Hepatitis B does not increase pancreatic cancer risk

A Henry Ford Hospital study observed that hepatitis B does not increase the risk for pancreas cancer and that only age is a contributing factor.

The results contradict a prior study in 2008 that suggested a link between pancreas cancer and prior hepatitis B infection. Hepatitis B is an inflammation of the liver caused by a viral infection.

Study results will be presented at the American Association for the Study of Liver Diseases' Annual Meeting in Boston.

Using data from Henry Ford Health System, physicians looked at more than 74,000 patients who were tested for hepatitis B between 1995 and 2008. In the overall analysis, only age was found to be a significant predictor for pancreas cancer.

"We looked at the occurence rate of pancreas cancer among hepatitis B-infected patients over a 13-year period and observed that we could not confirm a higher risk for those with a prior exposure to hepatitis B, as a previous study suggested," says Jeffrey Tang, M.D., gastroenterologist at Henry Ford Hospital and main author of the study.

"When other factors are considered such as age, race, sex, HIV status, and the presence of diabetes only older age and presence of diabetes proved significant, whereas previous exposure to hepatitis B was no longer an important variable".

As per the National Cancer Institute, more than 35,000 people in the U.S. die of pancreas cancer each year and 42,000 new cases are diagnosed. The survival rates for patients with pancreas cancer are poor.

An estimated 800,000 to 1.4 million people have chronic hepatitis B infection, as per the Centers for Disease Control and Prevention. In 2007, an estimated 43,000 people in the United States were newly infected with hepatitis B, eventhough a number of cases are not reported because a number of people do not have symptoms.

Posted by: Sue    Source

View the original article here

Genes and pancreatic cancer

Abnormalities in genes that repair mistakes in DNA replication may help identify people who are at high risk of developing pancreas cancer, a research team from The University of Texas M. D. Anderson Cancer Center reports in the Jan. 15 issue of Clinical Cancer Research
Defects in these critical DNA repair genes may act alone or in combination with traditional risk factors known to increase an individual's likelihood of being diagnosed with this very aggressive type of cancer.

"We consider DNA repair to be the guardian of the genome," said main author Donghui Li, Ph.D., professor in the Department of Gastrointestinal Medical Oncology at M. D. Anderson. "If something is wrong with the guard, the genes are more readily attacked by tobacco carcinogens and other damaging agents".

With this in mind, Li and her colleagues set out to identify DNA repair genes that could act as susceptibility markers to predict pancreas cancer risk. In a case-control study of 734 patients with pancreas cancer and 780 healthy individuals, they examined nine variants of seven DNA repair genes. The repair genes under investigation were: LIG3, LIG4, OGG1, ATM, POLB, RAD54L and RECQL.

The scientists looked for direct effects of the gene variants (also called single nucleotide polymorphisms) on pancreas cancer risk as well as potential interactions between the gene variants and known risk factors for the disease, including family history of cancer, diabetes, heavy smoking, heavy alcohol consumption and being overweight.

The M. D. Anderson team observed that the risk of developing pancreas cancer was 77 percent lower among individuals with the variant form of the LIG3 gene (LIG3 G-39A AA). In contrast, people who carried the variant form of the ATM gene (ATM D1853N AA) were more than twice as likely to develop the disease as those without the genetic variation.

When the researchers examined possible interactions between gene variants and known risk factors, they found no significant interplay between the abnormal DNA repair genes and smoking, heavy alcohol consumption or excess body weight. However, two of the gene variants (ATM D1853N and LIG4 C54T) did interact with diabetes to affect pancreas cancer risk.

For example, in comparison to non-diabetics with the ATM D1853N GG genotype, diabetics carrying the ATM D1853N GA/AA genotypes had more than triple the risk of developing pancreas cancer. Similarly, in comparison to non-diabetics with the LIG4 CC genotype, diabetics with the LIG4 CT/TT genotype had more than double the risk of developing the disease.

Li noted that the ultimate goal of this research is to identify high-risk individuals for closer scrutiny and follow up.

"We know that people with diabetes have a higher risk of developing pancreas cancer, but we don't know who will actually develop the disease and who will not," Li said. "The same is true for smokers. But we can't do Computerized axial tomography scans on every diabetic or every smoker.

"We need to develop biomarkers that will enable us to do a quick genetic test on a diabetic patient, heavy smoker or someone with a family history of pancreas cancer," she continued. "We could then do a screening test, identify those with the highest risk, and monitor them more closely".

U.

nderstanding the role of variant DNA repair genes in the development and prognosis of pancreas cancer would also give scientists more insight into their functional significance. This increased knowledge should promote the development of new therapeutic strategies to target these abnormal genes.

Posted by: Sue    Source

View the original article here

The Deadly Secrets Of Pancreatic Cancer

Main Category: Pancreatic Cancer
Article Date: 27 Oct 2012 - 0:00 PDT Current ratings for:
The Deadly Secrets Of Pancreatic Cancer

A large-scale study that defines the complexity of underlying mutations responsible for pancreatic cancers in more than 100 patients was published in Nature.

The analysis represents the first report from Australia's contribution to the International Cancer Genome Consortium (ICGC), which brings together the world's leading scientists to identify the genetic drivers behind 50 different cancer types.

Pancreatic cancer has the highest mortality rate of all the major cancers and is one of the few for which survival has not improved substantially over the past 40 years. It is the fourth-leading cause of cancer death.

Professor Sean Grimmond, from the Institute for Molecular Bioscience (IMB) at The University of Queensland, and Professor Andrew Biankin, from The Kinghorn Cancer Centre at Sydney's Garvan Institute of Medical Research/ St. Vincent's Hospital led an international team of more than 100 researchers that sequenced the genomes of 100 pancreatic tumours and compared them to normal tissue to determine the genetic changes that lead to this cancer.

"We found over 2,000 mutated genes in total, ranging from the KRAS gene, which was mutated in about 90 per cent of samples, to hundreds of gene mutations that were only present in 1 or 2 per cent of tumours," Professor Grimmond said. "So while tumours may look very similar under the microscope, genetic analysis reveals as many variations in each tumour as there are patients.

"This demonstrates that so-called 'pancreatic cancer' is not one disease, but many, and suggests that people who seemingly have the same cancer might need to be treated quite differently."

Professor Biankin said such individual genetic diagnoses and treatments represent the future of healthcare. "In this study, we found a set of genes, the axon guidance pathway, that is frequently damaged in pancreatic cancer patients and is associated with a potentially poorer outcome for those patients. It is a new marker of pancreatic cancer that can be used to direct prognoses and treatments.

"'Personalised medicine', where the molecular profile of a patient is matched to the best treatment, is the way the world is moving for many diseases, not just cancer."

"The challenge now will be in moving from population healthcare and a 'one drug fits all' model to personalised healthcare. First we must take the time to develop the necessary genetic knowledge and implement health systems to translate that knowledge effectively."

Professors Biankin and Grimmond acknowledged the vital assistance of the Australian Pancreatic Cancer Genome Initiative, a network of more than 20 hospitals and research institutions Australia-wide, with over 200 members - surgeons, pathologists, nurses and researchers - that all contributed to the project.

They also collaborated with colleagues from the Baylor College of Medicine and The Methodist Hospital Research Institute in Texas, the Ontario Institute for Cancer Research, Johns Hopkins University in Maryland, the University of California San Francisco, the University of Verona, the Cambridge Research Institute and the Sanger Centre in the UK.

The ICGC project is being funded through $27.5 million from the National Health and Medical Research Council of Australia (NH&MRC), its largest-ever single grant. NHMRC Chief Executive Officer, Professor Warwick Anderson said that "NHMRC is proud to have been the major funding contributor to this research, and I am delighted that breakthroughs have been made in understanding the genetic basis of this disease.

"This positive outcome is evidence of NHMRC supporting the very best research and researchers, and the importance of our involvement in strong national and international collaborations.

"The ultimate goal of our funding is healthier citizens, both in Australia and overseas, and this research will certainly lead to a better understanding of this issue."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our pancreatic cancer section for the latest news on this subject. FUNDING
As well as the NHMRC funding, we acknowledge the following additional funding support:
Commonwealth Department of Innovation, Industry, Science, Research and Tertiary Education (DIISRTE); Australian Cancer Research Foundation (ACRF); Queensland Government (NIRAP); The University of Queensland; Cancer Council NSW; Cancer Institute NSW; Avner Nahmani Pancreatic Cancer Research Foundation; R.T. Hall Trust; Petre Foundation; Jane Hemstritch in memory of Philip Hemstritch; Gastroenterological Society of Australia (GESA); American Association for Cancer Research (AACR) Landon Foundation – INNOVATOR Award; Royal Australasian College of Surgeons (RACS); Royal Australasian College of Physicians (RACP); Royal College of Pathologists of Australasia (RCPA).
Research Australia Please use one of the following formats to cite this article in your essay, paper or report:

MLA

n.p. "The Deadly Secrets Of Pancreatic Cancer." Medical News Today. MediLexicon, Intl., 27 Oct. 2012. Web.
12 Nov. 2012. APA

Please note: If no author information is provided, the source is cited instead.

