Nieuws alvleesklierkanker


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Nieuwe ontdekking maakt weg vrij voor behandeling alvleesklierkanker

Volgens een studie in het ‘Journal of Cancer Research wordt alvleesklierkanker, de derde belangrijke oorzaak van kanker gerelateerde sterfgevallen, als tweede belangrijke geprojecteerd tegen het jaar 2030. De vijfjaarsoverleving is slechts 8 procent wat betekent dat het de enige grote kanker is met een overlevingskans van één enkel cijfer. Ondanks de stijgende sterftecijfers zijn er te weinig financiële middelen voor onderzoek en weinig door de ‘Food and Drug Administration’ goedgekeurde behandelingen om de ziekte te bestrijden.

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Kunstmatige alvleesklierbehandeling werkt goed in proefonderzoek

Onderzoekers melden een doorbraak in de ontwikkeling van een kunstmatige alvleesklier (pancreas) voor diabetes en andere aandoeningen, die tot stand is gekomen door het combineren van technologieën: de mechanische, kunstmatige alvleesklier, en een transplantatie van de insulineproducerende cellen (eilandjes van Langerhans).

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Chinees kruiden extract kan helpen bij het elimineren van alvleesklierkankercellen

Onderzoekers van de universiteit van Minnesota ontdekken de werkzaamheid van Lei Gong Teng bij het blokkeren van een eiwit dat alvleesklier kankercellen helpt te overleven. De diagnose alvleesklierkanker kan verwoestend zijn. Deels door de agressieve celdeling en tumorgroei, ontwikkelt alvleesklierkanker zich snel en heeft een lage overlevingskans van vijf jaar (minder dan 5 procent).

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Oud Chinees medicijn tegen pancreaskanker

De schors van de Amoer kurkboom (Phellodendron amurense) is al eeuwenlang gekend in de Chinese geneeskunde. Nu wordt het door de wetenschap ingezet in de strijd tegen alvleesklierkanker met het potentieel voor nog meer toepassingen. UT Health Science Center onderzoeker A. Pratap Kumar onderzocht het kurkeik extract voor de behandeling van prostaatkanker en ontdekte dat dodelijk pancreaskankers vergelijkbare ontwikkelingstrajecten hebben met prostaattumoren.

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Roken, zwaar drinken gekoppeld aan eerder begin van pancreas kanker

University of Michigan Health System studie maakt een stap de richting te leren wanneer kanker screening moet starten. Degenen die zwaar roken en drinken, zouden op een vroegere leeftijd pancreas kanker kunnen ontwikkelen dan degenen die dat niet doen, volgens een studie geleid door een universiteit van Michigan Health System gastro-enteroloog. In de studie, gepubliceerd in het Amerikaanse tijdschrift over gastro-enterologie, werden zware rokers met alvleesklierkanker gediagnosticeerd rond leeftijd 62 en zware drinkers op de leeftijd van 61-bijna een decennium eerder dan de gemiddelde leeftijd van 72. Roken is een sterke risicofactor bij alvleesklierkanker en bij alcohol is aangetoond dat er oxidatieve schade aan de alvleesklier veroorzaakt wordt, waarin het patroon voor de inflammatoire trajecten die tot kanker leiden gezet wordt. De bevindingen wijzen er alleen op dat deze gewoonten eerder kunnen leiden tot de ontwikkeling van pancreas kanker in het leven.

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Alvleesklierkanker gebruikt fructose, zoals in westers voedsel voorkomt om tot groei te komen

Alvleesklierkankers gebruiken fructosesiroop, zoals die in veel westers voedsel voorkomt, om een weg te effenen die er voor zorgt dat celdeling versneld, volgens een studie van UCLA's Jonsson Comprehensive Cancer Center. Alhoewel breed bekend is dat kanker glucose gebruikt, een simpele suiker, om de groei te bevorderen,is dit de eerste keer dat er een verband is aangetoond tussen kankergroei en fructose, volgens een onderzoek van Dr. Anthony Heaney, een professor in de medicijnen en neurochirurgie van
Jonsson Cancer Center. Tussen 1970 en 1990 is het gebruik van HFCS met meer dan 1000% toegenomen volgens een artikel in april 2004, uitgegeven door American Journal of Clinical Nutrition. Voedsel producenten gebruiken HFCS,een mengsel van fructose en glucose, omdat het goedkoop is, makkelijk te vervoeren en te bewaren. En door het hoge zoetgehalte, is het kostendrukkend voor bedrijven om kleine hoeveelheden HFCS te gebruiken ipv duurdere alternatieven.

