DNA

New test genetically fingerprints tumors

Source: online.wsj.com
Author: Ron Winslow

In a fresh advance for the burgeoning field of personalized medicine, researchers have developed a blood test based on the DNA of tumors that could help tailor treatment for individual cancer patients.

The report, announced Thursday, represents one of the most tangible examples yet of how the ability to sequence a person’s entire genetic code could have a direct impact on patient care. There have been a flurry of reports on new sequencing technology that is yielding enormous amounts of information about genetics and disease, but that has yet to deliver much in the way of new treatment strategies.

“For cancer patients there hasn’t been much utility so far. This may prove to be one of the first useful approaches,” said Victor Velculescu, co-director of the cancer biology program at Johns Hopkins University’s Kimmel Cancer Center and senior author of the new study.

Much research involving whole-genome sequencing is aimed at finding differences in the individual letters that make up the genetic code. The belief is that those small alterations will point to molecular pathways that regulate disease, which would be potential targets for drug therapies.

The Hopkins researchers, writing in the journal Science Translational Medicine, took a different approach. They scanned the DNA of tumors taken from six patients with breast or colon cancer, looking not for tiny DNA changes, but what they call rearrangements in large sections of the genome of tumor cells. The DNA of tumors varies genetically from that of normal tissue, and the rearrangements are essentially a fingerprint of the cancer.

The findings suggest that by testing blood for this fingerprint, doctors will be able to learn whether a patient treated for cancer is free of disease or needs additional or more aggressive care.

“It’s a very clever use of the [sequencing] technology,” said Jeffery Schloss, program director for genome technology at the National Human Genome Research Institute, a division of the National Institutes of Health.

Dr. Schloss, who wasn’t involved with the Hopkins study, likened the approach to drawing a map. Sequencing the letters of the genetic code would be akin to plotting every house in a large neighborhood. The Hopkins team was looking only for neighborhoods—in particular, neighborhoods out of place compared with where they would be in normal tissue.

The uniqueness of such “neighborhood” rearrangements is what makes the DNA a good biomarker for the status of tumors, Dr. Velculescu said. A blood test can detect evidence of even minuscule levels of such alterations. That can indicate, for instance, whether a tumor may be progressing after initially responding to treatment or whether any residual disease is present after surgery to remove a tumor. That could help a doctor and patient decide what other treatment options to pursue.

In the study, researchers tracked for two years one patient whose disease initially responded to treatment and then recurred. Levels of the DNA marker in the patient’s blood accurately reflected the course of the disease, researchers said. The test wouldn’t help predict which drugs a patient is likely to respond to—that likely would require a more detailed DNA scan, researchers said.

This advance comes as the cost of sequencing a patient’s entire genome has fallen sharply—to less than $10,000 now from about $1 million three years ago, according to companies that make sequencing machines. Experts predict that the cost will soon get to about $1,000, potentially making it affordable for medical centers to routinely run the genome of patients with cancer and other diseases.

Currently, cancer doctors often use CT scans to check on the status of a tumor—at a cost of about $1,500, the Hopkins researchers said. They estimated the current cost of the DNA test at about $5,000 but suggest the cost will soon be comparable to a CT scan.

Hopkins has filed patents for the technology. Dr. Velculescu and two other co-authors of the paper are entitled to a share of royalties on sales of any products related to the research if it is commercialized. Further research is necessary to validate the approach with more patients and more cancer types, but researchers said such a test could be ready to use within two years and widely available “within several years.”

February, 2010|Oral Cancer News|

Human papillomavirus, p16 and p53 expression associated with survival of head and neck cancer

Source: 7thspace.com
Author: staff

P16 and p53 protein expression, and high-risk human papillomavirus (HPV-HR) types have been associated with survival in head and neck cancer (HNC). Evidence suggests that multiple molecular pathways need to be targeted to improve the poor prognosis of HNC.

Purpose:
This study examined the individual and joint effects of tumor markers for differences in predicting HNC survival. P16 and p53 expression were detected from formalin-fixed, paraffin-embedded tissues by immunohistochemical staining. HPV DNA was detected by PCR and DNA sequencing in 237 histologically confirmed HNC patients.

