New pancreas tumor registry

Charles J. Yeo, M.D., Samuel D. Gross Professor and Chair, Department of Surgery at Jefferson Medical College of Thomas Jefferson University, announces the establishment of the new Jefferson Pancreas Tumor Registry (JPTR).

"The purpose of the registry is to further study whether pancreas cancer occurs more frequently in families with a history of the disease," said Dr. Yeo, who is the principal investigator of JPTR. "It will also be used to determine the environmental and occupational risk factors to which pancreas cancer patients have been exposed."

The JPTR modeled after the National Familial Pancreas Tumor Registry is a longitudinal study in which participants may engage in long-term follow-up and receive information regarding scientific and epidemiological breakthroughs in pancreas cancer.

Participants are asked to complete a detailed questionnaire and may be asked to submit a blood sample and/or cheek swab. The questionnaires are designed to elicit the family health history of a patient with pancreas cancer or a non-affected family member, and to document exposure to occupational and environmental factors, such as residential radon, asbestos and second-hand tobacco smoke.

Research has shown that certain rare genetic conditions are linked to an increased risk of pancreas cancer, including familial breast-ovary cancer, familial melanoma, familial colon cancer, hereditary pancreatitis and Peutz-Jegher's syndrome (a rare hereditary condition that results in gastrointestinal polyps). "While we have not identified a causative gene yet to allow predictive testing for pancreas cancer, we can offer risk assessments and surveillance via imaging, blood tests and endoscopic ultrasound for patients with a strong family history of pancreas cancer," added Dr. Yeo.

Such high risk patients may be referred to a Jefferson gastroenterologist to discuss the pros and cons of invasive surveillance. The goal is to diagnose pancreas cancer earlier, when more therapy options are available. For persons who do develop pancreas cancer, Jefferson physicians may use the results of genetic testing to select the most effective treatment. Targeted treatment for pancreas cancer is becoming a reality, in part due to recent discoveries made in the laboratory of Jonathan Brody, Ph.D., assistant professor, Department of Surgery at Jefferson Medical College of Thomas Jefferson University, where molecular studies have clearly indicated survival advantages with the use of targeted chemotherapy.

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Smoking increases risk of metastatic pancreatic cancer

Smoking has once again been implicated in the development of advanced cancer. Exposure to nicotine by way of cigarette smoking may increase the likelihood that pancreatic ductal adenocarcinoma will become metastatic, as per scientists from the Kimmel Cancer Center at Jefferson. Their study was reported in the August edition of the journal Surgery
The culprit behind the increased metastasis potential may be an isoform (variant type) of a protein called osteopontin, as per Hwyda Arafat, M.D. Ph.D., an associate professor of Surgery at Jefferson Medical College of Thomas Jefferson University and a member of the Jefferson Pancreatic, Biliary & Related Cancers Center.

Nicotine promotes the expression osteopontin, and high levels of osteopontin have been reported in pancreatic ductal carcinoma (PDA). Dr. Arafat and her research team analyzed PDA samples and confirmed that the isoform, called OPNc, was also expressed on invasive PDA lesions. Prior studies have shown that OPNc is expressed in several invasive cancers, and supports metastatic behavior.

The scientists correlated OPNc expression with the patients' smoking history. OPNc expression was found on 87 percent of the invasive PDA lesions analyzed, of which 73 percent were from smokers. The OPNc expression also correlated with higher expression levels of osteopontin. Precancerous lesions expressed no OPNc.

"This is the first time a relationship between nicotine and OPNc expression has been identified," Dr. Arafat said. "These data are very exciting because now we can evaluate OPNc as a prognostic and diagnostic marker of invasive PDA lesions. "Because of the lower expression levels of OPNc in non-smokers, OPNc appears to be regulated by nicotine, which is another novel finding of this study. The exact role of OPNc in PDA remains to be defined, but it could provide a unique potential target to control pancreas cancer aggressiveness, particularly in people who smoke cigarettes".

Pancreas cancer is the fourth-leading cause of cancer death in the country, taking 34,000 lives a year. Only four percent of individuals with pancreas cancer live for five years after diagnosis.

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Smoking has once again been implicated in the development of advanced cancer. Exposure to nicotine by way of cigarette smoking may increase the likelihood that pancreatic ductal adenocarcinoma will become metastatic, as per scientists from the Kimmel Cancer Center at Jefferson. Their study was reported in the August edition of the journal Surgery

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Hepatitis B exposure and pancreatic cancer

HOUSTON - In a first-of-its-kind finding, scientists at The University of Texas M. D. Anderson Cancer Center have discovered that exposure to the hepatitis B virus (HBV) may increase the risk of pancreas cancer.