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Pieter Tau


Gerichte immunotherapie toont belofte voor gemetastaseerde
borstkanker, pancreatische kanker

De eerste experimenten met behulp van gerichte monoklonale antilichamen in combinatie met bestaande therapieën tonen belofte bij de behandeling van pancreatische kanker en gemetastaseerde borstkanker. Dit blijkt uit een onderzoek dat zal worden gepresenteerd door onderzoekers van de Universiteit van het Pennsylvania Abramson Cancer Center op de 2010-bijeenkomst van de American Society of
Clinical Oncology.

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Eric van Staalduinen


Lage hoeveelheid Arsenicum schaadt de hoeveelheid glucose bevorderende afscheiding van insuline in Beta-cellen van de alvleesklier

Chronische blootstelling aan hoge niveaus van anorganisch arsenicum wordt gerelateerd aan een breed spectrum van menselijke kwalen, inclusief type 2 diabetes. Een zeer belangrijke stap in de pathogenese (de wijze van ontstaan en ontwikkeling van een ziekte) van type 2 diabetes is een stoornis van glucose-bevorderende insulineafscheiding (GSIS) van ?-cellen. De reactieve zuurstofsoorten (ROS) die uit het glucosemetabolisme worden afgeleid dienen als één van de metabolische signalen voor GSIS. "Kern factor-erythroid 2 (Nrf2)" is een centrale overzettingsfactor die de cellulaire aanpassingsreactie op oxydatieve spanning regelt. Fu et al. (p. 864) hebben de hypothese getest dat de activering van Nrf2 en inductie van anti-oxyderende enzymen in antwoord op arsenicumblootstelling het signaleren van ROS en zo GSIS in aangekweekte cellen belemmert. De auteurs concluderen dat de lage niveaus van arsenicum een cellulaire aanpassing / oxydatieve spanningsreactie veroorzaken, die anti-oxyderende niveaus verhoogt, en het signaleren van/door ROS betrokken bij GSIS verstoort, en ook de celfunctie.

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Dennis Morrien


Zonder drainage minder complicaties bij operatie van alvleesklierkanker

In Nederland en veel andere landen krijgen patiënten die geopereerd moeten worden vanwege alvleesklierkanker voorafgaand aan de operatie standaard galwegdrainage.

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Bij alvleesklierkanker direct opereren

Patiënten met alvleesklierkanker moeten direct worden geopereerd aan de tumor, zonder dat er eerst een galwegdrainage plaatsvindt.

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Video - Belly Fat Can cause Pancreatic Cancer


Why could ethyl pyruvate attenuate severe acute pancreatitis?

Excessive activation of inflammatory mediator cascade during SAP is a major cause of distant organ injury and the high mortality. Cytokines such as TNF- alpha and IL-1 beta are released early in the development of systemic inflammatory response. This leaves a narrow therapeutic window for administration of therapeutics and delayed delivery of that anti-inflammatory therapeutics is not effective after the inflammatory mediator cascade has developed. A research article to be published on July 28, 2008 in the World Journal of Gastroenterology addresses this question. The research team led by Prof. Wang from Centre of Pancreatic Surgery of Xiehe Hospital, Tongji Medical College, Huazhong University of Sciecne and Technology, demonstrated that the serum levels of HMGB1 began to rise significantly at 12 h, and maintained at high levels up to 48 h after induction of experimental SAP in rats. The delayed kinetics indicated that HMGB1 may provide a broader therapeutic window for treating this lethal systemic inflammatory disease. EP was proved could inhibit HMGB1 release from macrophages and prevent the accumulation of serum HMGB1 levels in mice with lethal sepsis through inhibiting NF- kappaB and p38 MAPK signaling. The research, performed by this team, investigated whether delayed EP therapy attenuates experimental SAP via reducing serum HMGB1 levels in rats or not.

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Zinc transporters regulate pancreatic cancer

Zinc, an important trace element for healthy growth and development, can be related to pancreatic cancer. Too much ZIP4, a molecule that enables the transport of zinc into cells, promotes the growth and spread of pancreatic tumors cells, said a group of researchers from Baylor College of Medicine in Houston, the University of Texas M.D. Anderson Cancer Center and the University of Florida in Gainesville, in a report which appears online today in the Proceedings of the National Academy of Sciences.