Results:
Overexpression of p16 (p16+) and p53 (p53+) occurred in 38% and 48% of HNC tumors, respectively. HPV-HR was detected in 28% of tumors. Worse prognosis was found in tumors that were p53+ (disease-specific mortality: adjusted hazard ratios, HR=1.9, 95% CI: 1.04-3.4) or HPV (overall survival: adj. HR=2.1, 1.1-4.3) but no association in survival was found by p16 status.

Compared to the molecular marker group with the best prognosis (p16+/p53/HPV-HR: referent), the p16/p53+/HPV group had the lowest overall survival (84% vs. 60%, p<0.01; HR=4.1, 1.7-9.9) and disease-specific survival (86% vs.

66%, p<0.01; HR=4.0, 1.5-10.7). Compared to the referent, the HRs of the other six joint biomarker groups ranged from 1.6-3.4 for overall mortality and 0.9-3.9 for disease-specific mortality.

Conclusion:
The p16/p53/HPV joint groups showed greater distinction in clinical outcomes compared to results based on the individual biomarkers alone. This finding suggests that assessing multiple molecular markers in HNC patients will better predict the diverse outcomes and potentially the type of treatment targeted to those markers.

Author: Elaine SmithLinda RubensteinHenry HoffmanThomas HaugenLubomir Turek
Credits/Source: Infectious Agents and Cancer 2010, 5:4

February, 2010|Oral Cancer News|

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 by viral infections can also be prevented by making positive lifestyle changes to reduce these risks.

World Cancer Day was marked around the globe yesterday (Thursday 4 February) in an effort to highlight the link between infections and cancer.

Dr Carter said: ‘Thirty per cent of mouth cancer cases have been linked to a poor diet. Eating a balanced diet with plenty of fruit and vegetables, quitting smoking and cutting down on alcohol consumption lowers the risk of mouth cancer.’

The British Dental Health Foundation’s Mouth Cancer Action Month campaign, which runs each November in the UK with the message of ‘If In Doubt, Get Checked Out’, stresses the importance of following this advice by undertaking regular dental visits and self-examination.

February, 2010|Oral Cancer News|

HPV-associated base of tongue squamous cell carcinoma incidence increasing in Sweden

Source: www.hemonctoday.com
Author: staff

The incidence for base of tongue squamous cell carcinoma increased significantly in Sweden between 1998 and 2007, and by 2007, more than 80% of these cases were HPV-positive.

Various studies during the past 20 years have indicated that HPV is a risk factor for oropharyngeal cancer. However, few studies have assessed the specific sub-sites of the oropharynx.

In this study, researchers assessed the increased incidence of base of tongue cancer and the association of HPV in 109 patients diagnosed with base of tongue cancer between 1998 and 2007 in Stockholm, Sweden.

The researchers obtained diagnostic pretreatment paraffin-embedded tumor biopsies from 95 patients. DNA samples were obtained from 30-mcm paraffin-embedded base of tongue biopsy slices. Age at diagnosis ranged from 41 to 85 years.

From 1970 to 2007, the age-standardized incidence of base of tongue squamous cell carcinoma increased from 0.15 per 100,000 person-years between 1970 and 1974 to 0.47 per 100,000 person-years between 2005 and 2007.

HPV DNA was found in 75% of base of tongue cancer cases during this time. Of the HPV-positive tumors, 86% were HPV-16–positive and seven were HPV-33–positive.

During the study period, the incidence of HPV-positive base of tongue cancers persistently increased (see chart). A significant increase was found in the proportion of HPV-positive cancer between 1998 and 2001 compared with 2004 and 2007 (58% vs. 84%; P<.05).

When compared with patients with HPV-negative tumors, patients with HPV-positive tumors were likely to be stage IV (P<.02) and had less advanced T-stage (P<.05 for T2; P<.01 for T3); however, these patients had more advanced N-stage (P<.01 for N0; P<.01 for N2a-c).

Source: Attner P. Int J Cancer. 2010;doi:10.1002/ijc.24994.

February, 2010|Oral Cancer News|

1,000: the magic number in genomic research

Source: www.minnpost.com
Aurhor: Sharon Schmickle

The number 1,000 is emerging as a standard benchmark on the frontiers of genomic research.

In the 1000 Genomes Project — launched two years ago — American, British, Chinese and German scientists are sequencing the genomes of some 1,000 individuals from around the world in order to aid medical research as it relates to human genetic variation.

