New DNA therapy for advanced mouth cancer

Source: www.dentistry.co.uk Author: staff A research team has been awarded a patent after developing a new DNA therapy for head and neck cancer sufferers. Researchers from the University of Pittsburgh School of Medicine in the US, aims to develop a safe and effective alternative to standard chemotherapy treatments which cause debilitating side-effects. Based on a form of genetic therapy called ‘antisense', the new DNA therapy injections target the epidermal growth factor receptor (EGFR), blocking the growth of a protein which is found on the surface of many types of cancer cells. During the initial Cancer Institute study, led by Dr Jennifer Grandis, the injections were well-tolerated, and the tumours which were being targeted by the treatment disappeared or shrank considerably in more than a quarter of the patients. The British Dental Health Foundation has welcomed the latest development in treating this deadly disease. Chief executive Dr Nigel Carter said: 'These new findings show that this new DNA therapy can have the potential as both a safe and effective advanced cancer treatment. One of the major problems with mouth cancer is that it often presents in late stages, significantly reducing survival – so a late stage treatment is particularly welcome. 'Head and neck cancers have a strong association with environmental and lifestyle risk factors including smoking tobacco, alcohol consumption and the sexually transmitted human papilloma virus (HPV). 'Research has recently suggested that the HPV virus, transmitted via oral sex, could soon become the most common cause of mouth cancer.' Cancers caused [...]

2010-02-07T09:42:31-07:00February, 2010|Oral Cancer News|

GenVec receives orphan drug designation

Source: www.onemedplace.com Author: staff GenVec’s experimental drug to treat pancreatic cancer has been granted orphan drug status by the U.S. Food and Drug Administration (FDA). The drug candidate TNFerade stimulates the production of an immune system protein known for having anti-cancer effects. Shares in GenVec rose 25 percent following the announcement. Last summer, Gaithersburg, Maryland-based GenVec announced positive data from a Phase II/III clinical trial of TNFerade. The drug provided a 42.5% reduction in the risk of death when combined with standard treatment, when compared to standard treatment alone. TNFerade is also being explored as a candidate to treat esophageal cancer, rectal cancer, and head and neck cancer. Note: The FDA grants orphan drug designation to drugs that may be significantly more effective than currently existing treatments, and target conditions that affect less than 200,000 U.S. patients per year. Upon approval, drugs granted orphan status enjoy seven years of marketing exclusivity in the United States.

2009-11-08T12:07:30-07:00November, 2009|Oral Cancer News|

Researchers pinpoint a new enemy for tumor-suppressor P53

Source: biocompare.com Author: staff Researchers at The University of Texas M. D. Anderson Cancer Center have identified a protein that marks the tumor suppressor p53 for destruction, providing a potential new avenue for restoring p53 in cancer cells. The new protein, called Trim24, feeds p53 to a protein-shredding complex known as the proteasome by attaching targeting molecules called ubiquitins to the tumor suppressor, the team reported this week in the Proceedings of the National Academy of Sciences Online Early Edition. "Targeting Trim24 may offer a therapeutic approach to restoring p53 and killing tumor cells," said senior author Michelle Barton, Ph.D., professor in M. D. Anderson's Department of Biochemistry and Molecular Biology. The discovery is based on an unusual approach to studying p53, which normally forces potentially cancerous cells to kill themselves and is shut down or depleted in most human cancers. Studies of the p53 protein and gene tend to focus on cancer cell lines or tumors, where the dysfunction already is established, Barton said. "We wanted to purify p53 from normal cells to better understand the mechanisms that regulate it." The team developed a strain of mice with a biochemical tag attached to every p53 protein expressed. After first assuring that the tagged p53 behaved like normal p53, the team then used the tag, or hook, to extract the protein. "We could then identify proteins that were attached to p53, interacting with it, through mass spectrometry," Barton said. They found Trim24, a protein previously unassociated with p53 that is [...]

Cancer hope after cell discovery

Source: The Press Association (ukpress.google.com) Author: staff Scientists have announced they had identified a "new route" for messages to cells in fruit flies which could lead to the growth of breast, ovarian, head and neck cancer in people. The team at the University of Liverpool found signals from a molecule called Epidermal Growth Factor Receptor (EGFR) on the surface of a cell are fed through a protein called pico in flies, which has a similar protein in humans called Lamellipodin. This process controls and regulates cell growth and division and its discovery has been described as "important basic research" by the charity Cancer Research UK. The EGFR molecule sends signals that drive the growth of breast cancer, ovarian cancer and cancers of the head and neck in people. Lead author of the study and Cancer Research UK scientist Dr Ekaterina Lyulcheva, who is based at the University of Liverpool, said: "Before now, scientists knew about the presence of these molecules and their possible link to cancer, but no-one knew how they talked to each other, to ultimately control tissue growth. "We know EGFR is linked to cancer but we have not shown that Lamellipodin is used to drive the growth of cancer in humans. Lamellipodin is a similar protein to pico in fruit flies that has similar functions." Dr Lyulcheva said that although Lamellipodin and pico had similar functions more research in humans would need to be undertaken to discover if Lamellipodin was used to drive the growth of the [...]

2008-11-12T08:03:20-07:00November, 2008|Oral Cancer News|
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