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Tiny samples could yield big predictive markers for pancreatic cancer

A handful of proteins, detected in incredibly tiny amounts, may one day help doctors distinguish between a harmless lesion in the pancreas and a potentially deadly one, say researchers at Fox Chase Cancer Center. The researchers believe that these protein biomarkers, if confirmed in subsequent studies, could represent reliable indicators of pancreatic cancer or precancerous pancreatic lesions, which would allow for earlier, perhaps more successful, treatment. Their findings appear in the March issue of the journal Pancreas, available online now. "New technologies have become very good at identifying pancreatic cysts when they appear, but we know very little about how to categorize these cysts," says the study's senior author Anthony Yeung, Ph.D., molecular biologist and member of Fox Chase's faculty. "We can detect, in as little as 40 microliters of cyst fluids a group of proteins that might collectively be used as indicators of a potentially cancerous cyst." The difficulty of detecting pancreatic cancer early is one of the reasons that the disease remains one of the deadliest forms of cancer. In some cases, pancreatic cancer develops within small pancreatic cysts that are originally benign, but become cancerous over time. As high-resolution imaging techniques, such as magnetic resonance imaging (MRI), are used more often in clinical medicine, doctors are finding many more small, fluid-filled cystic lesions of the pancreas. "Many of these cysts are completely benign and have little or no risk of becoming cancerous. However, a subset of pancreatic cysts carry a real risk of becoming malignant over time," says co-author Jeffrey Tokar, M.D., Fox Chase gastroenterologist. "Many patients with pancreatic cysts are referred to us for endoscopic needle aspiration of fluid within the cyst, which is then sent to the laboratory and a variety of tests are commonly performed. However, while these tests can be useful, it often remains impossible to tell a patient their absolute risk of progression to cancer."

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Two New Therapies Show Promise for Cancer Patients

Clinical trial data and cutting-edge testing give key insights in the fight against basal cell carcinoma and pancreatic cancer. San Diego and Phoenix—April 15, 2008—Clinical researchers at Scottsdale Healthcare and TGen today announced the results of two clinical trials that show promise for patients battling cancer. The Phase I clinical trial findings, presented at the this weeks Annual Meeting of the American Association for Cancer Research by Daniel Von Hoff, MD, FACG, focused on basal cell carcinoma (BCC) and pancreatic cancer. The Arizona trials were conducted at TGen's Clinical Research Service (TCRS) at Scottsdale Healthcare, a strategic alliance between TGen and Scottsdale Healthcare’s Clinical Research Institute. Basal Cell Carcinoma In the first trial, a novel molecule, GDC-0449, shrinks tumors in basal cell carcinoma (BCC) while having limited side effects, including a loss of sense of taste, and a small amount of hair loss and weight loss, suggesting a viable new treatment option. GDC-0449 works by blocking a pathway — a series of chemical reactions within a cell— known as Hedgehog, containing two genes (PTCH and SMO) that lead to a known tumor-promoting gene called GLI1. Alterations in any of these genes have been shown to lead to basal cell carcinoma and other diseases. GDC-0449 is a chemical synthetic designed to replicate the properties of cyclopamine, a chemical found in nature.

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Calorie restricted diet prevents pancreatic inflammation and cancer

Prevention of weight gain with a restricted calorie diet sharply reduced the development of pancreatic lesions that lead to cancer in pre-clinical research reported today by researchers from the University of Texas at Austin and the University of Texas M. D. Anderson Cancer Center at the American Association for Cancer Research annual meeting.

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Jefferson Scientists’ Discovery May Help Explain Smoking-Pancreatic Cancer Link

If lung cancer and heart disease aren’t bad enough, cigarette smokers are also at higher risk for developing, among other things, pancreatic cancer. Now, researchers at the Kimmel Cancer Center at Jefferson in Philadelphia have preliminary evidence indicating one possible reason why. Data being presented April 13, 2008 during the Annual Meeting of the American Association for Cancer Research shows that they have found that nicotine in cigarettes increases the production of a protein that is known to promote cancer cell survival, invasion and spread.

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Therapies delivered by "trojan" peptides and through the use of nanotechnology may enhance the effectiveness of cancer treatment

Christina Kousparou, Ph.D., Head of Research at Trojantec Ltd, reported that using the Antennapedia protein as a "trojan horse" to pierce the outer layer of a cancer cell and deliver p21, a known tumor suppressor protein, successfully reduced malignant tumors in mice. Intravenous treatment with p21 by this method brought the cancer cell growth and death cycle to a halt and slowed tumor growth. Mice given this protein also lived longer than a control group of animals. Researchers had speculated that p21 would increase sensitivity to chemotherapy. The combination of p21 with chemotherapy resulted in total tumor eradication in 40% of animals and a reduction in tumor burden in 100% of animals.