Then there’s the goal of the $1,000 genome. Reduce the cost of accurately spelling an individual’s DNA to that level and we could see practical results from decades of genomic discovery — even at the clinical level. A research team from Complete Genomics Inc. in Mountain View, California, reported progress in that regard this week in the journal Science.

Now comes a new report from the “1,000 tumor” project at the University of Chicago’s Institute for Genomics and Systems Biology.

The Chicago scientists are working toward the goal of collecting and analyzing the genetic sequences and variations of every gene expressed by 1,000 tumors. One year into the three-year project, they have completed data for genes expressed by 100 tumors — primarily breast cancer, head and neck cancer, and leukemia. In the process, they have streamlined techniques for analyzing the remaining 900 tumors.

Meanwhile, by correlating genetic data with patient outcomes, the Chicago team has begun to identify genetic patterns within tumors that may help them predict how a cancer will behave. Eventually, the research should help identify which patients would benefit from which treatments.

We must have at least 1,000 genome projects around the world at this point in the research. Has anyone bothered to count?

The Mayo Clinic reported in November that its cancer research team in Arizona has completed its first whole human genome sequencing on a patient with multiple myeloma, a cancer of the bone marrow. Among other information, they captured an entire snapshot of the patient’s cancer cells through various stages of the disease.

Mayo teams in Rochester, Minn., are working on other genomic studies as are scientists at the University of Minnesota.

This will be a great field to watch in this new decade.

January, 2010|Oral Cancer News|

Liverpool scientists working on vaccine for mouth cancer

Source: www.liverpoolecho.co.uk
Author: Liza Williams

ONE central project the scientists and doctors are working on is a vaccine for mouth cancer. Liverpool researchers have found some cases are caused by the HPV virus – the same bug which causes cervical cancer. They have discovered that two-thirds of tonsil cancer tumour samples showed evidence of the HPV-16 gene.

The work is particularly important because the researchers are also seeing the rates of tonsil cancer doubling in non-smokers and non-drinkers – two of the main causes of the disease.

They have found a DNA test helps to predict whether a patient has HPV. This could be used to decide which treatment is best for the patient, because both chemo and radiotherapy are more successful in patients with the virus.

They are now developing a clinical trial for a HPV vaccine for head and neck cancer, like the jab given to teenage girls to prevent cervical cancer.

January, 2010|Oral Cancer News|

Scientists decode entire genetic code of cancer

Source: www.popsci.com
Author: Jeremy Hsu

And cigarette smokers get a free mutation in every pack

In a major step toward understanding cancer, one of the biggest problems bedeviling modern medicine, scientists have now cracked the genetic code for two of the most common cancers. This marks just the beginning of an international effort to catalog all the genes that go wrong among the many types of human cancer, the BBC reports.

Cracking the Cancer Code A cluster of breast cancer cells, with blue ones marking actively growing cells and yellow marking dying cells. Could scientists crack their code next?
Cracking the Cancer Code A cluster of breast cancer cells, with blue ones marking actively growing cells and yellow marking dying cells. Could scientists crack their code next?

Too much time spent under the sun apparently leads to most of the 30,000 mutations contained within the DNA code for melanoma, or skin cancer. Outside experts told the BBC that no previous study has managed to link specific mutations to their causes.

Wellcome Trust scientists also found more than 23,000 errors in the lung cancer DNA code, with most caused by cigarette smoke exposure. A typical smoker might get one new mutation, possibly harmless but also possibly a cancer trigger, for every 15 cigarettes that they smoke.

The new cancer maps could lead to better blood tests for diagnosing the respective cancers, as well as better targeted drugs. Blood tests might even reveal the DNA patterns that suggest cancer lies on the horizon.

The International Cancer Genome Consortium still expects to spend hundreds of thousands of dollars in cracking the code of the many human cancers. The U.S. has the job of studying cancers of the brain, ovary and pancreas, while the UK examines breast cancer. China is tasked with decoding stomach cancer, Japan is focused on liver cancer, and India has taken a crack at mouth cancer.

This painstaking research can only help futuristic treatment efforts, such as nanoparticle-targeted lasers and do-it-all nanoparticles that can track, tag and kill cancer cells. But those cancer-resistant mole rats should still count their lucky stars.

December, 2009|Oral Cancer News|

Microarray technologies in the diagnosis and treatment of head and neck cancer

Source: emedicine.medscape.com
Authors: Perminder S Parmar, MD et al.

