DNA – Page 3 – Oral Cancer News

Black raspberries reduce DNA damage in oral cancer survivors

Source: www.prweb.com Author: press release New research presented Wednesday, April 10, at the American Association for Cancer Research Annual Meeting 2013 in Washington, DC, suggests that a food-based cancer prevention study aimed at oral cancer survivors was effective at attenuating highly reactive oxygen molecules that can damage DNA and trigger cancer. In the study, a phase 1b clinical trial conducted at The Ohio State University, participants consumed 4 - 8 grams of black raspberries daily for six months. The berries were well tolerated by the participants and adherence to the regimen was good. This study provides compelling data that indicate biochemical markers of cancer-causing DNA damage were reduced in participants who adhered to the food-based regimen and supports other evidence from a phase 2 human trial linking application of black raspberry gel to precancerous lesions to a reduced risk of developing oral cancer. Black raspberries, not to be confused with blackberries, are almost exclusively grown in Oregon, on the west coast of the United States. They have been studied extensively because of their high concentration of certain phytonutrients and antioxidants. BerriProducts, an Oregon-based company, has been supplying black raspberry products to research universities across the country for the last four years.

Oral Cancer Foundation News Team - A2013-04-11T08:20:55-07:00April, 2013|Oral Cancer News|

Researchers document molecular tumor subtypes of head and neck cancer

Source: www.oncologynurseadvisor.com Author: Kathy Boltz, PhD Head and neck squamous cell carcinoma (HNSCC) is the seventh most common form of cancer in the United States. However, other than an association with the human papillomavirus (HPV), no validated molecular profile of the disease has been established. By analyzing data from DNA microarrays, a study has confirmed the presence of four molecular classes of the disease. Also, previous results have been extended by suggesting an underlying connection between the molecular classes and observed genomic events, some of which affect cancer genes. This study also demonstrated the clinical relevance of the classes and certain genomic events, paving the way for further studies and possible targeted therapies. "Cancer is a disease caused by alteration in the DNA and RNA molecules of tumors. A cancer results when broken molecules initiate a cascade of abnormal signals that ultimately results in abnormal growth and spread of tissues that should be under tight control within the body,” said Neil Hayes, MD, MPH, of the University of North Carolina Lineberger Comprehensive Cancer Center and of The Cancer Genome Atlas. "However, most common tumors, including head and neck cancer, have relatively little information in the public record as to how these signals coordinate to create different patterns of abnormalities. This study is among the largest ever published to document reproducible molecular tumor subtypes. Subtypes, such as those we describe, represent attractive models to understand and attack cancers for treatment and prognosis." The team analyzed a set of nearly 140 HNSCC [...]

Oral Cancer Foundation News Team - A2013-03-12T07:08:52-07:00March, 2013|Oral Cancer News|

DNA adducts linked to oral cancer in smokers

Source: www.news-medical.net Author: Sarah Guy, medwireNews Reporter Having a high susceptibility to certain types of DNA damage caused by tobacco smoking could significantly increase the risk for oral cancer, show results of a Taiwanese study. Levels of BaP 7,8-diol 9,10-epoxide (BPDE) - a metabolite of Benzo[a]pyrene, an important carcinogen found in cigarette smoke - correlated positively with smoking status in a cohort of individuals with oral cancer, report the researchers. The findings also indicate a significantly increased risk for oral cancer among individuals with high DNA adduct levels compared with their peers with low levels. "Based on our finding, we suggest that detected BPDE-like DNA adducts could be used as a biomarker for oral cancer risk," write Huei Lee (Taipei Medical University) and colleagues in the Archives of Oral Biology. The team analyzed BPDE-DNA adduct levels in oral tissue samples from 158 oral cancer patients and 64 individuals without cancer (controls), using immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). The results of these assays significantly and positively correlated , so that immunohistochemistry-negative patients did not have detectable DNA adduct levels using ELISA and vice versa. DNA adduct levels also positively correlated with smoking status among the cancer patients, note the researchers, with significantly higher adduct levels among smokers than nonsmokers, at 93.18 versus 0.04 adducts per 108 nucleotides. Lee and co-workers also observed that cancer patients had significantly higher DNA adduct levels than controls, at a range of 0-358.00 versus 0-39.50 adducts per 108 nucleotides. Indeed, DNA adduct level was an [...]

Oral Cancer Foundation News Team - A2013-01-05T15:32:56-07:00January, 2013|Oral Cancer News|