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New studies on the Mediterranean diet confirm its effectiveness for chronic disease prevention

Scientists of the Instituto de Nutrición y Tecnología de los Alimentos (Institute of Nutrition and Food Technology) of the University of Granada (UGR, Spain) have been doing research into the positive effects of Mediterranean diet's ingredients on health. Among these works, there is a new research line about pancreatic cancer cells. Emilio Martínez de Victoria Muñoz, director of the Institute, points out that in the study 'Influence of the ingredients of the Mediterranean diet on a cell line on pancreatic cancer cells' (UGR-Junta de Andalucía) they have manipulated the composition of the cell membrane providing olive oil, fish oil or an antioxidant typical of olive oil, analysing how such cells defend themselves from the aggressions which cause pancreatic alterations".The objective is to expose olive oil compounds (such as oleic acid) and fruit and vegetable antioxidants to "membranes of a pancreatic cancer cell line in such a way that they become more or less resistant to harmful stimulus which cause diseases such as cancer or pancreatitis".This way, the research work intends to correlate the composition of cell membranes with more or less resistance to suffering from different types of disease. The conclusions suggest that feeding and changes in membrane composition affect cell function and can therefore influence the prevention of certain diseases.

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Naturally-occurring apple compounds reduce risk of pancreatic cancer

Eating flavonol-rich foods like apples may help reduce the risk of pancreatic cancer, especially in smokers.

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Mesothelin engineered on virus-like particles provides treatment clues for pancreatic cancer

New understanding of a protein that spurs the growth of pancreatic cancer could lead to a new vaccine against the deadly disease, said researchers at Baylor College of Medicine in Houston in a report appearing in the current edition of the journal Molecular Cancer Therapeutics.

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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 pancreatic cancer. European investigators led by Prof. Matthias Löhr from the Karolinska Institute evaluated 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, compared 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. Löhr 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.”

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Study Finds Even Stronger Relationship Between High Body Mass Index, Pancreatic Cancer

In reviewing the weight history of pancreatic cancer patients across their life spans, researchers at The University of Texas M. D. Anderson Cancer Center have determined that a high body mass index in early adulthood may play a significant role in an individual developing the disease at an earlier age. The study, published in the June 24 issue of the Journal of the American Medical Association, also found that patients who are obese the year before diagnosis have a poorer outcome than those who are not. While excess weight is a known risk factor associated with pancreatic cancer, before now, few studies have looked at patients' body mass index (BMI) throughout their lifetime rather than simply at adulthood and/or year of disease diagnosis. "This is the first study to explore at which ages excess body weight predisposes an individual to pancreatic cancer," said Donghui Li, Ph.D., professor in M. D. Anderson's Department of Gastrointestinal Medical Oncology and the study's corresponding author. "With our epidemiological research, we aimed to demonstrate the relationship between BMI and risk of pancreatic cancer across a patient's life span and determine if there was a time period that specifically predisposes an individual to the disease, as well as the link between BMI and cancer occurrence and overall survival of the disease."

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Studies Spot Numerous Undiscovered Gene Alterations In Pancreatic and Brain Cancers

HHMI investigators have detected a multitude of broken, missing, and overactive genes in pancreatic and brain tumors, in the most detailed genetic survey yet of any human tumor. Some of these genetic changes were previously unknown and could provide new leads for improved diagnosis and therapy for these devastating cancers.

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Jefferson scientists find protein may be key in developing deadly form of pancreatic cancer

A tumor-blocking protein previously implicated in prostate and breast cancer development may also be behind the most aggressive type of pancreatic cancer. Researchers have discovered that the protein pp32 -- which normally applies the brakes on a cancer-causing gene -- is missing in an aggressive form of pancreatic cancer. Though the work is preliminary, the scientists say, the absent protein could eventually become a marker for the disease and a potential drug target.

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Taking the fight against cancer to heart

Hormones produced by the heart eliminated human pancreatic cancer in more than three-quarters of the mice treated with the hormones and eliminated human breast cancer in two-thirds of the mice. The treatment has not yet been tried in humans, but clinical trials are in the planning stages. The research will be presented at a symposium April 9 at the Experimental Biology 2008 conference in San Diego.