Introduction
Since the draft sequence of the human genome was published in 2001 (Lander, 2001), the Cancer Genome Anatomy Project index of tumor genes has classified more than 40,000 genes directly or indirectly involved in one or more cancers (Strausberg, 2001; Strausberg, 2000). Conventional techniques of gene investigation in cancer rely on the identification of single genetic alterations associated with disease. This has proven to be both time consuming and cost ineffective. The introduction of complementary DNA (cDNA) microarray technology in 1995 (Schena, 1995) has helped to facilitate the identification and classification of DNA sequence information and the assignment of functions to these new genes by allowing investigators to analyze expression of thousands of genes simultaneously in a single experiment.

Microarrays are a significant advance because they contain a very large number of genes and because of their small size. Therefore, microarrays are useful when one wants to survey a large number of genes quickly or when the study sample is small. Microarrays may be used to assay gene expression within a single sample or to compare gene expression in 2 different cell types or tissue samples, such as in healthy and diseased tissue. Because a microarray can be used to examine the expression of hundreds or thousands of genes at once, it promises to revolutionize the way gene expression is examined.

Methods
DNA microarrays are small solid supports onto which the sequences from thousands of different genes are attached at fixed locations. The supports themselves are usually glass microscope slides but can also be silicon chips or nylon membranes. The DNA is printed, spotted, or actually synthesized directly onto the support.

Messenger RNA (mRNA) from the sample of interest can serve as a template for producing complementary DNA (cDNA) in the presence of a reverse transcriptase enzyme. This cDNA can then be fluorescently labeled and hybridized to the target gene sequences on the microarray. A confocal scanner then reads the fluorescent intensity of each hybridized sequence in the array. The scanner that records the intensity value is linked to digital image analysis software, which produces a color-coded image of the array, and a quantitative value is recorded for each target gene. The intensity of fluorescence is analyzed and correlates with expression of the gene.

The data produced from a microarray experiment typically constitute a long list of measurements of spot intensities and intensity ratios, generated either by a pair-wise comparison of 2 samples or by a comparison of several samples with a common control. The challenge is to sort through this data to find meaningful results. Because of the complexity of the data sets generated by microarray experiments, the use of data-analysis software is essential. Several commercial and public data-analysis tools have been developed for this purpose.

Current Applications In Head And Neck Oncology
In recent years, the use of microarray technology has been of great interest in head and neck squamous cell carcinoma (HNSCCa). Microarrays may eventually help in the understanding of the disease and ultimately lead to improvements in diagnosis, treatment, and outcome (Warner, 2004). Furthermore, the quantitative and qualitative aspect of microarrays may eventually be exploited to screen for molecular markers of head and neck cancer (Sok, 2003). Numerous expression studies of HNSCCa have been performed (Sok, 2003; Belbin, 2002; Villaret, 2000; Leethanakul, 2000; Squire, 2002).

Belbin et al used complementary DNA (cDNA) microarrays that contained 9216 clones to measure global patterns of gene expression in HNSCCa. Through the use of statistical analysis, they identified 375 differentially expressed genes, which divided 17 patients with head and neck tumors into 2 clinically distinct subgroups based on gene-expression patterns. The results of their analysis demonstrated that gene-expression profiling can be used as a predictor of outcome and highlighted pathways, meriting exploration for possible links to outcome in HNSCC.

Using cDNA subtractive methodology in conjunction with microarray technology to screen for HNSCCa-specific genes, Villaret et al were able to identify 9 known genes that were significantly overexpressed in HNSCCa compared with healthy tissue specimens. In addition, they found 4 previously unidentified genes that were overexpressed in a subset of tumors.

Using a cDNA array of 588 known human cancer-related genes and 9 housekeeping genes, Leethanakul et al demonstrated a consistent decrease in the expression of differentiation markers, such as cytokeratins, and an increase in the expression of numerous signal-transducing and cell cycle regulatory molecules, as well as growth and angiogenic factors and tissue-degrading proteases. The authors also found that most HNSCCas overexpress members of the Wnt and Notch growth and differentiation regulatory system, suggesting that the Wnt and Notch pathways may contribute to squamous cell carcinogenesis.

In their study, Squire et al, using spectral karyotyping (SKY), comparative genomic hybridization (CGH), and microarrays, identified consensus regions of chromosomal imbalance and structural rearrangement in HNSCCa. The authors were able to demonstrate recurrent chromosomal alterations using CGH and SKY and to correlate them to expression array analysis.