DNA alone inadequate to identify HPV-related cancers

Source: www.oncologypractice.com Author: Mary Ann Moon Testing for the presence of human papillomavirus DNA alone, especially using polymerase chain reaction methods, is not adequate to identify which head and neck squamous cell carcinomas are caused by the virus, according to two studies published online Sept. 18 in Cancer Research. Identifying HPV-driven malignancies is important because they respond better to treatment and have better outcomes than those unrelated to HPV infection. Indeed, treatment of head and neck squamous cell carcinoma (HNSCC) may soon be guided by the tumor’s HPV status, since trials are now underway to determine whether de-escalation of chemo- and radiotherapy is safe and effective in such patients. At present, however, the biomarkers that are best suited to making this identification are unclear. Case Series Assesses Biomarkers In the first study, researchers assessed the usefulness of four biomarkers in determining which HNSCCs in a case series were driven by HPV. They began by examining fresh-frozen tumor biopsy samples from 199 German adults diagnosed as having oropharyngeal squamous cell cancer between 1990 and 2008. The four biomarkers were HPV-16 viral load, viral oncogene RNA (E6 and E7), p16INK4a, and RNA patterns similar to those characteristic of cervical carcinomas (CxCa RNA), said Dr. Dana Holzinger of the German Cancer Research Center at Heidelberg (Germany) University and her associates. The simple presence of HPV DNA in a tumor sample was found to be a poor indicator of prognosis, likely because it often signaled past HPV infections or recent oral exposure, rather than [...]

Oral Cancer Foundation News Team - A2012-09-24T13:36:21-07:00September, 2012|Oral Cancer News|

Predicting oral cancer

Source: www.dailyrx.com Oral cancers can occur anywhere in the mouth. As with any cancer, the sooner it’s found, the better. A new tool helps doctors know when oral cancer may be in a patient’s future. A recent study finds that a set of molecular markers can help judge which lesions in the mouth are most likely to turn into oral cancer. The Oral Cancer Prediction Longitudinal Study was conducted in Canada at the Oral Cancer Prevention Program at the BC Cancer Agency in Vancouver. "The results of our study should help to build awareness that not everyone with a low-grade oral premalignant lesion will progress to cancer," said Program Director, Miriam Rosin, PhD. "However, they should also begin to give clinicians a better idea of which patients need closer follow-up." Every year, cancer shows up in the mouths of nearly 300,000 people around the globe. Some of these start as spots – or lesions – in the mouth that have not yet become cancerous. It’s always been difficult to tell which of these pre-malignant lesions will progress to full blown cancer. In an earlier study, Rosin’s team had analyzed the DNA of tissue that eventually turned into oral cancer. This research provided a method for grouping patients according to risk. For this study, researchers examined pre-cancerous tissue from nearly 300 patients, who were followed over a period of years. These patients were placed into either low-, intermediate- or high-risk groups. Two additional DNA markers were used to zero in on [...]

Oral Cancer Foundation News Team - A2012-09-11T08:13:58-07:00September, 2012|Oral Cancer News|

Molecular markers help predict oral cancer progression

Source: DrBicuspid.com August 21, 2012 -- A group of molecular markers has been identified that can help clinicians determine which patients with low-grade oral premalignant lesions are at high risk for progression to oral cancer, according to data from the Oral Cancer Prediction Longitudinal Study published in Cancer Prevention Research (August 21, 2012). "The results of our study should help to build awareness that not everyone with a low-grade oral premalignant lesion will progress to cancer," said Miriam Rosin, PhD, director of the Oral Cancer Prevention Program at the British Columbia (BC) Cancer Agency, in a press release issued by the American Association of Cancer Research, which publishes the journal. "However, they should also begin to give clinicians a better idea of which patients need closer follow-up." In 2000, Rosin and colleagues used samples of oral premalignant lesions in which progression to cancer was known to have subsequently occurred to develop a method for grouping patients into low- or high-risk categories based on differences in their DNA. In their current population-based study, the researchers confirmed that this approach was able to correctly categorize patients as less or more likely to progress to cancer. They analyzed samples from 296 patients with mild or moderate oral dysplasia identified and followed over years by the BC Oral Biopsy Service, which receives biopsies from dentists and ear, nose, and throat surgeons across the province. Patients classified as high-risk had an almost 23-fold increased risk for progression. Next, the researchers added two additional DNA molecular [...]

Charlotte Parker2012-08-22T09:55:45-07:00August, 2012|Oral Cancer News|

Demystifying the immortality of cancer cells

Source: http://medicalxpress.com/ Author: In cancer cells, normal mechanisms governing the cellular life cycle have gone haywire. Cancer cells continue to divide indefinitely, without ever dying off, thus creating rapidly growing tumors. Swiss scientists have discovered a protein complex involved this deregulated process, and hope to be able to exploit it to stop tumor formation in its tracks. All our cells come equipped with an automatic self-destruct mechanism; they are programmed to die after a certain number of divisions. This internal clock is of great interest to cancer researchers, because most forms of cancer exhibit a defect in this innate timing mechanism. Cancer cells continue to divide indefinitely, long past the moment at which a normal cell would self-destruct. A team of researchers from professor Joachim Lingner’s laboratory at EPFL has learned how this defect is regulated in a tumor. Post-doctoral researcher Liuh-Yow Chen led the team in publishing an article appearing in the journal Nature on the 4th of July 2012. Their hope is that the discovery will provide new targets for drug therapies to combat the deadly disease. Cellular immortality, which is responsible for cancer formation, hearkens back to a critical function of the cells of the developing embryo. At the ends of every chromosome there is a special sequence of DNA known as a telomere, whose length is governed by the telomerase enzyme. This sequence represents the lifespan of the cell. Every time the cell divides, it is shortened, and when the telomere finally runs out, [...]