'The Deadly Secrets Of Pancreatic Cancer'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Heavy smokers, drinkers can face pancreatic cancer earlier in his life

Friday, October 5 HealthDay News)-drinkers and heavy smokers can develop pancreatic cancer at a younger age than other people, according to a new study.

The average age at which patients are diagnosed with pancreatic cancer is 72, according to the American Cancer Society.

But this study of more than 800 patients of pancreatic cancer that heavy smokers were diagnosed in above the age of 62 and drinkers at the age of 61 - a decade before the average age at the time of diagnosis.

Heavy smokers were defined as those who smoked more than one pack of cigarettes a day and drinkers were those who averaged three drinks per day.

The study also found drinkers were diagnosed with cancer of the pancreas at a younger age than those who drank other types of alcohol, such as wine or liquor from beer. But when the researchers took the amount of alcohol consumed in mind, the type of alcohol did not affect the age at diagnosis.

The good news was that they can reverse the harmful effects of heavy smoking and drinking. Ten years after renouncing their unhealthy habits, drinkers and former smokers did not have an increased risk of being diagnosed with cancer of the pancreas in an early age.

The study was published online on August 28 in the American Journal of Gastroenterology.

The findings could help determine at what age should begin detection of pancreatic cancer, once widespread screening is available.

"How to develop programs of research, an understanding of the influence of personal characteristics as the age of presentation is important to optimize the time of these projections," internal author of main study and gastroenterologist Dr. Michelle Anderson, Assistant Professor of medicine at the University of Michigan health system, said at a UMHS press release.

Although the study found associations between drinking, smoking and diagnosis of cancer of the pancreas at younger ages, did not demonstrate cause and effect relationships.

More information

The American cancer society has more about cancer of the pancreas.

Source: University of Michigan Health System, press release, October 01, 2012

Copyright © 2010 HealthDay. All rights reserved.

View the original article here

Steve Jobs Faces Uphill Battle Against Cancer: Experts

This news article has expired. Below you will find a short description about the news article and comments that were left by CancerCompass users.

Prognosis for rare neuroendocrine disease is poor, doctors say

View the original article here

Chemotherapy plus synthetic compound for pancreatic cancers

Human pancreas cancer cells dramatically regress when treated with chemotherapy in combination with a synthetic compound that mimics the action of a naturally occurring "death-promoting" protein found in cells, scientists at UT Southwestern Medical Center have found.

The research, conducted in mice, appears in today's issue of Cancer Research and could lead to more effective therapies for pancreatic and possibly other cancers, the scientists said.

"This compound enhanced the efficacy of chemotherapy and improved survival in multiple animal models of pancreas cancer," said Dr. Rolf Brekken, associate professor of surgery and pharmacology and the study's senior author. "We now have multiple lines of evidence in animals showing that this combination is having a potent effect on pancreas cancer, which is a devastating disease".

In this study, Dr. Brekken and his team transplanted human pancreatic tumors into mice, then allowed the tumors to grow to a significant size. They then administered a synthetic compound called JP1201 in combination with gemcitabine, a chemotherapeutic drug that is considered the standard of care for patients with pancreas cancer. They observed that the drug combination caused regression of the tumors.

"There was a 50 percent regression in tumor size during a two-week therapy of the mice," Dr. Brekken said. "We also looked at survival groups of the animals, which is often depressing in human therapeutic studies for pancreas cancer because virtually nothing works. We found not only significant decrease in tumor size, but meaningful prolongation of life with the drug combination".

The drug combination was also effective in an aggressive model of spontaneous pancreas cancer in mice.

The compound JP1201 was created in 2004 by UT Southwestern scientists to mimic the action of a protein called Smac. The scientists discovered Smac in 2000 and observed that this protein plays a key role in the normal self-destruction process present in every cell.

Cell death, or apoptosis, is activated when a cell needs to be terminated, such as when a cell is defective or is no longer needed for normal growth and development. In cancer cells, this self-destruct mechanism is faulty and lead to breaks in the cell-death cascade of events. The synthetic Smac, or Smac mimetic, developed at UT Southwestern inhibits these breaks, allowing the cell to die.

"In essence, we're inhibiting an inhibitor," Dr. Brekken said. "And we're allowing the apoptotic cascade to kick off, resulting in the death of cancer cells".

UT Southwestern scientists are using Smac mimetics in breast and lung cancer research, as well. Dr. Brekken said the next step is to develop a compound based on JP1201 that can be tested in humans in clinical trials.

Posted by: Sue    Source

View the original article here

New drug substantially extends survival in pancreatic cancer

A new form of chemotherapy that destroys new blood vessels that grow around tumors has produced excellent results in a phase II trial of patients with inoperable pancreas cancer, scientists report at the 33rd Congress of the European Society for Medical Oncology (ESMO) in Stockholm.

European researchers led by Prof. Matthias Lhr from the Karolinska Institute reviewed the efficacy and safety of three different doses of cationic lipid complexed paclitaxel (EndoTAG-1) administered twice weekly, in combination with weekly infusions of gemcitabine, in comparison to gemcitabine alone, in 200 patients with pancreatic adenocarcinoma.

"EndoTAG consists of charged particles that bind preferentially to the fast-growing endothelial cells in new blood vessels being formed by tumors," Prof. Lhr explained. "The drug, paclitaxel, is then released and thus directly reaches an important target in tumors, i.e. the vessels. Paclitaxel itself is not very efficient in pancreratic cancer".

After following patients for a year, the scientists observed that therapy with such combination led to a substantially extended median survival time in comparison to standard treatment. Patients given gemcitabine alone survived on average 7.2 months, in comparison to up to 13.6 months for patients who received repeated doses of the combination (EndoTAG plus gemcitabine).

"These results are the best I have ever seen in palliative therapy in pancreas cancer," Prof. Lhr said. "The results are really excellent and a phase III study is in the making".

Posted by: Sue    Source

Did you know?
A new form of chemotherapy that destroys new blood vessels that grow around tumors has produced excellent results in a phase II trial of patients with inoperable pancreas cancer, scientists report at the 33rd Congress of the European Society for Medical Oncology (ESMO) in Stockholm.

View the original article here

Why Cancer Symptoms May Elude M.D.

FRIDAY, Feb. 24 (HealthDay News) -- Diagnosing cancer is more difficult in certain groups of patients, according to a British study.

Researchers analyzed data gathered from more than 41,000 patients with 24 types of cancer who were treated in 158 hospitals across England. They found that 77 percent of those who saw their family doctor about suspicious symptoms were referred to a hospital after only one or two consultations.

However, the study found that women, young people, non-white patients and patients with less common cancers were more likely to see their family doctor three or more times before they were referred to a hospital.

The researchers identified large differences in the promptness of family doctors in England to diagnose different types of cancer. Patients with symptoms of multiple myeloma, lung and pancreatic cancer required many more consultations with their family doctor before they were referred to a hospital, compared to patients with more common cancers such as breast, melanoma and testicular.

For example, almost 51 percent of patients with the blood cancer multiple myeloma required multiple visits to their family doctor before referral, compared with less than 8 percent of breast cancer patients.

Differences in the nature and characteristics of symptoms may explain why certain cancers are more difficult to diagnose, the researchers said. For example, multiple myeloma is especially difficult to diagnose because it mimics other conditions, while a breast lump may readily suggest cancer, the authors said.

They also said that doctors may be less likely to consider cancer in younger patients and may have communication difficulties with patients from different ethnic groups, which may explain why cancer diagnoses can take longer in these patients.

The study appears online Feb. 24 in The Lancet Oncology.

"These findings highlight limitations in current scientific knowledge," lead author Georgios Lyratzopoulos, of Cambridge University, said in a journal news release. "Medical research in recent decades has prioritized improving cancer treatments, but knowledge about the 'symptom signature' of common cancers and practical solutions on how best to diagnose them is still emerging."

Martin Guilliford, of King's College London, wrote in an accompanying editorial that the findings raise several questions that should be tested in future research.

He said some of those questions are: "Do modes of cancer presentation vary systematically between different groups of patients? Are (family doctors) more reluctant to refer young or non-white patients for investigation of possible cancer? Are participants in these groups less willing to accept a referral to investigate possible cancer?"

More information

The American Academy of Family Physicians has more about cancer diagnosis and tests.

SOURCE: The Lancet Oncology, news release, Feb. 21, 2012

Copyright © 2012 HealthDay. All rights reserved.