In their study, Sok et al, using hierarchical clustering analysis, revealed that the gene-expression profiles obtained from a panel of 12,000 genes could distinguish tumor from nonmalignant tissues. Gene expression changes were reproducibly observed in 227 genes, representing previously identified factors associated with neoplasia. Furthermore, significant expression of the collagen type XI alpha-1 gene and a novel gene were reproducibly observed in all 9 tumors, whereas these genes were virtually undetectable in their corresponding, adjacent nonmalignant tissues.

Future
Despite strides in prevention and advances in treatment, cancer of the head and neck remains a disease of considerable morbidity and mortality. The use of complementary DNA (cDNA) microarray technology to explore gene expression on a global level is rapidly evolving. Although still in its infancy, cDNA microarray technology may prove helpful in the diagnosis, prognosis, and management of head and neck cancer.

Authors and affiliations:
James M Pearson, MD, Staff Physician, Department of Otolaryngology – Head and Neck Surgery, New York Eye and Ear Infirmary; Stimson P Schantz, MD, Head, Department of Otolaryngology, Division of Head and Neck Surgery, New York Eye and Ear Infirmary

November, 2009|Oral Cancer News|

At our throats

Source: www.forbes.com
Author: Matthew Herper

Oncologist Maura Gillison was looking for patients with tonsil cancer for a clinical study several years ago. The first enlisted was a malpractice lawyer, followed by a doctor, then a scientist. She joked to a colleague that all she needed was a rear admiral. In walked a member of the military brass. All were in their 30s, 40s and 50s.

People in their prime didn’t used to get throat tumors. Head-and-neck cancer, as doctors call it, was a disease of older problem drinkers who also chain-smoked (more men than women). Years of exposure to scotch and Lucky Strikes would damage the DNA of cells lining the throat, leading to cancer.

But Gillison, 44, a professor at Ohio State University, was among the first researchers to make a startling realization: The old cigarettes-and-alcohol form of the disease was being eclipsed by a new form, caused by the same human papilloma virus (HPV) that causes cervical cancer. The tumors grow in the tonsils or in the tissue that remains after tonsillectomy. The only good news is that the prognosis for these patients is better than for the old disease.

Gillison and researchers at the National Cancer Institute estimate that 4,000 people, 75% of them men, develop this new form of throat cancer annually. That’s only a tenth of head-and-neck cases, but it’s half as many people as get cervical cancer in the U.S. More worrisome, Gillison’s work shows HPV tonsil cancer is increasing at a rate of 5% a year, unusual growth for a cancer diagnosis, even though throat infection with the HPV strain that causes it is exceedingly rare. Any spread of the virus could make the number of cases increase dramatically. “I’m very worried,” says Otis Brawley, chief medical officer of the American Cancer Society. Skeptics say the association is not proven, and that too much of the work comes from just Gillison.

Both Gillison and Brawley think a solution may exist: Vaccinate all boys, starting as early as age 9, with Merck’s HPV vaccine, Gardasil, now heavily promoted for cervical cancer. Gardasil, however, is already the source of all sorts of controversy. Antivaccine groups oppose it because of its high costs ($360 for three shots) and alleged side effects; the FDA says the vaccine is safe. GlaxoSmithkline is developing its own HPV vaccine.

Gillison spent three years trying to draw Merck’s attention to HPV tonsil cancer. Finally, she is working with Merck to design a study to see if Gardasil can affect HPV infection in the throat. Merck admits studying the problem is “challenging” but says the potential is big.

Interested in cancer-causing viruses, Gillison started work on the HPV problem in 1996 when she was finishing her Ph.D. and oncology training at Johns Hopkins University. She signed up with a group studying HPV and cervical cancer. But she switched to studying throat cancer patients after finding a few research papers reporting cases in which tumors had the DNA of the HPV virus inside them.

She was shocked to find a substantial number of throat tumors had the HPV type. She also noticed something dramatic when she organized HPV patients by the year they were born. Starting with patients born in 1935, there had been an increase in the number of cases every single year.

Researchers realized that a big change in sexual behavior in the 1950s and 1960s–mainly, that people had more sexual partners–had allowed a virus that had been rare to spread throughout the population. Some researchers say gay men and women seem underrepresented, possibly because they catch the virus elsewhere in the body and develop immunity.