The study, reported in the Oct. 1 edition of the Journal of Clinical Oncology, also suggests that patients with this lethal form of cancer treated with chemotherapy may face danger of reactivation of their HBV.

Pancreas cancer is diagnosed in 37,000 people in the United States each year, and more than 34,000 people die of the disease annually, as per the American Cancer Society. It is often diagnosed in the late stages and is particularly perplexing because few risk factors are known.
Manal Hassan, M.D., Ph.D.

Credit: M. D. Anderson Cancer Center

"If this study is validated, it will give us more information about the risk factors of pancreas cancer and possibly even help prevent it in some cases," said lead author Manal Hassan, M.D., Ph.D., assistant professor in M. D. Anderson's Department of Gastrointestinal Medical Oncology.

HBV and hepatitis C virus (HCV) are major global health problems, affecting about 2 percent of the population worldwide. In the United States 1.25 million people have chronic HBV, while 3.2 million have chronic HCV. These systemic viruses can harm the body in a variety of ways, including traveling through the bloodstream and damaging tissues throughout the body.

The word "hepatitis" means "inflammation of the liver," and prior research has shown HBV and HCV are major causes of liver cancer. Little is known about their roles in other cancers. However, the proximity of the liver to the pancreas and the fact the pancreas and liver share common blood vessels and ducts make the pancreas a potential target for hepatitis viruses.

While this is the first study to examine whether exposure to HBV and HCV increases risk for pancreas cancer, other research has indicated chronic HBV infection may impair pancreatic function and that HBV may replicate in the pancreas, Hassan said.

In this study, which began in 2000, 476 M. D. Anderson patients with early pancreas cancer were identified. Additionally, 879 people without pancreas cancer were matched with the patients by age, gender and race. All participants were interviewed for demographic and risk factors information.

Then scientists tested the blood of all participants for the presence of HCV and HBV antibodies, which indicate past exposure to HCV and HBV.

The prevalence of past exposure to HBV was significantly higher (7.6 percent) in people with pancreas cancer than in healthy people (3.2 percent). However, exposure to HCV was not significantly different in the two groups.

In addition, the study confirmed previously reported risk associations of cigarette smoking, history of diabetes and a family history of pancreas cancer.

People exposed to HBV may develop occult, or hidden, HBV infection. In these cases, the M. D. Anderson scientists say, there is a potential for reactivation of HBV during chemotherapy, the most common therapy for pancreas cancer. Chemotherapy may suppress the immune system, leading to viral replication of the HBV, the scientists explained.

"If these results are validated, physicians might want to test pancreas cancer patients for HBV before administering chemotherapy," said senior author James Abbruzzese, M.D., professor and chair of M. D. Anderson's Department of Gastrointestinal Medical Oncology and associate medical director of the Gastrointestinal Center. "Reactivation of HBV could potentially cause liver damage and even liver failure".

Scientists stress these early results need to be studied further and plan to collaborate with other institutions to compare results among other populations and people who are actually infected with the virus. If they are confirmed, these results may offer new insight into pancreas cancer, possibly even preventing some cases in the future.

"We are working hard to try to understand the factors that are risks to developing pancreas cancer, especially modifiable risks," Abbruzzese said. "If these results are confirmed, people who are at risk might be able to help prevent pancreas cancer by getting an HBV vaccine".

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Study Identifies Components Responsible For Therapy-Blocking Solid Stress, Suggests Therapeutic Cancer Strategies

Main Category: Pancreatic Cancer
Also Included In: Lung Cancer;  Breast Cancer
Article Date: 24 Sep 2012 - 1:00 PDT Current ratings for:
Study Identifies Components Responsible For Therapy-Blocking Solid Stress, Suggests Therapeutic Cancer Strategies

It's a high-pressure environment within solid tumors. Abnormal blood and lymphatic vessels cause fluids to accumulate, and the uncontrolled proliferation of cancer cells within limited space leads to the buildup of what is called solid stress. Both types of pressure can interfere with the effectiveness of anticancer treatments, but while strategies have been developed that reduce fluid pressures, little has been known about the impact of solid stress or potential ways to alleviate it. Now a Massachusetts General Hospital (MGH) research team has identified factors that contribute to solid stress within tumors, suggesting possible ways to alleviate it, and has developed a simple way to measure such pressures.