View the original article here

Malaria drug for pancreatic cancer?

Researchers report they have shrunk or slowed the growth of notoriously resistant pancreatic tumors in mice, using a drug routinely prescribed for malaria and rheumatoid arthritis.

The pre-clinical results, which will appear in the recent issue of the journal Genes & Development and is currently published on its web site, have already prompted the opening of a small clinical trial in patients with advanced pancreas cancer, one of the deadliest and hardest-to-treat forms of cancer, said the investigators, led by Alec Kimmelman, MD, PhD, a radiation oncologist at Dana-Farber.

"We are seeing robust and impressive responses in pancreas cancer mouse models," said Kimmelman, whose laboratory specializes in studies of pancreas cancer, the fourth-leading cause of cancer death in the United States. The oral drug, hydroxychloroquine, is inexpensive, widely available, and causes relatively mild side effects, he said. A second, planned clinical trial will combine the drug with radiation.

"While these findings are indeed exciting and a cause for optimism, one needs to be mindful that so far the effects, while impressive, have only been shown in mice," said Ronald DePinho, MD, director of the Belfer Institute for Applied Cancer Science at Dana-Farber. "I eagerly await to see how the human studies will progress".

A new therapy avenue would be extremely welcome in pancreas cancer. The National Cancer Institute estimates that 43,140 people were diagnosed in 2010 and 36,800 died. Despite some recent gains with targeted molecular agents and combination regimens, only about 6 percent of patients live five years, and the median survival is less than six months.

Hydroxychloroquine is a form of the drug chloroquine, which is used to prevent and treat malaria and also prescribed for autoimmune diseases, including lupus and rheumatoid arthritis. These compounds have recently stirred much interest in cancer research, because they inhibit a process called autophagy (from the Greek for "self-eating") that is elevated in cancer cells.

Autophagy is present in normal cells as well, but at a much lower level. The process enables cells to break down and eliminate proteins, such as damaged cell membranes and worn-out organelles like mitochondria. But it is also a survival strategy. When nutrients are scarce, cells can digest and feed on their own non-critical proteins to avoid starvation.

Cancer cells also use autophagy to outwit chemotherapy therapy. Research has shown that cancer cells can activate this process in response to a variety of cancer therapys, allowing them to survive during the stress of treatment. But, as Kimmelman noted, autophagy can also be a cell-death mechanism. Cancer scientists are intensely studying ? and debating ? how to manipulate autophagy as a potential method to slow tumors' growth or make them more sensitive to other therapies.

In their research reported in Genes & Development, Kimmelman and his colleagues were stunned to find that autophagy was turned on at all times in pancreas cancer cell lines ? not just under conditions of stress, therapy or starvation. "This was a big surprise," he said. "These cells weren't deprived of nutrients; they were swimming in all the nutrients they could ever want." This suggested that for some unknown reason, pancreas tumors are highly dependent on autophagy, and therefore potentially uniquely good candidates for autophagy-inhibiting therapy.

In their next experiments, the team administered chloroquine to several different pancreas cancer cell cultures, and also tested its effects in three types of mouse models. In the laboratory cultures, they reported, the drug "markedly decreased" the growth of the tumor cells, showing that the cells were heavily dependent on autophagy to for continued growth.

In vivo testing involved three types of mouse models ? human pancreas cancer cells placed under the rodents' skin (xenografts); human cells injected into the animals' pancreases (orthotopic transplants); and a genetic model (mice bioengineered to develop native pancreatic tumors).

The response to chloroquine was "profound" in the xenograft models, Kimmelman said: All eight untreated mice died of their cancer within 140 days, while only one of eight treated mice had died by 180 days.

The drug's effects were less dramatic but still impressive in the orthotopic and genetic mouse models, the scientists said. The tumors that developed in the genetically pancreas cancer-prone mice were, like their equivalent in human patients, extremely resistant to all therapys. Among other properties, these tumors were embedded in tough, fibrous tissue that is difficult for drugs to penetrate.

Nevertheless, the researchers reported that chloroquine therapy as a single agent increased the rodents' survival by 27 days compared with untreated control mice. This is encouraging, Kimmelman commented, because even the newest targeted drugs aimed at pancreas cancer "don't have much effect in this genetic mouse model".

The Dana-Farber trial of hydroxychloroquine, led by Kimmelman and oncologist Brian Wolpin, MD, is designed to enroll 36 pancreas cancer patients in whom first- or second-line therapys have failed. The drug is taken in pill form twice a day. Results won't become available for at least a year, said Kimmelman.

Kimmelman said the next step will be to investigate the combination of hydroxychloroquine with radiation in patients with operable pancreas cancer.

"This is a very interesting and promising approach, attacking the Achilles' heel in pancreas cancer's defenses," commented Robert Mayer, MD, of Dana-Farber's Center for Gastrointestinal Oncology. "But it's too early to say whether hydroxychloroquine should be added to chemotherapy, and what the risks and benefits might be, so we want to examine it in a clinical trial".

Kimmelman's lab is also investigating other forms of cancer that might be good candidates for inhibition of autophagy by the drug. He said that their work, as well as recent findings from other labs, suggests that those cancers appears to be ones that are primarily driven by the KRAS oncogene ? as nearly all pancreatic tumors are.

Posted by: Sue    Source

View the original article here

Oral Bacteria Linked To Increased Risk Of Pancreatic Cancer

Editor's Choice
Main Category: Pancreatic Cancer
Also Included In: Dentistry
Article Date: 02 Oct 2012 - 12:00 PDT Current ratings for:
Oral Bacteria Linked To Increased Risk Of Pancreatic Cancer

Gum disease and pancreatic cancer may be associated with one another, according to the British Dental Health Foundation.

Published in the journal Gut, the study found that certain types of bacterium present in the formation of gum disease is linked to a 2 times higher risk of developing pancreatic cancer. On the other hand, oral bacteria that is not harmful resulted in a 45% decreased risk of pancreatic cancer.

A 2007 study, conducted by the same researchers, found that men with a history of periodontal disease had a 64% increased risk of pancreatic cancer than men who did not.

The experts say they cannot yet prove that gum disease increases the risk of pancreatic cancer, but they say that the new research is evidence that there is a significant association between the two.

Earlier studies have said there is a correlation between the two diseases. However, it is not clear whether certain bacteria found in gum disease are a cause or a result from pancreatic cancer.

Signs and symptoms of pancreatic cancer, which depend on the size, tissue type, and location of the tumor may include: Loss of appetiteWeight loss Jaundice (yellowish coloring of eyes and skin)Upper abdomen painTrousseau sign - a medical sign present in certain cancersClinical depressionDiabetes mellitusDominique Michaud, a Brown University epidemiologist, said: "This is not an established risk factor. But I feel more confident that something is going on. It's something we need to understand better."

Co-lead author of the study, Jacques Izard from the Forsyth Institute and Harvard University agreed with Michaud. He explained, "We need to further investigate the importance of bacteria in pancreatic cancer beyond the associated risk."

The study found that pancreatic cancer was responsible for 7,901 deaths out of 20,104, and in England, a mere 4% of pancreatic cancer patients lived for more than 5 years.

Chief Executive of the British Dental Health Foundation, Dr Nigel Carter OBE, said that if there is even the slightest evidence of an association between pancreatic cancer and gum disease, this should be enough to remind people of how critical good oral health is.

He said:

"This research provides further ammunition to the growing belief these two disease could be related.

There is no escaping the fact that poor oral health has some role to play, as a number of studies are now starting to show. What we must remember is oral health is relatively simple to maintain. The Foundation's three key messages- brushing your teeth for two minutes twice a day using a fluoride toothpaste, cutting down on how often you have sugary foods and drinks and visiting the dentist regularly, as often as they recommend- are a great starting point for maintaining good oral health.

If you have swollen gums that bleed regularly when brushing, bad breath, loose teeth or regular mouth infections appear, it is likely you have gum disease. If any of these symptoms persist, your dentist may be able to help you."

Written by Christine Kearney
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our pancreatic cancer section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

n.p. "Oral Bacteria Linked To Increased Risk Of Pancreatic Cancer." Medical News Today. MediLexicon, Intl., 2 Oct. 2012. Web.
12 Nov. 2012. APA

Please note: If no author information is provided, the source is cited instead.

'Oral Bacteria Linked To Increased Risk Of Pancreatic Cancer'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Progress in Pancreatic cancer treatment

For the first time scientists have shown that by inhibiting the action of an enzyme called TAK-1, it is possible to make pancreas cancer cells sensitive to chemotherapy, opening the way for the development of a new drug to treat the disease.

