DNA

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|

Identification of highly radiosensitive patients may lead to side effect-free radiotherapy

Source: www.ecancermedicalscience.com
Author: staff

An international group of scientists has taken the first step on the road to targeting radiotherapy dosage to individual patients by means of their genetic characteristics, a radiation oncologist told Europe’s largest cancer congress, ECCO 15 – ESMO 34, in Berlin today. Professor Dirk de Ruysscher, from Maastricht University Medical Centre, Maastricht, The Netherlands, said that his team’s work might provide the basis for personalised radiotherapy in which, with a simple blood test, doctors may be able to select the optimal radiation dose for a particular patient.

The team of scientists from The Netherlands, Belgium, Germany, and Canada studied a group of patients with hypersensitivity to radiation therapy, drawn from the largest world-wide database available – the European Union-funded Genetic pathways for the prediction of the effect of irradiation (GENEPI) study, which integrates biological material with patient data and treatment specifications. The database included information from more than 8000 European patients.
“Part of this project is the establishment of a sub-database in which very rare patient characteristics are brought together with the hypothesis that their genetic traits will enable the characterisation of molecular pathways related to radio-sensitivity,” explained Professor de Ruysscher. “A major problem for radiation oncologists at present is that we are bound by the need to avoid damage to normal tissues. This means that the dose of radiation generally used is governed by the response of the most radiosensitive patients, and this may lead to many patients receiving lower than optimal doses, hence affecting the ability to deliver a higher dose that may result in better local tumour control.”

A tissue bank including skin fibroblasts (the structural framework of skin cells), whole blood, lymphocytes (white blood cells involved in the immune system), plasma, and lymphoblastic (immature lymphocyte) cell lines from patients who were known to be hypersensitive to radiation was established from patients in Europe and Canada.

When compared with a control group, also drawn from the GENEPI study, the hypersensitive patients showed either severe side effects occurring at very low radiation levels, or severe side effects lasting for more than four weeks after the end of radiotherapy and/or requiring surgery, or severe late side effects occurring or persisting more than 90 days after the end of radiotherapy.

The scientists identified 33 such patients, 10 males and 23 females, of whom 11 (two males and nine females) ultimately proved to be really hypersensitive to radiation, underlining the rarity of this condition. Their mean age was 61.6 plus or minus 8.5 years (range 49 – 74). One patient had non-small cell lung cancer, six breast cancer, two head and neck cancer and one lymphoma. The radiation doses, the overall treatment times, and the follow-up times all fell within the usual parameters.

“The severe side effects included acute skin reactions, extreme skin thickening or fibrosis, lung tissue inflammation and blindness due to optical nerve damage,” said Professor de Ruysscher. “Although radiotherapy is a highly effective way of treating cancer, it is important that we are able to identify the patients who will react badly to it and adjust their dosage accordingly.”

Radiotherapy works by causing DNA damage in cells in a particular area so that they destroy themselves. Because cancer cells reproduce more and are undifferentiated (lacking the ability to become a more specialised cell type), they are less able to repair the damage caused by radiotherapy than are differentiated, normal cells which can usually repair themselves. However, some of the normal cells surrounding the treatment site may also be damaged during radiotherapy, and it is this damage that leads to side effects.

Scientists already know that different types of tumours respond differently to radiotherapy; highly radiosensitive cancer cells such as leukaemias can be killed by quite low radiation doses, whereas melanomas need such a high dose that it would be unsafe to use radiation therapy in this case. The finding that individuals, as well as tumours, react differently will enable doctors in the future to target doses even more carefully, taking into account not just the radiosensitivity of the tumour type but also the potential reaction of the particular patient to treatment.

“We hope that the EU will fund a successor project to elucidate genetic pathways in combination with other patient data so that we can make predictive models that can be implemented in standard clinical practice,” said Professor de Ruysscher. “We believe that, if we can understand what it is going on at a molecular level, we may be able to develop a blood test that will allow us to know precisely how an individual patient will react to radiotherapy, and to target the dose accordingly. Such personalised treatment will be a major advance, allowing us to minimise both radiotherapy doses and unpleasant side effects, while treating the tumour in the most effective way possible. Perhaps even more importantly, it will enable us to give higher doses to many patients and hence improve control of their tumours.”

September, 2009|Oral Cancer News|

Perceptronix Reports Clinical Study Underway to Evaluate OralAdvance(TM) for Early Detection of Oral Cancer

Source: www.earthtimes.org
Author: press release

Perceptronix Medical Inc. announces that a clinical study of OralAdvance(TM), a test for the early detection of oral cancer, is now underway. The clinical study will assess the performance of OralAdvance(TM) compared to the gold standard biopsy and histology for its ability to differentiate between visually suspicious oral lesions with cancer or pre-cancer and visually suspicious benign oral lesions.