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New Options When An Old Enemy Returns

Pancreatic cancer is one of the most challenging malignancies to treat, and recurrence is common, even after initial treatment with surgery and radiation. When the cancer does return, treatment options are often limited to chemotherapy, but researchers at Georgetown University Hospital’s Lombardi Comprehensive Cancer Center are utilizing the precision allowed by CyberKnife® to see if radiosurgery is a viable treatment option in select patients. “When treating recurrent pancreatic tumors, there are a number of factors to evaluate before we can consider radiosurgery as an additional treatment option,” explains Christopher Lominska, M.D., lead author of the study and a resident in radiation medicine at Lombardi. “First, treatment must be safe, which is demonstrated in this study. We also designed a treatment that can be delivered in a short period of time -- a critically important quality-of-life factor in this patient population.”

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New technique invented to reveal pancreatic stem cells

Just like those absconders chased by police all over the world, everybody can tell about their good deeds but none really knows how to recognize them. Yet, as of today, thanks to a study just published in the Proceedings of the National Accademy of Sciences (PNAS) and authored by Nobel Laureate for Medicine in 2007 Mario Capecchi and by the researcher from the Catholic University of Rome Eugenio Sangiorgi, we now know how to reveal the stem cells camouflaged in the pancreas.A stem cell is a cell capable of generating all the other cells constituting the same tissue (sometimes also called "adult stem cell"). "Reading the newspapers sometimes one would doubt it – says Sangiorgi – but we don't know many things about stem cells. It might look odd, but for instance we don't have a method to distinguish a priori between a stem cell and any other cell in the same tissue. We can only infer that a cell really is a stem cell by observing its behaviour". In other words, when a researcher encounters a tissue, it's not immediately possible to identify with certainty and thus isolate a stem cell. In some case, like in the meadows, we now know where they are located and how to single them out – and hence we have been capable of successful life saving transplants for many years. But in the case of the pancreas, as in that of many other tissues, until some years ago we doubted that these special cells were even present there. "Together with Professor Capecchi, we had already designed in the past a novel way to mark the stem cells in a tissue: a sort of little flag, capable of helping us to effectively label the cells we were looking for", explains Sangiorgi. In order to achieve this, Capecchi and Sangiorgi used a molecular switch, that is a piece of DNA, which activates itself once the mouse under scrutiny takes a special drug. When the switch is "on", a special fluorescent protein is produced (and, as a matter of fact, the study about this type of proteins won the Nobel Prize in Chemistry last October). The luminous cells are indeed the long-sought stem cells. "In order to understand that these are really stem cells, we need only to wait", comments Sangiorgi. "A normal cell is sooner or later destined to die. A stem cell, instead, retains its capacity to renew itself and replicate. Thus, if we can still observe, many months later, that a cell is still alive, that means it is indeed a stem cell – or a cell derived directly from the division of a stem cell". In the newly published article, Sangiorgi and Capecchi have shown with their technique that a particular subset of the pancreatic cells, the so-called acinar cells, are indeed stem cells. The truly interesting aspect of their results is that these cells also produce important digestive enzymes.

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M. D. Anderson Study Finds Even Stronger Relationship Between High Body Mass Index, Pancreatic Cancer

In reviewing the weight history of pancreatic cancer patients across their life spans, researchers at The University of Texas M. D. Anderson Cancer Center have determined that a high body mass index in early adulthood may play a significant role in an individual developing the disease at an earlier age. The study, published in the June 24 issue of the Journal of the American Medical Association, also found that patients who are obese the year before diagnosis have a poorer outcome than those who are not. While excess weight is a known risk factor associated with pancreatic cancer, before now, few studies have looked at patients' body mass index (BMI) throughout their lifetime rather than simply at adulthood and/or year of disease diagnosis. "This is the first study to explore at which ages excess body weight predisposes an individual to pancreatic cancer," said Donghui Li, Ph.D., professor in M. D. Anderson's Department of Gastrointestinal Medical Oncology and the study's corresponding author. "With our epidemiological research, we aimed to demonstrate the relationship between BMI and risk of pancreatic cancer across a patient's life span and determine if there was a time period that specifically predisposes an individual to the disease, as well as the link between BMI and cancer occurrence and overall survival of the disease." Pancreatic cancer is the fourth leading cause of cancer death in men and women in this country. It is a highly lethal disease - according to the American Cancer Society, more than 42,470 persons will be diagnosed and 35,240 will likely die from the disease in 2009. The median survival for patients with the disease is less than 10 months and the five-year survival rate is less than five percent. Obesity and smoking are the major modifiable risk factors associated with the disease; it's estimated that 25 percent of the pancreatic cancer cases are associated with the former and 27 percent with the latter, said Li. While the number of adults smoking is on the decline, the number of adults dangerously overweight is on the rise. In the U.S., obesity in adults has increased by 60 percent in the last 20 years, and is considered an epidemic by the Centers for Disease Control. "With our study, we hoped to better understand the cause-and-effect relationship between this modifiable risk factor that contributes to the development of pancreatic cancer, in hopes that high-risk individuals can be identified and preventive measures discovered for this lethal disease," said Li.

