain-injured patient. NewYork-Presbyterian, which is ranked sixth on the U.S.News & World Report’s list of top hospitals, also comprises NewYork-Presbyterian Hospital/Columbia University Medical Center, Morgan Stanley Children’s Hospital of NewYork-Presbyterian, NewYork-Presbyterian Hospital/Westchester Division and NewYork-Presbyterian Hospital/The Allen Pavilion. Weill Cornell Medical College is the first U.S. medical college to offer a medical degree overseas and maintains a strong global presence in Austria, Brazil, Haiti, Tanzania, Turkey and Qatar. For more information, visit http://www.nyp.org and http://www.med.cornell.edu.

NewYork-Presbyterian Hospital
425 East 61st St., Fl. 7
New York, NY 10021
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http://www.nyp.org

Successful treatment depends on the early detection of fibrosis and cirrhosis. Currently, detection involves a surgical liver biopsy, which is an unpleasant, expensive procedure and carries some risk. Patients and doctors would prefer tests that are “not invasive” such as a blood test to detect and monitor liver disease.

Lead investigators Drs. Anand Mehta and Timothy Block report in the upcoming Journal of Virology, which appears online next week and in print February 2008, their discovery that the blood of most, if not all, people they tested with a diagnosis of liver cirrhosis, contains high levels of a special antibody that recognizes a carbohydrate sugar commonly found on bacteria. Detection of this antibody in the blood of an affected person correlates very well with a diagnosis of increasing fibrosis and cirrhosis in the new study.

“This is a fascinating discovery and is important because, if confirmed, the test could help us replace liver biopsy as a method for staging liver disease. In addition, it may be teaching us something about how liver disease occurs,” said David Thomas, M.D., Chief, Infectious Diseases, Johns Hopkins School of Medicine, Baltimore, MD.

Working with the National Cancer Institute (NCI) Early Detection Research Network, the researchers have been able to test this approach in 300 blood samples from people with liver disease, and can conduct the new test in thousands. Although the test is still experimental and more is needed before it can be used to monitor disease, the discovery is promising.

“If this work is validated, it may offer a new, non-invasive way to test for liver disease, allowing people to either avoid biopsy or to know when they really need one. It also implies that bacteria may have a much bigger role in initiating liver disease than realized, and even lead to new therapies,” said Block.

Complications from bacteria in people with cirrhosis are well understood; however, bacteria are not usually seen early in the disease. The significance of this new discovery may suggest earlier treatments with antibiotics could benefit patients with chronic liver disease.

About the Hepatitis B Foundation

The Hepatitis B Foundation is the only national nonprofit organization solely dedicated to finding a cure and improving the quality of life for those affected with hepatitis B worldwide through research, education and patient advocacy.

Hepatitis B Foundation

http://www.hepb.org

The research contributes to a growing body of evidence on the link between leg length and health.

The findings are based on almost 4300 women between the ages of 60 and 79, who had been randomly selected from 23 British towns.

Standing and seated height were measured to include leg and trunk length, and blood samples were taken to measure levels of four liver enzymes, ALT, GGT, AST and ALP.

These enzymes indicate how well the liver is working and whether it has been damaged. ALP is also an indicator of bone disease, such as osteoporosis.

The women were also quizzed in detail about their medical history, lifestyle, and social class, all of which are likely to influence health and stature.

Complete information was available for just over 3600 of the women.

The analysis showed that the longer the leg length, the lower were levels of ALT, GGT, and ALP. ALT levels, in particular, were lowest among the women with the longest legs.

ALT and ALP were highest among those women with the shortest trunk length.

The findings held true after adjusting for influential factors such as age, childhood social class, adult alcohol consumption, exercise, and smoking.

And the results remained the same after excluding those women who already had liver cancer, diabetes, cardiovascular disease, or osteoporosis.

“Our interpretation of the results is that childhood exposures, such as good nutrition that influence growth patterns also influence liver development and therefore levels of liver enzymes in adulthood and/or the propensity for liver damage,” say the authors.

Greater height may boost the size of the liver, which may decrease enzyme levels so ensuring that the liver is able to withstand chemical onslaught much more effectively, they add.

There may also be factors in common with the increased risks of other diseases, as ALT, GGT, AST and ALP are also associated with diabetes and cardiovascular disease, they say.

The association between height components (leg and trunk length) and adult levels of liver enzymes
Journal of Epidemiology and Community Health 2007; 62: 48-53

TMC435350-C201 is a phase IIa proof-of-concept, blinded, randomized, placebo-controlled trial to assess the effectiveness, safety, tolerability, and pharmacokinetics of four different dose regimens of TMC435350 (25 mg daily, 75mg daily, 200mg daily, 400mg daily). 96 treatment-naïve and 24 treatment-experienced patients with chronic genotype-1 HCV infection will be enrolled in the trial which will be conducted at more than 20 sites in Europe. Patients will receive either TMC435350 or placebo once daily (qd) for 28-days. Standard of Care (SoC) treatment, peginterferon alpha-2a (Pegasys®) and ribavirin (Copegus®), will be provided for 48 weeks or, optionally, for 24 weeks for those patients with an undetectable HCV viral load at Week 4 and who remain undetectable at Week 20. Patients will be followed-up for 24 weeks after the end of SoC to allow evaluation of sustained virologic response (SVR).