"Traditionally cancer research has focused on cancer cells and, more recently, on the biochemical microenvironment of tumors," says Rakesh Jain, PhD, director of the Steele Laboratory for Tumor Biology at MGH and senior author of the study in the Proceedings of the National Academy of Sciences. "Our work shows that the physical or mechanical microenvironment plays an equally important role in tumor progression and treatment resistance."

Jain and his colleagues have been leaders in understanding the impact of elevated fluid pressures that make it difficult for drugs to enter and permeate tumors. Their work showed that fluid pressures are relieved when antiangiogenesis drugs normalize the abnormal blood vessels characteristically found within solid tumors, improving the effectiveness of other anticancer therapies. But that approach can only work if vessels have not been squeezed shut by solid stress in surrounding tissues. In recent studies Jain's team showed that solid stress also increases the invasiveness of cancer cells.

The current study was designed to develop techniques that measure solid stress in tumors, to identify factors that contribute to the generation of this solid stress and to determine whether previously compressed blood vessels would open when stress-inducing components were depleted. Based on predictions from mathematical models, the MGH-based team developed a remarkably simple way to measure solid stress within tumor tissues.

In experiments using both tumors experimentally grown in mice and tumors removed from human patients, the researchers found that, when a solid tumor is cut in two, each segment begins to swell along the sliced surface, releasing stored solid stress. In contrast, when a sample of normal tissue is cut in two, the separated halves of tissue retain their size and shape (links to video files below). Measuring the extent of shape relaxation along with other mechanical properties of tumor tissue enabled calculation of the amount of solid stress within a tumor sample.

Sample of breast tumor grown in mouse expands after cutting, releasing solid stress *

Sample of normal mouse kidney tissue, showing no change in shape after cutting **

Additional experiments utilizing the newly developed technique identified several components that contribute to increased solid stress within tumors, including the proliferation not only of cancer cells but also of fibroblasts and other components of the tumor's extracellular matrix. In pancreatic tumors implanted into mice, the researchers showed that inhibition of a pathway leading to the growth of fibroblasts reduced solid stress associated with tumor growth and opened up compressed blood and lymphatic vessels, which could both relieve fluid pressure and improve the delivery of chemotherapy drugs.

The authors note that their results may explain why the use of antiangiogenesis drugs has not improved treatment of highly fibrotic tumors - including dangerous pancreatic, lung and breast cancers - and suggest that a strategy targeting both aspects of intratumor pressure should be explored. "Now that we have seen how tumors exploit physical forces to facilitate progression and treatment resistance, we need to learn how to tame these fluid and solid forces to improve treatment outcomes," says Jain, the Cook Professor of Radiation Oncology (Tumor Biology) at Harvard Medical School. "We urgently need to identify safe pharmaceutical agents that reduce solid stress and then add them judiciously to current treatments."

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. * http://www.pnas.org/content/suppl/2012/08/29/1213353109.DCSupplemental/sm01.mov
** http://www.pnas.org/content/suppl/2012/08/29/1213353109.DCSupplemental/sm02.mov
Co-lead authors of the PNAS paper are Triantafyllos Stylianopoulos, PhD, and John D. Martin of the Steele Laboratory. Additional co-authors are Vikash Chauhan, Saloni Jain, Benjamin Diop-Frimpong, Yves Boucher, PhD, and Lance Munn, PhD, Steele Lab; Nabeel Bardeesy, PhD, MGH Center for Cancer Research; Barbara Smith, MD, MD, and Cristina Ferrone, MD, MGH Department of Surgery; and Francis J. Horniceki, MD, PhD, MGH Orthopaedic Oncology. The study was supported by grants from the National Institutes of Health and the Department of Defense.
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New therapies promising some against pancreatic cancer

Tuesday, June 19, HealthDay News)-giving four weeks of a specific drug before chemotherapy improved response rates in a small group of patients with advanced pancreatic cancer, report researchers at the University of Michigan.

The results are "very, very preliminary", said Dr. Jay Brooks, Chairman of Hematology and Oncology at the Ochsner of Baton Rouge, Louisiana, health system but you can show "a minimum of at least progress in the understanding of the biology of the disease. Pancreatic cancer is incredibly difficult to treat cancer".

The findings were presented Tuesday during a press conference at the American Association for the Conference on cancer research on cancer of the pancreas in Lake Tahoe, Nevada

The drug, GDC-0449, directs the signaling pathway Sonic Hedgehog, which lights up when cancer is present.