Dr Davide Melisi told Europe's largest cancer congress, ECCO 15 ESMO 34 [1], in Berlin today (Thursday 24 September) that resistance to chemotherapy was the greatest challenge to treating pancreas cancer.

"Pancreas cancer is an incurable malignancy, resistant to every anti-cancer therapy. Targeting TAK-1 could be a strategy to revert this resistance, increasing the efficacy of chemotherapy," said Dr Melisi, who until the start of September was a Fellow at the M.D. Anderson Center in Houston (Texas, USA); he has now moved to a staff position at the National Cancer Institute in Naples (Italy). "During the past few years we have been studying the role played by a cytokine or regulatory protein called Transforming Growth Factor beta (TGFbeta) in the development of pancreas cancer. Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance".

Dr Melisi and colleagues investigated the expression of TAK-1 (TGFbeta-Activated Kinase-1) in pancreatic cell lines and developed a drug that was capable of inhibiting TAK-1. They tested the activity of the TAK-1 inhibitor on its own and in combination with the anti-cancer drugs gemcitabine, oxaliplatin and SN-38 (a metabolite of the anti-cancer drug irinotecan) in cell lines, and the activity of the TAK-1 inhibitor combined with gemcitabine against pancreas cancer in mice.

"The use of this TAK-1 inhibitor increased the sensitivity of pancreatic cells to all three chemotherapeutic drugs. By combining it with classic anti-cancer drugs, we were able to use doses of drugs up to 70 times lower in comparison with the control to kill the same number of cancer cells. In mice, we were able to reduce significantly the tumour volume, to prolong the mice survival, and to reduce the toxicity by combining the TAK-1 inhibitor with very low doses of a classic chemotherapeutic drug, gemcitabine, that would have been ineffective otherwise," said Dr Melisi.

The use of gemcitabine on its own against the cancer in mice was ineffective because of the drug resistant nature of the disease. However, once it was combined with the TAK-1 inhibitor, Dr Melisi and colleagues saw a 78% reduction in tumour volumes. "The median average survival for the control, TAK-1 inhibitor, gemcitabine on its own, or TAK-1 inhibitor combined with gemcitabine was 68, 87, 82 and 122 days respectively," he said.

"This is the first time that TAK-1 has been indicated as a relevant target for the therapy of a solid tumour and that it is a valid approach to reverting the intrinsic drug resistance of pancreas cancer. The TAK-1 inhibitor used in this study is an exciting drug that warrants further development for the therapy of pancreas cancer. In the near future, we will study whether it is also able to make other chemotherapeutic agents, such as oxaliplatin, 5-FU or irinotecan, work against pancreas cancer in mice.

"Our main goal is to translate this combination approach from the bench to the bedside, conducting a clinical trial that could demonstrate the safety of this TAK-1 inhibitor in combination with gemcitabine, and its efficacy, in pancreas cancer patients".

Posted by: Sue    Source

View the original article here

Chemoradiation for pancreatic cancer better

The addition of the drug gemcitabine with chemoradiation for the therapy of patients who had surgery for pancreas cancer was linked to a survival benefit, eventhough this improvement was not statistically significant, as per a research studyin the March 5 issue of JAMA.

Despite the potential benefits of surgically removing cancer involving the pancreas, there is a 50 percent to 85 percent rate of local relapse linked to liver and intra-abdominal failure and a 5-year survival of less than 20 percent, as per background information in the article. The frequency and pattern of failure makes the combination of added postoperative chemotherapy and radiation an important consideration. The drug gemcitabine has been shown to improve outcomes compared with the drug fluorouracil.

William F. Regine, M.D., of the University of Maryland Medical Center, Baltimore, and his colleagues conducted a study to assess if the addition of gemcitabine to the supplemental therapy of fluorouracil chemoradiation (chemotherapy plus radiation) improved survival for patients who had a portion of their pancreas removed as a therapy for pancreas cancer (surgical resection). The randomized controlled phase 3 trial included 451 patients enrolled between July 1998 and July 2002 at 164 U.S. and Canadian institutions, with follow-up through August 2006. Patients received chemotherapy with either fluorouracil (n = 230) or gemcitabine (n = 221) for three weeks previous to chemoradiation treatment and for 12 weeks after chemoradiation treatment (with fluorouracil).

The scientists observed that patients with pancreatic head (a part of the pancreas) tumors (n = 388) had a median (midpoint) survival of 20.5 months and 3-year survival of 31 percent in the gemcitabine group vs. 16.9 months and 22 percent in the fluorouracil group. A certain level of hematologic (involving abnormalities in the blood cell counts) toxicity (grade 4) was 1 percent in the fluorouracil group and 14 percent in the gemcitabine group without a difference in neutropenia (a blood disorder) or infection. There were no differences in the ability to complete chemotherapy or radiation treatment.

The addition of gemcitabine to [supplemental] fluorouracil-based chemoradiation was linked to a survival benefit for patients with resected pancreas cancer, eventhough this improvement was not statistically significant, the authors write.

Patients in the study had the lowest rate of cancer recurring in its original location than in other prior studies. The tumor came back in the same area in 23 percent of the patients, in comparison to 40 percent to 60 percent of patients in other studies. At least 70 percent of the patients in this study experienced spread of their cancer to other parts of the body, a process that is known as systemic metastasis.

Laboratory correlative studies from [this trial] are ongoing and are evaluating molecular genetic alterations that promote local and systemic relapse. Future trials should emphasize novel systemic therapys to reduce systemic metastases and modern image-guided radiation to prevent local recurrence while reducing radiation-correlation toxic effects.

(JAMA. 2008;299[9]:1019-1026. Available pre-embargo to the media at www.jamamedia.org).

Editors Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Editorial: Adjuvant Therapy for Surgically Resected Pancreatic Adenocarcinoma

In an accompanying editorial, James L. Abbruzzese, M.D., of the University of Texas M. D. Anderson Cancer Center, Houston, offers suggestions on how to improve outcomes for pancreas cancer patients with surgical resection.

First, the lessons regarding the optimal selection of patients for surgical resection need to be exported more effectively into the high-surgical volume setting. Second, further work is needed to determine which patients are most likely to benefit from chemoradiation and, if this modality is going to evolve, further emphasis should be placed on the development of more effective radiation sensitizers.

Third, based on interindividual differences in drug metabolism and DNA repair, it appears that patients who are more likely to benefit from current chemotherapy and chemoradiation strategies can be defined prospectively. These individualized approaches should be examined in prospective clinical trials.

Finally, and most importantly, efforts must be redoubled to develop a new generation of promising therapeutics, and the commitment must be increased to understand and test them in prospectively defined patient subsetsnot the means to detect marginal or incremental improvements in clinical trials of large numbers of unselected patients.

Posted by: Sue    Source

View the original article here

No Cancer Risk From Long-Acting Insulin: Studies

MONDAY, June 11 (HealthDay News) -- Three studies should squelch fears that taking a form of insulin called insulin glargine (Lantus) increases the risk of cancer, researchers say.

Prior research had suggested an increase in cancer risk with Lantus, an injectable drug used to treat diabetes. "But, the worry we had that Lantos might be associated with cancer seems not to be the case, and people should continue using insulin," said Dr. Spyros Mezitis, an endocrinologist at Lenox Hill Hospital in New York City, who wasn't involved in these studies.

Lantus is a long-acting insulin, meaning patients need only one shot a day, rather than multiple injections, and it's easy to use, Mezitis added.

People using glargine often have type 1 diabetes, a condition in which the body can't make insulin, which is needed to regulate the amount of sugar in the blood. People with type 2 diabetes, the form linked to being overweight and sedentary, may also take insulin if lifestyle and dietary changes don't control their blood-sugar levels.

In the United States, where obesity and type 2 diabetes are soaring, Mezitis said he expects to see many more insulin users in years to come.

In each study, researchers wanted to see if there was any connection between daily doses of insulin and cancer.

The results were scheduled for presentation Monday at a meeting of the American Diabetes Association in Philadelphia.

In one study, Laurel Habel, a research scientist at the Kaiser Permanente Northern California Division of Research, and colleagues looked at the risk of cancer among 115,000 patients taking either glargine or an intermediate-acting insulin called NPH. This is usually taken twice a day.

"We looked at prostate, breast and colon cancer and all cancers combined," Habel said. "We saw no evidence that there was any relationship between glargine and the risk of these cancers."

In addition, no risk of cancer was noted among patients who switched from another long-acting insulin to glargine or in people who started on glargine first, Habel said.

But, these findings are based on short-term use of the drugs -- median duration was less than 1.5 years -- and she said additional follow-up is needed to evaluate cancer risk over the long-term. Cancer can take years to decades to develop, Habel noted.

In another trial, researchers from the University of North Carolina (UNC) looked at the risk of cancer in more than 52,000 people taking glargine or NPH.