In the phase I study TMC435350 was administrated at 200 mg qd for five days to patients chronically infected with genotype-1 hepatitis C virus (HCV). The viral load reductions met the target set for the trial. These results will be submitted for presentation at the Annual Meeting of the European Association for the Study of the Liver in Milan in April 2008

The earlier phase I study results were reported at the AASLD Liver Meeting in Boston, November 2-6 2007. They showed that in this study TMC435350 was generally well-tolerated when given to HCV-negative healthy volunteers at single oral doses up to 600 mg, and at 5 days of oral doses up to 400 mg. The plasma levels of TMC435350 24 hours after day 5 dosing at 200 mg qd were more than 250-fold in excess of the HCV replicon EC50 value.

The principal causes of liver fibrosis/cirrhosis in Japan and China are viral infection by the Hepatitis B virus or Hepatitis C virus. Alcohol abuse and fatty liver may also lead to liver fibrosis. Fibrosis is a complicated disease process during which liver cells are replaced with scar tissue and gradually damages liver function. Inflammation is usually the first step of this process. In China alone, it is estimated that 130 million people are infected with and carrying the HBV virus. A significant percentage of them will develop liver fibrosis/cirrhosis, frequently resulting in mortality.

Liver fibrosis has a very large patient population in Japan, China, and many other Asian countries. Liver disease is also called a “National Disease” in China. “F351 may provide a breakthrough therapy for liver fibrosis patients at risk of developing cirrhosis complication‚” stated Ying Luo‚ Ph.D., Chief Executive Officer of GNI, Ltd. and Shanghai Genomics, Inc. “This will be our second product in clinical trials, which represents a major milestone and expands our product portfolio. The IND approval demonstrates our R&D and regulatory team’s capability and our determination to develop new drugs for diseases prevalent in Asia, especially in Japan and China,” continued Dr. Luo.

“The initiation of this clinical study follows years of our research on key inflammatory signaling pathways in human cells and in animals‚” added Jun Wu‚ Ph.D., Chief Scientific Officer of GNI, Ltd. and Shanghai Genomics, Inc. “We have shown that F351 specifically inhibits over-production of collagen by liver fibroblasts following inflammatory insults. The possibility to intervene in such inflammatory process has enormous relevance to the treatment of fibrotic diseases in humans.”

About GNI

Founded in 2001, GNI is a clinical-stage international drug development company with its headquarter in Japan and major operation in China. GNI has successfully mapped gene regulatory networks via a complex process of reverse-engineering. Furthermore, GNI has developed the technology required to apply this data to drug development and discovery. In June 2005, GNI acquired Shanghai Genomics, which operates an integrated drug discovery and development platform in Shanghai, China. The combined strength of GNI and Shanghai Genomics has resulted in research collaborations with major international pharmaceutical companies. In August 2007 GNI was listed on the Mothers market of the Tokyo Stock Exchange (ticker symbol: 2160). For further information, please visit http://www.gene-networks.com and http://www.shanghaigenomics.com.

This press release contains “forward-looking” statements, including statements related to GNI’s plans to pursue development of product candidates and the timing thereof. Any statements contained in this press release that are not statements of historical fact may be deemed to be forward-looking statements. Words such as “continue,” “could,” “may,” and similar expressions are intended to identify these forward-looking statements. There are a number of important factors that could cause GNI’s results to differ materially from those indicated by these forward-looking statements, including risks associated with the timing and success of clinical trials and the commercialization of product candidates. GNI does not undertake any obligation to update forward-looking statements.

“What is tragic about this situation,” said Dr. Douglas Dieterich, Professor of Medicine, Liver Diseases, Mount Sinai School of Medicine and Chairman of the Board of the Greater New York City Chapter of ALF, “is that innocent people are now at risk of contracting potentially deadly viruses: hepatitis B, hepatitis C, and HIV.

Although most Americans are familiar with HIV, most do not know about hepatitis B and C, the two most common forms of chronic liver disease. Hepatitis B is 100 times more infectious and hepatitis C four times more infectious than HIV. More than 5 million Americans have hepatitis B or C. Viral hepatitis exhibits few if any symptoms, and the undetected illness can progress to a point where treatment may no longer be effective. These viral infections can lead to cirrhosis, liver cancer and death if untreated.

“When it comes to hepatitis, for example, many doctors don’t know how it is transmitted or when to test their patients,” said Dieterich. “Testing can allow for early diagnosis and treatment, preventing the virus from developing into cirrhosis of the liver or cancer.”

Although hepatitis B is vaccine-preventable, there is no complete cure for those already infected. And while hepatitis C can be treated successfully for half of those infected, there is no vaccine to protect the uninfected. Hepatitis B and C infection can be avoided by using only sterile needles for tattoos or body piercing, avoiding injection drugs, and practicing safer sex.

“ALF works on many fronts in order to combat liver disease,” said Rick Smith, the President and CEO of the American Liver Foundation. “Unfortunately, one of the greatest obstacles to overcoming liver disease is the ignorance and the stigma attached to it. That is why we provide medical seminars for physicians as well as awareness campaigns for the general public.”

About the American Liver Foundation

The American Liver Foundation is the nation’s leading nonprofit organization promoting liver health and disease prevention. ALF provides research, education and advocacy for those affected by liver-related diseases including hepatitis. Please visit the American Liver Foundation’s Web site at http://www.liverfoundation.org.