Activation of the pathway seems to contribute to the healing characteristics of pancreatic cancer, which makes it more difficult for chemotherapy drugs penetrate and do their job.

The hypothesis of the researchers who giving GDC-0449 before chemotherapy can improve the effectiveness of chemotherapy and its initial results indicate that it may be the case.

GDC is already used for basal cell carcinoma advanced under the name of Erivedge (vismodegib).

Twenty-one patients with previously untreated metastatic pancreatic cancer received four weeks of GDC, given in pill form once a day, and then chemotherapy with the drug Gemcitabine.

Biopsies taken both before the GDC and three weeks later showed reduction of the tumor in five patients, while other four patients achieved disease «stable», which means that the tumor was not declining or growing.

The drug was most effective in patients who initially had high levels of expression of Hedgehog.

Hedgehog levels are especially high in cancer cells. Is human trafficking, "a subset of cells identified in many cancers, including cancer of the pancreas, which is believed not only to boost the growth of tumor but that are also particularly resistant to standard chemotherapy and radiation therapies," explained the study author Dr. Edward Kim, a medical oncologist at the cancer center integral of the University of Michigan in Ann Arbor.

"I think this trial here is a step back in the right direction to find exactly what is happening. I would say that reading the summary response rate was very high. It means that you would normally see a 5 or 9% chance of getting a response to Gemcitabine, and here in this situation I think that at least 23 percent, 25 percent, "said the President of the Conference Dr. Daniel Von Hoff, medical Chief and distinguished professor at the Translational Genomics Research Institute and Professor of medicine at the clinic Mayo in Rochester"", Minn. "went beyond what would normally be expected".

"I'm very interested in seeing the final outcome of this," said Von Hoff. "The good news is that these inhibitors of Hedgehog does not add any substantial toxicity any".

A second study presented at the Conference, this one done in mice, found a protein which makes cells to stubbornly refuse to respond to the treatment of pancreatic cancer.

Blocking the protein, known as RLIP76, in mice with cancer of the pancreas to "complete regression" in tumors, said the lead author of the study Dr. Sanjay Awasthi, Professor of medical oncology Endocrinology and therapeutic research and diabetes and metabolism at the city of Hope Cancer Center in Duarte, California.

RLIP76 transports chemicals killer of chemotherapy drugs and radiation out cells until they can do their job. It tends to be more RLIP76 in cancer cells of the pancreas that in human cells healthy.

Beating later RLIP76 levels also seemed have antidiabetic effects, as these mice showed decreases in the blood sugar, cholesterol and triglycerides.

Awasthi said that he and his colleagues expect to move forward with this molecule, possibly as a medicine against diabetes and cancer to.

Awasthi is the founder of Terapio, the company that manufactures the RLIP76 recombinant protein to treat poisoning by radiation. Terapio is not involved with any application of the protein to treat cancer.

Papers presented at medical meetings normally are considered preliminary until published in a magazine.

More information

The U.S. National Cancer Institute has more about cancer of the pancreas.

SOURCES: Dr. Jay Brooks, Chairman of Hematology / Oncology, Ochsner, Baton Rouge, Louisiana; health system May 19, 2012, the press conference with medical oncologist Edward Kim, M.D., Ph.d., centro integral de cancer the University of Michigan, Ann Arbor, Michigan; Sanjay Awasthi, M.D., Professor, medical oncology and therapeutic research and diabetes, Endocrinology and metabolism, city of Hope Cancer Center, Duarte, California; Daniel D. Von Hoff, M.D., physician in Chief and distinguished Professor, Institute of Translational Genomics Research and Professor of medicine, Mayo Clinic, Rochester, Minn.

Copyright © 2010 HealthDay. All rights reserved.

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vitamin B6. B12 and folate, may decrease pancreatic cancer risk

Scientists exploring the notion that certain nutrients might protect against pancreas cancer observed that lean individuals who got most of these nutrients from food were protected against developing cancer. The study also suggests this protective effect does not hold true if the nutrients come from vitamin supplements.

As per a research findings reported in the June 1 issue of Cancer Research, a journal of the American Association for Cancer Research, researchers combined data from four large studies and observed that people who were at or below normal body weight decreased their risk for developing pancreas cancer if they took in high levels of vitamin B6, vitamin B12, and folate from food. The study determined that their risk was 81 percent, 73 percent, and 59 percent lower, vitamin B6, vitamin B12, and folate respectively, compared with participants who did not eat as much of these nutrients or who weighed more. As per the researchers, that was the only statistically significant finding from the study, which is the largest yet to look at these nutrients and pancreas cancer risk.