Oral Cancer Foundation News Team - A2012-07-08T06:54:32-07:00July, 2012|Oral Cancer News|

Genes May Link Disparate Diseases

Source: The Wall Street Journal Diseases that strike different parts of the body—and that don't seem to resemble each other at all—may actually have a lot in common. Scientists have identified the genetic basis for many separate diseases. Now, some researchers are looking at how the genes interact with each other. They are finding that a genetic abnormality behind one illness may also cause other, seemingly unrelated disorders. Sometimes diseases are tangentially linked, having just one gene in common. But the greater the number of shared genetic underpinnings a group of diseases has, the greater the likelihood a patient with one of the illnesses will contract another. Researchers have found evidence, for example, that there is a close genetic relationship between Crohn's disease, a gastrointestinal condition, and Type 2 diabetes, despite the fact the two conditions affect the body in very distinct ways. Other illnesses with apparently close genetic links are rheumatoid arthritis and Type 1 diabetes, the form of the disease that usually starts in childhood, says Joseph Loscalzo, chairman of the department of medicine at Brigham and Women's Hospital in Boston. This network approach, known among scientists as systems biology, could change the way medical specialists view and treat disease, according to some researchers. Rather than only looking to repair the parts of the body that are directly affected by illness, "we should be looking at what the wiring diagram [inside of cells] looks like," says Albert-László Barabási, a physicist at Northeastern University's Center for Complex Network Research [...]

Charlotte Parker2012-05-02T10:33:24-07:00May, 2012|Oral Cancer News|

HPV DNA, E6?I-mRNA expression and p16(INK4A) immunohistochemistry in head and neck cancer – how valid is p16(INK4A) as surrogate marker?

Source: HighWire- Stanford University It has been proposed that p16(INK4A) qualifies as a surrogate marker for viral oncogene activity in head and neck cancer (HNSCC). By analyzing 78 HNSCC we sought to validate the accuracy of p16(INK4A) as a reliable marker of active HPV infections in HNSCC. To this end we determined HPV DNA (HPVD) and E6?I mRNA (HPVR) expression status and correlated these results with p16(INK4A) staining. In tonsillar SCC 12/20 were HPVD+ and 12/12 of these showed active HPV infections whereas in non-tonsillar SCC 10/58 were HPVD+ and 5/10 showed active HPV infections. Thus, we prove about 8% of non-tonsillar SCC to be also correlated with HPV-associated carcinogenesis. Strikingly, 3/14 (21.4%) of tonsillar and non-tonsillar HPVD+/HPVR+ cases did not show p16(INK4A) overexpression and these cases would have been missed when applying initial p16(INK4A) staining only. However, in 13 cases negative for HPV, DNA p16(INK4A) was overexpressed. In conclusion, our data confirm tonsillar SCC to be predominantly but not only associated with active HPV infections. Furthermore, our data show that p16(INK4A) overexpression is not evident in a subgroup of HNSCC with active HPV infection. Definitive HPV data should therefore be utilised in diagnostics and treatment modalities of HPV positive and HPV negative HNSCC patients, resulting in a paradigm shift regarding these obviously different tumour entities. This news story was resourced by the Oral Cancer Foundation, and vetted for appropriateness and accuracy.

Charlotte Parker2012-04-17T12:58:24-07:00April, 2012|Oral Cancer News|

Oral HPV infection affects 7% of the US population

Source: www.onclive.com Author: Ben Leach Approximately 7% of Americans are infected with oral human papillomavirus (HPV), and men are 3 times as likely to be infected as women, according to an analysis that helps define a leading factor in the rise of oropharyngeal cancer. The findings of the HPV prevalence study were presented at the Multidisciplinary Head and Neck Symposium in Phoenix, Arizona, in January and concurrently published in the Journal of the American Medical Association.1 The cross-sectional study was based on samples taken from 5579 men and women between the ages of 14 to 69 years that were obtained at mobile examination centers as part of the National Health And Nutrition Examination Survey (NHANES) 2009-2010. The samples were obtained through an oral rinse and gargle, with subsequent DNA samples used to determine HPV type. Demographic data were obtained using standardized interviews. HPV prevalence in the overall study population was 6.9% (95% confidence interval [CI], 5.7%-8.3%). HPV type 16, which accounts for 90% of HPVpositive oropharyngeal squamous cell carcinomas, was the most common form, affecting 1.0% of the study population (95% CI, 0.7%-1.3%). Prevalence of HPV was significantly higher in men versus women (10.1% [95% CI, 8.3%- 12.3%] for men compared with 3.6% [95% CI, 2.6%- 5.0%] for women; P < .001]). Sexual contact was identified as a major factor in the rate of infection, with 7.5% of those who had experienced any form of sexual contact (95% CI, 6.1%-9.1%) infected, compared with 0.9% (95% CI, 0.4%-1.8%; P < .001) [...]

Oral Cancer Foundation News Team - A2012-03-14T12:09:29-07:00March, 2012|Oral Cancer News|