Over two years of follow-up, the researchers found no association between either form of insulin and the risk for any cancer.

The UNC team used data from the Northern European Study of Insulin and Cancer, which included more than 447,000 patients, and found no spike in cancer risk for glargine or any other insulin.

"There was absolutely no association at all between the risk of cancer and any form of insulin," researcher Peter Boyle, president of the International Prevention Research Institute in Lyon, France, said during a Monday press conference. The researchers had looked for risk of all cancers, plus risks for cancers of the breast, lung, pancreas, lung, colon and prostate.

"There was absolutely no causal association," he added.

In yet another study, Dr. Hertzel Gerstein, a professor of medicine at McMaster University in Hamilton, Ontario, Canada, and colleagues found no raised risk of cancer or heart disease in a study of insulin involving more than 12,500 participants.

"At the end of the day, the study showed that one injection of insulin a day had a neutral effect on heart attacks, strokes and deaths. In addition, it had no effect on other outcomes like cancers," Gerstein said.

No protective effects on cardiovascular health or cancer were seen from insulin either, according to the report, published in the June 11 online edition of the New England Journal of Medicine.

Data and conclusions presented at medical meetings should be considered preliminary until published in a peer-reviewed medical journal.

More information

For more information on diabetes, visit the American Diabetes Association.

SOURCES: Laurel Habel, Ph.D., research scientist, Kaiser Permanente Northern California Division of Research, Oakland, Calif.; Hertzel Gerstein, M.D., professor, medicine, McMaster University department of medicine, Hamilton, Canada; Spyros Mezitis, M.D., endocrinologist, Lenox Hill Hospital, New York City; June 11, 2012, news conference, Peter Boyle, Ph.D., president, International Prevention Research Institute, Lyon, France; June 11, 2012, presentations, American Diabetes Association meeting, Philadelphia; June 11, 2012, New England Journal of Medicine, online

Copyright © 2012 HealthDay. All rights reserved.

View the original article here

Finding pancreatic cancer early

A cancer scientist from Johns Hopkins has convinced an international group of colleagues to delay their race to find new cancer biomarkers and instead begin a 7,000-hour slog through a compendium of 50,000 scientific articles already published to assemble, decode and analyze the molecules that might herald the furtive presence of pancreas cancer.

With limited resources available for the exhaustive and expensive testing that needs to be done before any candidate can be considered a bona fide biomarker of clinical value, it's important to take stock of the big picture and strategize, says Akhilesh Pandey, M.D., Ph.D., an associate professor in the McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, and founder and director of the Institute of Bioinformatics in Bangalore, India.

Having mined the literature to amass 2,516 potential biomarkers of pancreas cancer, Pandey and his team are publishing their compendium on April 6 in PLoS Medicine They systematically cataloged the genes and proteins that are overexpressed in pancreas cancer patients, then characterized and compared these biomarker candidates in terms of how worthy each is of further study.

More than 200 genes are shortlisted because they were reported in four or more published studies to be overexpressed meaning that the proteins they make are in higher abundance in people with pancreas cancer than in people without the disease. This qualifies them as "excellent candidates" for the further studies that are needed to validate them as sensitive and specific biomarkers, note the authors.

Pandey says he was motivated by the fact that even leading cancer researchers had no real idea about how a number of candidate biomarkers for pancreas cancer had already been identified, much less how they stacked up against each other in terms of clinical value in detecting early stages of the disease. Such biomarkers are highly valued because they gallop Paul Revere-like through the bloodstream and can signal early warnings of clinically invisible cancers and other diseases.

"Curation and databases are not very sexy concepts," says Pandey. "But we can't keep doing the exciting new discovery stuff and never take the time to catalog our results and share them."

Taking pancreas cancer biomarkers to prove the value of such a strategic "big picture" approach, Pandey says it could serve as a basis for other disease-marker research.

"For the first time with pancreas cancer and potentially with any cancer we have a handle on the number of candidates already identified and a real sense of how big an army we should send on the mission of further testing them," says Pandey.

Pandey's ultimate goal is to ferret out the best protein biomarker for pancreas cancer a molecule that reveals itself in an accessible bodily fluid and therefore can be detected with ease and accuracy just like the protein biomarker that's made early on by a developing fetus and is exploited by at-home pregnancy tests.

The "gold standard" pancreas cancer biomarker would possess both high sensitivity and specificity for early diagnosis. Cancer, at its most basic, is an abnormal population of cells that produce specific molecules biomarkers which healthy, cancer-free bodies do not. Cancer also tends to be incipient, Pandey says.

The ideal biomarker would allow for easy diagnosis when a cancer is still young, before it spreads to other organs. It could also help clinicians make informed decisions about therapys and better predict of outcomes, Pandey says: "Biomarkers could tell us who should undergo surgery, who should get chemotherapy, and in which people a cancer is likely to recur." .

Biomarker discovery is an exploding area of research, Pandey says, yielding ever-increasing amounts of data more than any one person can hope to keep track of, unless it's all strategically collected for widespread study.

"We want to initiate a trend by proving the importance of collection and cataloging," Pandey says, "which are exercises that a number of might view as tedious".

The team's next step is to create a searchable Web database that is universally available and free.

Posted by: Sue    Source

View the original article here

Gum Disease Bacteria Linked To Pancreatic Cancer Risk

Main Category: Pancreatic Cancer
Also Included In: Dentistry
Article Date: 01 Oct 2012 - 2:00 PDT Current ratings for:
Gum Disease Bacteria Linked To Pancreatic Cancer Risk

The British Dental Health Foundation believes new scientific research presented is a further indication of a possible link between pancreatic cancer and gum disease.

The latest research, presented in the journal Gut, found one of the bacterium key in the development of gum disease was associated with a two-fold increase in risk for pancreatic cancer. The study also discovered those with non-harmful oral bacteria had a 45 per cent lower risk of pancreatic cancer.

Although researchers cannot confirm whether gum disease contributes towards a higher risk of developing pancreatic cancer, the research is a further indication of a potential link between the two diseases.

Previous research has also drawn an association between bacteria responsible for gum disease and pancreatic cancer, although in both cases it remains unclear whether the presence of particular types of bacteria are a cause or effect of pancreatic cancer.

The paper's corresponding author Dominique Michaud, epidemiologist at Brown University, commented: "This is not an established risk factor. But I feel more confident that something is going on. It's something we need to understand better."

Co-lead author Jacques Izard, of the Forsyth Institute and Harvard University concurred. He said: "We need to further investigate the importance of bacteria in pancreatic cancer beyond the associated risk."

Pancreatic cancer accounted for 7,901 deaths in 20104, while only four per cent of people in England survived the disease for more than five years. Given these statistics, Chief Executive of the British Dental Health Foundation, Dr Nigel Carter OBE, believes any link between the two diseases should provide a timely reminder about the importance of good oral health.

Dr Carter said: "This research provides further ammunition to the growing belief these two diseases could be related.

"There is no escaping the fact poor oral health has some role to play, as a number of studies are now starting to show. What we must remember is oral health is relatively simple to maintain. The Foundation's three key messages - brushing your teeth for two minutes twice a day using a fluoride toothpaste, cutting down on how often you have sugary foods and drinks and visiting the dentist regularly, as often as they recommend - are a great starting point for maintaining good oral health.

"If you have swollen gums that bleed regularly when brushing, bad breath, loose teeth or regular mouth infections appear, it is likely you have gum disease. If any of these symptoms persist, your dentist may be able to help you."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our pancreatic cancer section for the latest news on this subject. Dominique S Michaud, Jacques Izard et al., Pancreatic cancer: Original article: Plasma antibodies to oral bacteria and risk of pancreatic cancer in a large European prospective cohort study., Gut gutjnl-2012-303006Published Online First: 18 September 2012 doi:10.1136/gutjnl-2012-303006

http://www.cancerresearchuk.org/cancer-info/cancerstats/types/pancreas/?script=true

The British Dental Health Foundation

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

n.p. "Gum Disease Bacteria Linked To Pancreatic Cancer Risk." Medical News Today. MediLexicon, Intl., 1 Oct. 2012. Web.
12 Nov. 2012. APA

Please note: If no author information is provided, the source is cited instead.

'Gum Disease Bacteria Linked To Pancreatic Cancer Risk'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Blood Test Developed That Accurately Detects Early Stages Of Lung, Breast Cancer In Humans

Main Category: Lung Cancer
Also Included In: Breast Cancer;  Pancreatic Cancer
Article Date: 28 Sep 2012 - 1:00 PDT Current ratings for:
Blood Test Developed That Accurately Detects Early Stages Of Lung, Breast Cancer In Humans

Researchers at Kansas State University have developed a simple blood test that can accurately detect the beginning stages of cancer.