“Unlike many other types of cancer, the incidence and mortality rates of oral cancer have not shown significant improvement over the past 30 years. By the time most oral cancers are diagnosed, they are already symptomatic late-stage disease. At Perceptronix we are dedicated to changing this paradigm towards early detection for better patient outcomes,” says Dr. Bojana Turic, President and CEO of Perceptronix.

Patients for the blinded study will be recruited from the BC Cancer Agency’s Vancouver and Fraser Valley Centres.

“We are pleased to be able to participate in the evaluation of the test in a clinical setting with technology that was developed in partnership with scientists at the BC Cancer Agency’s Research Centre, and we are hopeful that the test will have a positive impact on the early detection of oral cancer,” says Dr. Allan Hovan (Provincial Professional Practice Leader, Program in Oral Oncology/Dentistry, BC Cancer Agency).

Currently, the death rate for oral cancer is higher than that of cervical cancer, Hodgkin’s disease, cancer of the brain, liver, testes, kidney, or malignant melanoma. High death rate associated with oral cancer could be reduced significantly by putting clinical and technological emphasis on early detection.

– When oral cancer is detected in its later stages, the five-year survival rate is approximately 50%

– When oral cancer is detected in its early stage, the five-year survival rate is 80% or higher

– Currently, only 36% of all oral cancers are detected in their early stage.

About OralAdvance(TM)
OralAdvance(TM) is a new quantitative cytology test based on analysis of oral brush specimens. The test provides an objective measure of gross DNA abnormality to determine the pre-malignant or malignant nature of a lesion. OralAdvance(TM) offers a new and useful option to assess suspicious lesions when a biopsy is not warranted or possible.

About Perceptronix Medical Inc.
Perceptronix Medical Inc. (Vancouver, Canada) is a private cancer diagnostics laboratory specializing in the provision of innovative early cancer detection tests based on quantitative cytology. The Company’s DNA image cytometry technology was developed in partnership with the BC Cancer Agency (Canada). Quantitative cytology provides physicians with an innovative cytopathology assessment based on an objective measure of large-scale DNA abnormality that can indicate precancerous or cancerous changes. The company has developed proprietary tests for the early detection of lung cancer and oral cancer using its DNA cytometry technology and offers quantitative cytology analysis of various tissues.

HPV data may aid vaccine’s effectiveness

Source: health.usnews.com
Author: staff

The majority of invasive cervical cancers in New Mexico in the 1980s and 1990s contained DNA from human papillomavirus type 16 (HPV16) and HPV type 18 (HPV18), says a new study. It also found that women diagnosed with HPV16- or HPV18-positive cancers were an average of five years younger than those diagnosed with cancers associated with other HPV types. The HPV vaccine (Gardasil) protects against infections caused by HPV16 and HPV18, so the new findings may have implications for future cancer screening programs, the researchers said.

The researchers analyzed U.S. data in the Surveillance, Epidemiology and End Results registry and identified 1,213 cases of in situ cervical cancer diagnosed between 1980 and 1999, as well as 808 cases of invasive cervical cancer diagnosed between 1980 and 1999 in New Mexico.

HPV16 DNA was found in 53.2 percent of invasive cervical cancers, HPV18 DNA was found in 13.1 percent, and HPV45 DNA in 6.1 percent. HPV16 DNA was found in 56.3 percent of in situ cervical cancers, HPV31 DNA in 12.6 percent, and HPV33 DNA in 8 percent.

Patients’ median age at diagnosis of invasive cancer with HPV16 and HPV18 was 48.1 years, and 45.9 years, respectively. Median age at diagnosis of invasive cancer with other HPV genotypes was 52.3 years. The study is in the March 24 online issue of the Journal of the National Cancer Institute.

“To our knowledge, this is the largest study of its kind conducted in a U.S. population,” wrote a team led by Cosette M. Wheeler, of the University of New Mexico Health Sciences Center in Albuquerque.

“This study of HPV genotypes in New Mexico provides important baseline data for evaluating the effectiveness of nearly implemented HPV-based technologies, HPV vaccines, and HPV screening in the prevention of cervical cancer,” she said. “Moreover, these data can guide the future application of these technologies to maximize the cost-effective, public health benefits of these interventions.”