What appears to happen is that one strain of the HPV virus, which is transmitted largely through oral sex, but also by French kissing or even just sharing a water glass, suppresses two anticancer genes.

HPV tonsil cancer is not as lethal as traditional throat cancers, but the treatment is still brutal. Martin Duffy, a 69-year-old Boston economist and consultant who doesn’t smoke and has run 40 Boston marathons, dropped 30 pounds to 120 pounds while being treated with Erbitux and radiation. He was diagnosed with tonsil cancer in February and is slowly recovering.

The death rate in head-and-neck cancer has been dropping, but doctors are still discouraged: It turns out the less threatening virus was responsible for many of those cancers. James Rocco, a head-and-neck surgeon at the Massachusetts Eye & Ear Infirmary, says, “We’re probably doing no better than we were 30 years ago.”

October, 2009|Oral Cancer News|

DNA test could be key to targeting treatments for head and neck cancer

Source: news.biocompare.com
Author: staff

It is estimated that more than 7,000 people are diagnosed with head and neck cancer each year in the UK and approximately 3,500 cases result in death. These cancers include tumours of the mouth, lips, throat and voice-box, and some have been linked to the sexually transmitted infection, HPV-16. Scientists at Liverpool analysed the DNA of more than 90 cancerous tissue samples to look for genes that indicated infection.

The team found that nearly two thirds of tonsil tumour samples showed evidence of the HPV-16 gene. It is thought that chemical alterations in the virus’s DNA trigger the production of proteins that can alter the rate at which cells grow and repair. This strongly increases the possibility of subsequent cancer development. Recent studies have found, however, that patients who have the HPV infection when they are diagnosed with cancer, respond better to chemotherapy or radiation therapy than those that do not have the infection. The work will be presented at the National Cancer Research Institute’s (NCRI) Cancer Conference in Birmingham today.

Mr Richard Shaw, from the School of Cancer Studies, explains: “Recent evidence demonstrates the possible involvement of HPV in the development of tonsil cancer, particularly in non-smokers. Interestingly, the treatment efficiency of chemotherapy and radiation, seems to differ between HPV positive and negative cases. We also need to find out why only a small percentage of people with this common infection develop this cancer. Our study, however, gives us a new lead towards a risk marker.

“It is thought that HPV interacts in the cell with genes controlling the chemical modification of DNA, which affects gene expression and tumour behaviour. Our study shows that HPV may be a trigger of tonsil cancer, independent of the known common causes, such as smoking or drinking. The work also suggests that a DNA test to determine the activity of HPV, could be used to identify the most effective treatment for each individual patient.

“Liverpool has the largest centralised head and neck oncology practice in the UK and our data show a doubling in the rate of non-drinkers and non-smokers presenting with tonsil cancer. As head and neck cancer is one of the cornerstones of the new CR-UK Cancer Centre in Liverpool, we are pleased to be making real progress in this area of research.”

Researchers are now working to develop a clinical trial for a therapeutic HPV vaccine in head and neck cancer.

Note:
1.The study, supported by the Royal College of Surgeons, is presented at the NCRI Cancer Conference on Monday, 5 October.

2. The Liverpool Cancer Research UK Centre focuses on understanding how cancers start and behave, how to develop better treatments with fewer side effects and how to tackle cancer in low-income communities where survival is lowest. As one of the first CR-UK Centres, Liverpool will set the pace for national and international progress in cancer of the pancreas, head and neck and blood. It will also concentrate on pioneering the latest techniques in surgery, radiotherapy and the treatment of children’s cancers.

3. The School of Cancer Studies brings together the considerable cancer research activities of the Divisions of Haematology, Pathology and Surgery & Oncology. The School forms a major part of the recently formed Liverpool CR-UK Cancer Centre..

4. The National Cancer Research Institute (NCRI) was established in April 2001. It is a UK-wide partnership between the government, charity and industry which promotes co-operation in cancer research among the 21 member organisations for the benefit of patients, the public and the scientific community. NCRI Cancer Conference is the UK’s major forum for showcasing the best British and international cancer research.

5. The University of Liverpool is a member of the Russell Group of leading research-intensive institutions in the UK. It attracts collaborative and contract research commissions from a wide range of national and international organisations valued at more than £93 million annually.

October, 2009|Oral Cancer News|