In less than an hour, the test can detect breast cancer and non-small cell lung cancer -- the most common type of lung cancer -- before symptoms like coughing and weight loss start. The researchers anticipate testing for the early stages of pancreatic cancer shortly.

The test was developed by Stefan Bossmann, professor of chemistry, and Deryl Troyer, professor of anatomy and physiology. Both are also researchers affiliated with Kansas State University's Johnson Cancer Research Center and the University of Kansas Cancer Center. Gary Gadbury, professor of statistics at Kansas State University, helped analyze the data from tests with lung and breast cancer patients. The results, data and analysis were recently submitted to the Kansas Bio Authority for accelerated testing.

"We see this as the first step into a new arena of investigation that could eventually lead to improved early detection of human cancers," Troyer said. "Right now the people who could benefit the most are those classified as at-risk for cancer, such as heavy smokers and people who have a family history of cancer. The idea is these at-risk groups could go to their physician's office quarterly or once a year, take an easy-to-do, noninvasive test, and be told early on whether cancer has possibly developed."

The researchers say the test would be repeated a short time later. If cancer is confirmed, diagnostic imaging could begin that would otherwise not be routinely pursued.

According to the American Cancer Society, an estimated 39,920 breast cancer deaths and 160,340 lung cancer deaths are expected in the U.S. in 2012.

With the exception of breast cancer, most types of cancer can be categorized in four stages based on tumor growth and the spread of cancer cells throughout the body. Breast and lung cancer are typically found and diagnosed in stage 2, the stage when people often begin exhibiting symptoms such as pain, fatigue and coughing. Numerous studies show that the earlier cancer is detected, the greater chance a person has against the disease.

"The problem, though, is that nobody knows they're in stage 1," Bossmann said. "There is often not a red flag to warn that something is wrong. Meanwhile, the person is losing critical time."

The test developed by Kansas State University's Bossmann and Troyer works by detecting increased enzyme activity in the body. Iron nanoparticles coated with amino acids and a dye are introduced to small amounts of blood or urine from a patient. The amino acids and dye interact with enzymes in the patient's urine or blood sample. Each type of cancer produces a specific enzyme pattern, or signature, that can be identified by doctors.

"These enzyme patterns can also help distinguish between cancer and an infection or other diseases that commonly occur in the human body," Bossmann said. "For example, a person who smokes a lot of cigars may develop an inflammation in their lungs. That will drive up some of the markers in the test but not all of them. Doctors will be able to see whether there was too much smoke inhalation or if there is something more serious going on. False-positives are something that we really want to avoid."

Once the test is administered, comprehensive results -- which include enzyme patterns -- are produced in roughly 60 minutes.

Bossmann and Troyer have designed a second testing method that is anticipated to produce the same results in about five minutes. The team recently received $305,000 in funding for this project from the National Science Foundation's Division of Chemical, Bioengineering, Environmental and Transport Systems.

In addition to early detection, researchers say the test can be tweaked to monitor cancer. For example, patients being treated with drugs can be observed for drug effectiveness. Similarly, doctors can use the dye in the test to determine if the entirety of a tumor has been successfully removed from a patient after surgery.

Researchers evaluated the test's accuracy on 32 separate participants in various stages of breast or lung cancer. Data was collected from 20 people with breast cancer -- ranging in age from 36 to 81 years old -- and 12 people with lung cancer -- ranging in age from 27 to 63 years old.

Twelve people without cancer were also tested as a control group. This group ranged in age from 26 to 62 years old.

A blood sample from each participant was tested three times. Analysis of the data showed a 95 percent success rate in detecting cancer in participants, including those with breast cancer in stages 0 and 1 and those with lung cancer in stages 1 and 2.

Tests detecting for pancreatic cancer are anticipated to begin in October as part of Bossmann and Troyer's collaboration with Dr. Stephen Williamson at the University of Kansas Medical Center. Blood samples from triple-negative breast cancer patients will be tested this fall in collaboration with Dr. Priyanka Sharma, who is also at the University of Kansas Medical Center.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our lung cancer section for the latest news on this subject. Funding for the study -- titled "Functionalized Bimagnetic Core/Shell Fe/FE3O4 Stealth Nanoparticles for Diag & Treatment Cancer" -- was originally provided through a subcontract of a National Institutes of Health phase II Small Business Innovation Research grant to NanoScale Corp., a Manhattan-based company that manufactures, markets and commercializes advanced products and technologies, and by the Johnson Cancer Rsearch Center at Kansas State University. A Small Business Innovation Research grant is awarded to small businesses with a university partner for the purpose of accelerating research to enter the commercial marketplace.
Kansas State University Please use one of the following formats to cite this article in your essay, paper or report:

MLA

n.p. "Blood Test Developed That Accurately Detects Early Stages Of Lung, Breast Cancer In Humans." Medical News Today. MediLexicon, Intl., 28 Sep. 2012. Web.
12 Nov. 2012. APA

Please note: If no author information is provided, the source is cited instead.

'Blood Test Developed That Accurately Detects Early Stages Of Lung, Breast Cancer In Humans'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Telomere Length In Blood Cells Could Lead To Test For Pancreatic Cancer

Main Category: Pancreatic Cancer
Also Included In: Genetics;  Blood / Hematology
Article Date: 25 Oct 2012 - 0:00 PDT Current ratings for:
Telomere Length In Blood Cells Could Lead To Test For Pancreatic Cancer

A new study shows that a blood marker is linked to pancreatic cancer, according to a study published by scientists at the University of Wisconsin Carbone Cancer Center and Mayo Clinic.

First author Dr. Halcyon Skinner, assistant professor of population health sciences at the University of Wisconsin School of Medicine and Public Health, says the study is the first time pancreatic cancer risk has been linked to differences in telomeres' length in blood cells.

"This suggests a new avenue to identify those with pancreatic cancer or those at risk of developing the cancer in the future,'' he says.

Skinner's colleagues at Mayo Clinic took blood samples from more than 1,500 people - 499 of them with a diagnosis of pancreatic cancer and 963 of them cancer-free control subjects. Specifically, the scientists were interested in the length of the telomeres - the end caps on chromosomes - found in white blood cells. They found a direct relationship with the risk of pancreatic cancer: the shorter the telomeres, the more likely a person was to have pancreatic cancer.

Telomeres maintain the stability of genes, and are known to shorten with age as cells divide. People of the same chronological age can have vastly different telomere lengths. In other words, some people's cells can by viewed as biologically older than cells from other people the same age.

"We know that people with many factors that are classically unhealthy also tend to have shorter telomeres. Those who have had stressful lives, exposed to chronic inflammation, have poor glucose control or smoked cigarettes tend to have shorter telomeres, and that can set the stage for genetic damage,'' Skinner explains.

Shortened telomeres in the blood have already been associated with other types of cancer, including colon cancer.

"We found the same relationship with pancreatic cancer, and for the vast majority of our participants, there was a direct linear relationship," he says, "the shorter the telomere, the higher the likelihood of pancreatic cancer."

But because shorter telomere length is also associated with the development of other cancers and other diseases of aging, measurement of telomere length alone is not a specific marker for pancreatic cancer.

Dr. Lisa A. Boardman, of Mayo Clinic, who led the overall study, says that future studies need to address if telomere length and other markers of pancreatic cancer should be combined to create a test that could be used clinically.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our pancreatic cancer section for the latest news on this subject. Skinner and UW colleagues Ron Gangnon and Kristin Litzelman led the design and data analysis of the study. It is being published in Cancer Epidemiology, Biomarkers and Prevention, a journal of the American Association for Cancer Research.
Skinner's work was supported by the National Institutes of Health (K07 CA109361).
University of Wisconsin-Madison Please use one of the following formats to cite this article in your essay, paper or report:

MLA

n.p. "Telomere Length In Blood Cells Could Lead To Test For Pancreatic Cancer." Medical News Today. MediLexicon, Intl., 25 Oct. 2012. Web.
12 Nov. 2012. APA

Please note: If no author information is provided, the source is cited instead.

'Telomere Length In Blood Cells Could Lead To Test For Pancreatic Cancer'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Whole Genome Sequencing Of Multiple Pancreatic Cancer Patients

Main Category: Pancreatic Cancer
Also Included In: Genetics
Article Date: 12 Oct 2012 - 0:00 PDT Current ratings for:
Whole Genome Sequencing Of Multiple Pancreatic Cancer Patients

Whole genome sequencing - spelling out all 3 billion letters in the human genome - "is an obvious and powerful method for advancing our understanding of pancreatic cancer," according to a new study from TGen, Mayo Clinic and Scottsdale Healthcare.

The Translational Genomics Research Institute (TGen) demonstrated that the use of WGS "represents a compelling solution to obtaining detailed molecular information on tumor biopsies in order to provide guidance for therapeutic selection," concluded the study published by the journal PLOS ONE.