April, 2009|Oral Cancer News|

Discovery may result in new test to determine predisposition to cancer

Source: www.biocompare.com
Author: staff

Researchers at UCLA’s Jonsson Comprehensive Cancer Center have developed an assay that may be used to help identify new genes that can predict a predisposition to cancer. The study, published in the April issue of Radiation Research, was done in yeast and mammalian cells.

Cancer cells show persistent genetic instability and the researchers, led by Robert Schiestl, have discovered a mechanism that switches on that genetic instability. If they can uncover and understand the molecular pathways at work in promoting genetic instability, they may be able to develop ways to switch that mechanism off, restoring stability.

“We all have several hundred cells in our body that go crazy every day, and they’re taken out by our immune system,” said Schiestl, a professor of pathology, radiation oncology and environmental health sciences and a Jonsson Cancer Center scientist. “What’s important is that those cells don’t grow and spread and invade other regions of our body. Cancer cells are able to grow, spread and invade because the continued genetic instability can disturb the cellular program and create a growth advantage. Unfortunately, the immune system is not very effective at taking cancer cells out.”

The assay determines the efficiency of the repair mechanism when DNA suffers a double-strand break, when both strands in the double helix are severed. These breaks cause genetic instability and are particularly dangerous because they can lead to genome rearrangements or deletions of certain genes that, when gone, result in cancer.

“Every cell has double strand breaks all the time,” said Schiestl, senior author of the study. “It is how the cell tries to fix these breaks that is key, the capacity and the efficiency of the repair so no further harm occurs.”

A cell that can’t efficiently repair itself could result in cancer.

In the study, researchers irradiated cells to create double strand breaks. They wanted to determine if a double strand break occurs in one area of the DNA is the instability limited to that area or also evident elsewhere. The standard thinking was that the genetic instability would be localized to the area of the break. However, Schiestl and his team showed that a break in one area has an “in trans” effect, meaning the instability could surface anywhere.

“What we have shown now in this paper is that DNA damage at one position in the genome, causes a certain mechanism of genetic instability all over the genome,” Schiestl said.

Specifically, the team irradiated cells and then transformed them with a DNA fragment that detects the efficiency and the accuracy of double strand break repair. The key in this experiment was that the DNA fragment was not irradiated. In this way, the researchers could demonstrate that the radiation triggered a specific mechanism of double strand break repair in the DNA fragment that did not receive any radiation. The effect was still noticeable after almost all the DNA damage the radiation caused in the cells was repaired, showing that the mechanism that is induced by the radiation is independent of the actual damage caused by the radiation.

Schiestl had previously shown that a single DNA double strand break also induces genetic instability all over the genome at sites that are not damaged, again a proof that double strand breaks induce genetic instability in trans.

Interestingly, many cancer cells show an elevated induction of the specific DNA double strand break repair mechanism found induced in trans in this study, as if the cancer cells had this mechanism somehow induced and were not able to switch it off.

“Now we have to identify the mechanism of the pathway, identify the genes involved in inducing that pathway and that might give us targets that we can inhibit with drugs to try to reduce genetic instability,” Schiestl said. “That could lead to a cancer treatment. Any time you can stop the growth of a cancer, you’ve won. It doesn’t damage other tissues or spread to other organs. We might be able to stop the instability before it results in cancer.”

Note:
1. The research was funded in part by a National Institutes of Health grant and a NASA graduate student fellowship. Other members of Schiestl’s team included Zorica Scuric, Cecilia Chan and Kurt Hafer.

April, 2009|Oral Cancer News|

Genetic Changes Outside Nuclear DNA suspected to trigger more than half of all cancers

Source: www.newswise.com
Author: staff

A buildup of chemical bonds on certain cancer-promoting genes, a process known as hypermethylation, is widely known to render cells cancerous by disrupting biological brakes on runaway growth. Now, Johns Hopkins scientists say the reverse process — demethylation — which wipes off those chemical bonds may also trigger more than half of all cancers.

One potential consequence of the new research is that demethylating drugs now used to treat some cancers may actually cause new cancers as a side effect.

“It’s much too early to say for certain, but some patients could be at risk for additional primary tumors, and we may find that they need a molecular profile of their cancer before starting demethylating therapy,” says Joseph Califano, M.D., professor of otolaryngology–head and neck surgery and oncology at Johns Hopkins.

The findings, based on studies of normal and cancer cells from human mouth, nose and throat tissue, provide more evidence that important regulators of gene activity occur outside as well as inside DNA in a cell’s nucleus.