All we can say is that a person who has reason to be concerned about their risk of developing this cancer, which is relatively rare but quite deadly, should maintain a normal weight and eat their fruit and vegetables, said the studys lead investigator, Eva Schernhammer, M.D., Dr.P.H., an assistant professor of medicine at Harvard Medical School.

The scientists also say that they uncovered another interesting trend - that some people who received these nutrients from multivitamin pills had an increased risk of developing the disease. As per the researchers, individuals who said they used multivitamins, and whose blood showed traces of these nutrients, had a 139 percent increased relative risk of developing pancreas cancer.

This is a preliminary, but intriguing, finding because it suggests that something in the vitamins may fuel pancreas cancer growth, Dr. Schernhammer said.

This isnt the first study to suggest that folate, and vitamin B6 and B12 - so called one carbon nutrients - are protective against pancreas cancer if they come from food, but not if they come from multivitamins, Dr. Schernhammer said.

One large Finnish study found one carbon food nutrients were linked to a decreased risk of developing pancreas cancer, but that vitamin pills were not helpful. Two other large American studies also found the food nutrients to be protective, but that vitamin use was linked to a higher, yet non-significant risk of developing the cancer.

In this study, scientists combined four large prospective cohort studies, The Womens Health Initiative, and three from the Harvard School of Public Health: the Nurses Health Study, the Health Professionals Follow-up Study, and the Physicians Health Study. From this large database, they performed a prospective nested case-control study to examine plasma concentrations of the nutrients from participants who had donated blood and answered questionnaires about their food intake and vitamin use before any cancer developed. Their analysis included 208 pancreas cancer cases and 623 cancer-free control cases.

No one knows why vitamin pills may not help ward off cancer, or why, in this study, it might have a deleterious effect, Dr. Schernhammer said, but some research in animals suggests that if there is a dormant tumor, folate and other similar vitamins may stimulate growth. That might be particularly true if a person did not take in enough of these nutrients consistently through diet, and then suddenly started taking multivitamins in an effort to become healthy, she said.

People believe that dietary intake of these nutrients reflects a lifelong healthy eating habit, and in those cases, these nutrients may be protective, but they could have an opposite effect if they are used in a person with an occult cancer, Dr. Schernhammer said. It might all depend on whether a person is cancer-free at the time they start using these nutrients.

The same kind of association has been found with use of soy, which is an estrogen-rich food, she said. Women who have eaten soy all their lives, such as people in Asia, have a reduced risk of developing breast cancer, but some studies have observed that increased soy intake in women who have not eaten it before appears to be harmful.

The scientists say their study cannot definitively say that one carbon nutrients either pose a benefit or a hazard to most people, but they note that it is the best analysis that can be performed outside of a randomized clinical trial.

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Potential To Improve Human Cancer Studies Using Novel Pig Model

Main Category: Melanoma / Skin Cancer
Also Included In: Pancreatic Cancer;  Biology / Biochemistry
Article Date: 26 Jul 2012 - 1:00 PDT Current ratings for:
Potential To Improve Human Cancer Studies Using Novel Pig Model

A naturally occurring line of immunodeficient pigs can support the growth of human tumors injected under their skin, offering a promising new large animal model for studying human cancers and testing new drugs and treatment strategies. The ability of human melanoma cells and pancreatic carcinoma cells to grow in these pig models is described in an article in BioResearch Open Access, a new bimonthly peer-reviewed open access journal from Mary Ann Liebert, Inc.. The article is available free online at the BioResearch Open Access website.*

Mathew Basel and colleagues, Kansas State University (Manhattan, KS) and Iowa State University (Ames), highlight the advantages that pig disease models offer, as they are anatomically and physiologically more closely related to humans than traditional rodent animal models. As a result, findings from studies in large animal models such as pigs are more likely to translate into similar outcomes in humans. The authors present their findings in the article "Human Xenografts Are Not Rejected in a Naturally Occurring Immunodeficient Porcine Line: A Human Tumor Model in Pigs." **

"This novel animal model has the potential to become a highly useful model in cancer research studies, in addition to providing significant opportunities for drug discovery and other translational applications," says Editor-in-Chief Jane Taylor, PhD, MRC Centre for Regenerative Medicine, University of Edinburgh, Scotland.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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