Examining three patients, the study spelled out the DNA of normal cells and compared that to the DNA of cells from biopsies of pancreatic adenocarcinoma (PAC), which makes up 95 percent of all pancreatic cancer tumors. Pancreatic cancer is the fourth leading cause of cancer death in the U.S.

Using next-generation sequencing, the study generated an average of 132 billion mappable bases, or data points, for each patient, resulting in the identification of 142 cellular genetic coding events, including mutations, insertions and deletions, and chromosomal copy number variants.

"This study is the first to report whole genome sequencing findings in paired tumor/normal samples collected from (three) separate PAC patients," said the report, which also was compiled with the collaboration of Mayo Clinic in Arizona, Arizona State University, and the Virginia G. Piper Cancer Center Clinical Trials at Scottsdale Healthcare, which is a partnership between TGen and Scottsdale Healthcare.

In all three case studies, the report found multiple potential therapeutic targets, highlighting the need to study the full spectrum of the genome and re-emphasizing the need to develop multiple avenues of therapeutics to match the specific medical challenges of each patient.

"Cancer, and specifically here pancreatic cancer, is a highly complex disease that ultimately will require a variety of treatment methods to control, and ultimately to cure," said Dr. Daniel Von Hoff, TGen's Physician-In-Chief, and Chief Scientific Officer for the Virginia G. Piper Cancer Center at Scottsdale Healthcare.

"This study shows that, as we continue to generate more information by sequencing the whole genomes of patients, we will continue to discover - with ever more confidence - the specific mechanisms that cause this cancer," said Dr. Von Hoff, one of the study's senior authors and one of the world's leading authorities on pancreatic cancer.

"We are very pleased to be working together with TGen in bringing hope and state of the art therapy to our patients at the Mayo Clinic Comprehensive Cancer Center," said Keith Stewart, M.B., Dean of Research at Mayo Clinic in Arizona, and the study's other senior author.

In the case of Patient 1, for example, genes previously associated with PAC were identified, including BRCA2, TP53, CDKN2A, MYC, SMAD4 and KRAS. But the study also made new discoveries. "Although BRCA2 mutations have been identified in PAC, the deletion we identify here in exon 10 of BRCA2 has not been previously reported," the study said.

Multiple therapeutics based on these findings were applied to Patient 1, who initially "showed a complete response,'' but developed drug resistance after six months.

"The BRCA2 deletion is likely the driving mutation in this patient as the loss of DNA repair functions permits the occurrence of mutations," the study said. "This finding and association provides evidence of the utility of performing whole genome analysis of patients in order to identify less common mutations that may be relevant for therapeutic selection."

WGS for Patient 2 and Patient 3 also uncovered multiple potential therapeutic targets through the identification of mutations and copy-number changes. In addition, RNA sequencing, or whole transcriptome analysis, of Patient 2 and Patient 3 revealed gene expression data that provided more information about likely affected biological processes.

Cellular pathway analysis of all sequencing data was also performed to identify processes that may be the most heavily impacted by cellular and gene expression alterations.

"As we continue to sequence patients, we will acquire a better understanding of the compendium of events that have a role in the disease, and strengthen our knowledge base for identifying and developing improved therapeutics," said Winnie Liang, Ph.D., Assistant Director of TGen's Collaborative Sequencing Center and one of the co-lead authors of the study.

"This study has demonstrated the feasibility of applying genome sequencing approaches toward eventual personalization and precision of therapy for patients with pancreatic cancer," said Dr. Mitesh Borad, hematologist/oncologist at Mayo Clinic in Arizona and co-author of the study. "Current studies are focusing on application of this approach in the clinical setting in a real time fashion."

Co-author Dr. Michael Demeure, Clinical Professor of TGen's Rare Cancer Unit and Scientific Director of the Endocrine and Rare Tumors Program at the Virginia G. Piper Cancer Center at Scottsdale Healthcare, said, "Whole genome sequencing provides us with the genetic blueprint and knowledge that is needed to crack the complex mysteries surrounding pancreatic cancer. For rare cancers where the data pool is relatively small, the potential for progress is particularly encouraging."

This groundbreaking study - Genome-wide characterization of pancreatic adenocarcinoma patients using next generation sequencing - was funded by: the National Foundation for Cancer Research, the Randy Pausch Scholarship Fund, and the Seena Magowitz Foundation. Additional support was provided by the Mayo Clinic Comprehensive Cancer Center, the U.S. Department of Health and Human Services, and supercomputing resources funded by the National Institutes of Health.

"This study represents a major step forward in the quest to find a cure for this cancer, which took the life of my mother, Seena. We are working harder than ever with TGen and others to continue this fight," said Roger Magowitz, President and co-founder of the Seena Magowitz Foundation.

"Whole genome sequencing is a new approach toward finding better treatments and to making these treatments available to cancer patients who need them now. We cannot emphasize enough the need for this kind of research," said Franklin C. Salisbury Jr., President of the NFCR.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our pancreatic cancer section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

n.p. "Whole Genome Sequencing Of Multiple Pancreatic Cancer Patients." Medical News Today. MediLexicon, Intl., 12 Oct. 2012. Web.
12 Nov. 2012. APA

Please note: If no author information is provided, the source is cited instead.

'Whole Genome Sequencing Of Multiple Pancreatic Cancer Patients'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Genetic code for form of pancreatic cancer

Researchers at Johns Hopkins have deciphered the genetic code for a type of pancreas cancer, called neuroendocrine or islet cell tumors. The work, described online in the Jan. 20 issue of Science Express, shows that patients whose tumors have certain coding "mistakes" live twice as long as those without them.

"One of the most significant things we learned is that each patient with this kind of rare cancer has a unique genetic code that predicts how aggressive the disease is and how sensitive it is to specific therapys," says Nickolas Papadopoulos, Ph.D., associate professor at the Johns Hopkins Kimmel Cancer Center and director of translational genetics at Hopkins' Ludwig Center. "What this tells us is that it appears to be more useful to classify cancers by gene type rather than only by organ or cell type."

Pancreatic neuroendocrine cancers account for about five percent of all pancreas cancers. Some of these tumors produce hormones that have noticeable effects on the body, including variations in blood sugar levels, weight gain, and skin rashes while others have no such hormone "signal".

In contrast, hormone-free tumors grow silently in the pancreas, and "a number of are difficult to distinguish from other pancreas cancer types," as per Ralph Hruban, M.D., professor of pathology and oncology, and director of the Sol Goldman Pancreatic Cancer Research Center at Johns Hopkins.

For the newly released study, the team investigated non-hormonal pancreatic neuroendocrine tumors in 68 men and women. Patients whose tumors had mutations in three genes ? MEN-1, DAXX and ATRX ? lived at least 10 years after diagnosis, while more than 60 percent of patients whose tumors lacked these mutations died within five years of diagnosis.

The Johns Hopkins team, which previously mapped six other cancer types, used automated tools to create a genetic "map" that provides clues to how tumors develop, grow and spread.

Within the code are individual chemicals called nucleotides, which pair together in a pre-programmed fashion to build DNA and, in turn, a genome. Combinations of these nucleotide letters form genes, which provide instructions that guide cell activity. Changes in the nucleotide pairs, called mutations, can create coding errors that transform a normal cell into a malignant one.

In the first set of experiments, the Johns Hopkins researchers sequenced nearly all protein-encoding genes in 10 of the 68 samples of pancreatic neuroendocrine tumors and compared these sequences with normal DNA from each patient to identify tumor-specific changes or mutations.

In another set of experiments, the researchers searched through the remaining 58 pancreatic neuroendocrine tumors to determine how often these mutated genes appeared.

The most prevalent mutation, in the MEN-1 gene, occurred in more than 44 percent of all 68 tumors. MEN-1, which has been previously associated with a number of cancers, creates proteins that regulate how long strands of DNA are twisted and shaped into dense packets that open and close depending on when genes need to be activated. Such a process is regulated by proteins and chemicals that operate outside of genes, termed "epigenetic" by scientists.

Two other usually mutated genes, DAXX and ATRX, which had not previously been associated with cancer, also have epigenetic effects on how DNA is read. Of the samples studied, mutations in DAXX and ATRX were found in 25 percent and 17.6 percent, respectively. The proteins made by these two genes interact with specific portions of DNA to alter how its chemical letters are read.

"To effectively detect and kill cancers, it appears to be important to develop new diagnostics and therapeutics that take aim at both epigenetic and genetic processes," says Kenneth Kinzler, Ph.D., professor of oncology at the Johns Hopkins Kimmel Cancer Center and co-director of the Ludwig Center at Johns Hopkins.