“While cancer-causing and other mutations alter vital protein-making pathways by rewriting the gene’s DNA code, epigenetic changes affect genes without changing the code itself. The new studies tell us that such changes occur not only when methyl groups bond to a gene’s on-off switch, but also when they come unglued,” says Califano.

Califano says sporadic reports of demethylation as a tool in activating cancer-promoting genes led his team to develop a systematic way to discover these epigenetic changes and show how the process is linked to cancer.

To gather their evidence, Califano and his group treated two cell lines from normal oral tissue with the demethylating drug 5-azacytidine and collected a list of genes that were activated as a result. They used special silicon chips carrying pieces of genetic material that allow thousands of genes to be analyzed at one time to locate genes activated by demethylation.

The list was cross-referenced with genes “turned on” in 49 head and neck cancer samples and 19 normal tissue samples. In all, Califano and his team found 106 genes specific to head and neck cancer that were activated by the demethylation process. “Some of the genes regulate growth, others metabolize sugars and some have already been linked to cancer development,” says Califano, who is director of head and neck cancer research at the Milton J. Dance Jr. Head & Neck Center at Greater Baltimore Medical Center. A report on this work appears on March 23 in PLoS One.

Further analysis by the Johns Hopkins team revealed a single connection among 106 genes: methylation within them is regulated by another gene called BORIS. BORIS acts as a “master regulator,” recruiting other proteins to demethylate a coordinated set of genes and signaling the development of cancer. According to the scientists, nearly 60 percent of a wide range of cancers, including head and neck and lung cancer, have high levels of BORIS expression.

He envisions that agents like 5-azacytidine may need to be combined with a “BORIS blocker,” a drug that has yet to be developed to protect patients who need demethylating therapies.

The research is funded by the Flight Attendant Medical Research Institute, the National Institute of Dental and Craniofacial Research, and the National Cancer Institute.

Research participants included Ian M. Smith, Chad A. Glazer, Suhail K. Mithani, Michael F. Ochs, Wenyue Sun, Sheetal Bhan, Andrew Gray, Chunyan Liu, Steven S. Chang, Kimberly L. Ostrow, William H. Westra, Shahnaz Begum and Mousumi Dhara from Johns Hopkins; and Alexander Vostrov, Ziedulla Abdullaev and Victor Lobanenkov from the National Institutes of Health.

Source:
Johns Hopkins Medicine

March, 2009|Oral Cancer News|

Perceptronix reports clinical study underway to evaluate OralAdvance(TM) for early detection of oral cancer

Source: www.earthtimes.org
Author: press release

Perceptronix Medical Inc. announces that a clinical study of OralAdvance(TM), a test for the early detection of oral cancer, is now underway. The clinical study will assess the performance of OralAdvance(TM) compared to the gold standard biopsy and histology for its ability to differentiate between visually suspicious oral lesions with cancer or pre-cancer and visually suspicious benign oral lesions.

“Unlike many other types of cancer, the incidence and mortality rates of oral cancer have not shown significant improvement over the past 30 years. By the time most oral cancers are diagnosed, they are already symptomatic late-stage disease. At Perceptronix we are dedicated to changing this paradigm towards early detection for better patient outcomes,” says Dr. Bojana Turic, President and CEO of Perceptronix.

Patients for the blinded study will be recruited from the BC Cancer Agency’s Vancouver and Fraser Valley Centres.

“We are pleased to be able to participate in the evaluation of the test in a clinical setting with technology that was developed in partnership with scientists at the BC Cancer Agency’s Research Centre, and we are hopeful that the test will have a positive impact on the early detection of oral cancer,” says Dr. Allan Hovan (Provincial Professional Practice Leader, Program in Oral Oncology/Dentistry, BC Cancer Agency).

Currently, the death rate for oral cancer is higher than that of cervical cancer, Hodgkin’s disease, cancer of the brain, liver, testes, kidney, or malignant melanoma. High death rate associated with oral cancer could be reduced significantly by putting clinical and technological emphasis on early detection.

– When oral cancer is detected in its later stages, the five-year survival rate is approximately 50%

– When oral cancer is detected in its early stage, the five-year survival rate is 80% or higher

– Currently, only 36% of all oral cancers are detected in their early stage.

About OralAdvance(TM)
OralAdvance(TM) is a new quantitative cytology test based on analysis of oral brush specimens. The test provides an objective measure of gross DNA abnormality to determine the pre-malignant or malignant nature of a lesion. OralAdvance(TM) offers a new and useful option to assess suspicious lesions when a biopsy is not warranted or possible.

