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