The Johns Hopkins team also observed that 14 percent of the samples studied contained mutations in a gene family called mTOR, which regulates cell signaling processes. Papadopoulos says that patients with tumors containing such alterations in the mTOR pathway could be candidates for therapy with mTOR inhibitor drugs.

"This is a great example of the potential for personalized cancer treatment," says Hruban. "Patients who are most likely to benefit from a drug can be identified and treated, while patients whose tumors lack changes in the mTOR pathway could be spared the side effects of drugs that may not be effective in their tumors".

Posted by: Sue    Source

View the original article here

Link Between Smoking AndPancreatic Cancer

Scientists at Michigan State University have added yet another piece to the puzzle that links cigarette smoking with cancer of the pancreas, one of the deadliest forms of cancer.

In research reported in the recent issue of the International Journal of Cancer, MSUs James Trosko and his colleagues zeroed in on the mechanism by which a healthy cell turns malignant.

Specifically, they observed that the chemicals produced by the burning of tobacco products polycyclic aromatic hydrocarbons, or PAHs interfere with communication between the bodys cells. More importantly, the work showed that some of these chemicals dont necessarily initiate the cancer, but rather contribute to the promotion of it.

"These PAH chemicals are correlation to the multistage, multimechanism process of carcinogenesis, not by mutating the stem cell, but by triggering the stem cell thats been previously mutated to proliferate," said Trosko, a professor of pediatrics and human development. "This finding has major implications, including the possibility that dietary intervention might interrupt or even reverse the promotion of pancreas cancers".

Until now, most researchers thought that specific PAHs produced by burning tobacco mutated genes which, in turn, triggered the cancer mechanism.

"We take issue with this interpretation," Trosko said. "We dont think that the PAH chemicals cause mutations which then lead to cancer".

Pancreas cancer is one of the more deadly forms of cancer, with an average survival rate of only about a year. Its projected that more than 37,000 Americans will be diagnosed with pancreas cancer in 2007.

Trosko noted that PAHs are formed when any substance containing certain proteins is burned, including foods.

"PAHs are all over," he said. "When you grill a steak or a hamburger, for example, you get exactly the same class of chemicals".

This research is the culmination of nearly 30 years of work in Troskos lab. It was in 1979 that Trosko, colleagues and students demonstrated that tumor-promoting chemicals interfered with a cells ability to communicate with other cells. Later, this group isolated adult human pancreatic stem cells from human pancreatic tissue.

Subsequent published findings indicated that these stem cells appeared to be targets for cancer.

"Since we had the system here in our lab, we decided to see if PAHs would act as a tumor promoter," he said. "And sure enough they did".

The good news is that people who quit smoking can dramatically improve their chances of avoiding cancers.

"If these chemicals act like cancer promoters and not initiators," Trosko said, "then quitting smoking can assist in interrupting the process".

Posted by: Sue    Source

View the original article here

Determining Risk for Pancreatic Cancer

In the latest clinical trial for a technique to detect pancreas cancer, scientists found they could differentiate cells that are malignant from those that are benign, pre-malignant, or even early stage indicators called mucinous cystic lesions.

Pancreas cancer is dangerous to screen for, yet deadly if ignored. The pancreas is extremely sensitive--biopsies can lead to potentially fatal complications--but with few symptoms, the cancer is commonly detected too late.

The disease is the fourth largest cause of cancer-related deaths in the United States, with a five-year survival rate of less than 5 percent. If doctors can find ways to identify early precursor lesions, the disease can be prevented in most individuals.

Reporting online Feb. 10, 2009, in the journal Disease Markers, scientists from Northwestern University and Evanston Northwestern Healthcare report convincing results with their minimally invasive methods for detecting pancreas cancer.

"This technique allows us to detect changes in cells that look normal using microscopy," says co-author Vadim Backman of Northwestern University. "This level of detail allows us to detect cancer in its earliest stages".

Their techniques, called four-dimensional elastic light scattering fingerprinting (4D-ELF) and low-coherence enhanced backscattering spectroscopy (LEBS), identify the cancer and its precursors by analyzing light refracted through cells in the duodenum, a section of the small intestine adjacent to the pancreas.

"I'm excited about this work," said Leon Esterowitz, the National Science Foundation (NSF) biophotonics program director who helped fund this study and the development of the 4D-ELF and LEBS technologies. "I believe these results are very promising, and the techniques have a high probability of success for not just detecting early pancreas cancer, but pre-cancer, so doctors can go ahead and treat the patient while there's still a chance to defeat the disease." Esterowitz added. "For pancreas cancer, this could lead to not only an excellent prognosis, but perhaps even a cure".

While earlier success had shown that the techniques could tell malignant from non-malignant tissue without resorting to a biopsy, the newly released study of 203 individuals was the first to show the method can identify various disease stages and risk factors, including a possible signature correlation to "family history".

The researchers' approach had a sensitivity of 95 percent for determining healthy tissue from malignant tissue and may be the most successful yet developed for detecting pancreatic diseases at curable stages and for identifying high-risk individuals.

"These optical techniques have shown promise for detecting both colon and pancreas cancer," says Backman. "Our hope is to continue to test the ability to detect other forms of cancer, which would greatly expand the impact of the technology." In ongoing work, the scientists will continue to refine their instrumentation and hope to validate the recent findings with further clinical trials.

Posted by: Sue    Source

View the original article here

Antioxidants may help cut pancreatic cancer risk, study suggests

Monday, July 23, HealthDay News)-a diet high in antioxidants such as selenium and vitamins C and E can reduce the risk of cancer of the pancreas in up to two-thirds, suggests a new study.

The study is observational in nature and can only suggest an association, not a cause and effect relationship. However, British researchers say that if further research confirms a direct link, this type of diet can prevent the 8 percent of pancreatic cancer cases.

An expert said that there has been much research into the relationship between diet and cancer.

"" The years there have been many attempts to find dietary causes of cancer, said Dr. Vincent Vinciguerra, Chief of Oncology and Hematology at North Shore-LIJ Monter Cancer Center in Lake Success, New York "it is estimated that 35 percent of cancers are related to carcinogens in the diet. Antioxidants have been subject to numerous essays because in theory it could be fundamental in the prevention of carcinogenesis."

In the new study, researchers led by the Dr. Andrew Hart of the University of East Anglia tracked the health of more than 23,500 people long-term, 40 to 74 years who entered the study between 1993 and 1997. Each participant maintains a food diary detailing the types, quantity and method of preparation for each food you ate for seven days.

After 10 years, 49 participants (55 per cent of whom were men) had been diagnosed with pancreatic cancer. In 2010, the number of participants diagnosed with pancreatic cancer increased to 86 (44 per cent were men). On average, patients survived six months after diagnosis.

The researchers found that people with greater intake of selenium were half as likely to develop cancer of the pancreas than those with the lowest consumption. Those who consume greater ingestion of three antioxidants, selenium and vitamins C and E--were 67 percent less likely to develop pancreatic cancer compared with those with the lowest consumption.

The study was published online July 23 in the journal Gut.

Previous studies using antioxidant supplements have not produced results as encouraging, but this may be because the antioxidants in food behave differently than the supplements, they told Hart and colleagues.

Vinciguerra agreed that the research so far on this issue has been "conflicting".

For example, he said, there was "a recent study involved prevention of cancer of prostate with vitamin E and selenium [that] showed no benefit".

"Selenium has also served in a study to prevent the lung cancer, that was negative," he added. "Vitamin C also has no proven prevention activities."

Even so, food and cancer may interact differently depending on the type of tumor, said Vinciguerra.

"The current study using food diaries is expected that it is providing useful information on this disease, which is often highly lethal," he said. "Prevention information should be prosecuted".

"The next step would be to do a prospective study of antioxidants in patients with increased risk of pancreatic cancer to verify the current findings," said Vinciguerra.

Meanwhile, he said, "we are recommending diets low in fat, red meat decreased [and] more fruits, vegetables, chicken and fish for our cancer patients, that like most provides antioxidants that hopefully it provides some degree of preventing recurrence.

Pancreatic cancer kills more than 250,000 people worldwide each year. Only 3 percent of people diagnosed with the disease live longer than five years. Genes, smoking and type 2 diabetes are all risk factors, but the diet is believed to play a role also.

The American Cancer Society more recent estimates for cancer of the pancreas in the United States for 2012 are: 43,900 on new cases and a few 37.400 deaths by the disease. The risk of pancreatic cancer is about one in 71, according to the society.

More information

The American cancer society has more about cancer of the pancreas.

SOURCES: Chief of Vincent Vinciguerra, M.D., Don Monti Division of Oncology/Hematology, North Shore LIJ Monter Cancer Center, Lake Success, New York; Gut, press release, July 23, 2012

Copyright © 2010 HealthDay. All rights reserved.

View the original article here