About Perceptronix Medical Inc.
Perceptronix Medical Inc. (Vancouver, Canada) is a private cancer diagnostics laboratory specializing in the provision of innovative early cancer detection tests based on quantitative cytology. The Company’s DNA image cytometry technology was developed in partnership with the BC Cancer Agency (Canada). Quantitative cytology provides physicians with an innovative cytopathology assessment based on an objective measure of large-scale DNA abnormality that can indicate precancerous or cancerous changes. The company has developed proprietary tests for the early detection of lung cancer and oral cancer using its DNA cytometry technology and offers quantitative cytology analysis of various tissues.

February, 2009|Oral Cancer News|

Variations in gene DNA boost drinkers’ cancer risk

Source: www.washingtonpost.com
Author: staff

Variations in the DNA of certain genes can increase the risk of cancer in people who drink alcohol, according to researchers who reviewed studies on alcohol consumption, genetic polymorphisms and cancer.

Their analysis suggests that such variations, called gene polymorphisms, in two enzymes — alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) — involved in metabolizing alcohol significantly increase alcohol drinkers’ risk of cancers of the head and neck and the esophagus.

The researchers looked at the effect of gene variations in other enzymes involved in alcohol and folate metabolism but found there wasn’t enough data to fully assess the effect of those gene variants on cancer risk.

They said that currently available data does not allow for a quantitative evaluation by meta-analysis of the link between gene variations and cancer risk in people who drink alcohol.

“We have highlighted the need for large, multicenter studies and for approaches to the study of multiple polymorphisms,” wrote Dr. Nathalie Druesne-Pecollo and colleagues at the French National Institute of Agronomical Research.

The review was published in the February issue of the The Lancet Oncology.

Previous research has shown a clear link between alcohol consumption and health risk, according to background information in the review. Recent figures show that drinking alcohol was a major contributing factor in the development of almost 400,000 cancers worldwide in 2002. In that same year, 323,900 cancer deaths (3.6 percent of all cancer deaths) were alcohol-related.

Source:
The Lancet Oncology, news release, Jan. 30, 2009

February, 2009|Oral Cancer News|

HPV testing followed by cytology and repeat HPV testing may improve cervical cancer screening

Source: JNCI Journal of the National Cancer Institute 2009 101(2):69
Author: staff

The use of human papillomavirus (HPV) DNA testing as an initial screening step followed by triage with a standard Pap test (cytology) and repeat HPV DNA testing may increase the accuracy of cervical cancer screening, according to a study in the Jan. 13 online issue of the Journal of the National Cancer Institute. Compared to cytology alone, the screening strategy improved detection of precancerous growths without a substantial increase in the number of false-positive tests.

Randomized trials have shown that using DNA testing for HPV—which is known to cause cervical cancer—in screening programs would increase detection of cervical intraepithelial neoplasia (CIN) compared with cytology. However, HPV DNA testing also results in a substantial increase in false-positive tests, which lead to unnecessary and costly retesting.

In the current study, Joakim Dillner, M.D. of Lund University in Malmö, Sweden, and colleagues compared the efficacy of 11 different screening strategies that used HPV DNA testing, cytology, or a combination of the two. To evaluate the different strategies the investigators retrospectively analyzed data from 6,257 women who were enrolled in the intervention arm of a large randomized screening trial, called Swedescreen, in which HPV DNA testing was used in addition to standard cytology.

As seen in previous trials, the use of HPV DNA testing in conjunction with cytology increased the screening efficacy, detecting 35 percent more cases of CIN grade 3 or worse, compared with cytology alone. The strategy, however, doubled the number of tests required. By contrast, the use of the HPV primary screen with cytology and repeat HPV testing resulted in a 30 percent higher detection rate compared to cytology alone, with only a 12 percent increase in the number of tests required. In this approach, all women with HPV infections detected on the primary screening went on to have a standard Pap test; those with normal cytology then had a repeat HPV DNA test at least 1 year later.

“In conclusion, our data indicate that using HPV DNA testing as primary screening followed by cytological triage and repeat HPV DNA testing of women with normal cytology who are HPV DNA positive after at least 1 year is a feasible strategy for incorporating HPV testing in primary cervical screening because it improves sensitivity and maintains a high [positive predictive value], thus minimizing unnecessary referrals,” the authors write.

Citation:
Naucler P, et al. Efficacy of HPV DNA Testing with Cytology Triage and/or Repeat HPV DNA Testing in Primary Cervical Cancer Screening. J Natl Cancer Inst 2009;101: 88–99.

January, 2009|Oral Cancer News|