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How does ellagic acid exert anti-cancer effect on pancreatic cancer cells?

A research group from the University of California Los Angeles investigated the anti-cancer properties of ellagic acid. They found that ellagic acid has strong pro-apoptotic and anti-proliferative effects on pancreatic cancer cells.

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Jefferson Scientists Deliver Toxic Genes to Effectively Kill Pancreatic Cancer Cells

A research team, led by investigators at the Department of Surgery at Jefferson Medical College of Thomas Jefferson University and the Kimmel Cancer Center at Jefferson, has achieved a substantial “kill” of pancreatic cancer cells by using nanoparticles to successfully deliver a deadly diphtheria toxin gene. The findings – set to be published in the October issue of Cancer Biology & Therapy – reflect the first time this unique strategy has been tested in pancreatic cancer cells, and the success seen offers promise for future pre-clinical animal studies, and possibly, a new clinical approach. The researchers found that delivery of a diphtheria toxin gene inhibited a basic function of pancreatic tumor cells by over 95 percent, resulting in significant cell death of pancreatic cancer cells six days after a single treatment. They also demonstrated that the treatment targets only pancreatic cancer cells and leaves normal cells alone, thus providing a potential ‘therapeutic window.’ Further, they are targeting a molecule that is found in over three-quarters of pancreatic cancer patients. “For the pancreatic cancer world, this is very exciting,” says the study’s lead author, molecular biologist Jonathan Brody, Ph.D., assistant professor, Department of Surgery at Jefferson Medical College of Thomas Jefferson University, who works closely with the Samuel D. Gross Professor and Surgeon, Charles J. Yeo, M.D. “There are no effective targeted treatments for pancreatic cancer, aside from surgery for which only a minority of patients qualify. We are in great need of translating the plethora of molecular information we know about this disease to novel therapeutic ideas.

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Study could help target new pancreatitis treatments

Pancreatitis is often a fatal condition, in which the pancreas digests itself and surrounding tissue. Scientists have previously found that alcohol can trigger the condition by combining with fatty acids in the pancreas, which leads to an excessive release of stored calcium ions. Once calcium ions enter cell fluid in the pancreas it activates digestive enzymes and damages the cells. The team, in collaboration with the RIKEN Brain Science Institute in Japan, have now identified channels within special stores that allow calcium to enter the fluid inside pancreatic cells. They have also found that toxic calcium release can be significantly reduced if the gene responsible for the production of these channels is ‘deleted’ (or knocked-out). Professor Ole Petersen, from the University’s School of Biomedical Sciences, explains: “The pancreas releases enzymes into the gut, where they become activated and digest our food. When these digestive enzymes are activated inside the cells, however, they start to digest the pancreas itself, causing serious damage and often death. Alcohol is widely recognised as one of the triggers for this process, but the reasons behind it have been unclear.

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Mayo Clinic finds new pathology tests double sensitivity to detect bile duct and pancreatic cancers

Pancreatic cancer and bile duct cancer are difficult to diagnose and often fatal because they are discovered in the advanced stages of the disease. Researchers have developed new tests that double the ability to detect bile duct and pancreatic cancers, according to a Mayo Clinic study published in the June issue of Gastroenterology. Pancreatobiliary tumors such as bile duct cancer (cholangiocarcinoma) and pancreatic cancer often present as strictures, or a narrowing of the duct that can either be caused by benign inflammation or cancer. Physicians insert an endoscope down the throat and into the bile duct and pancreas region to examine possible tumors; however, the narrowness of the bile duct makes it difficult to distinguish benign and malignant strictures. In this study, 498 patients with pancreatobiliary duct narrowing underwent an endoscopic procedure, and cell brushings were taken. Brushings were then analyzed by routine cytology, digital image analysis and fluorescence in situ hybridization (FISH) to determine the various tests' effectiveness and sensitivity in detecting and diagnosing cancer. While traditional cytology analysis relies on identifying abnormally shaped cells, the FISH test detects malignant cells using colored probes visible with a fluorescence microscope. Since cancer cells have an abnormal amount of DNA, by FISH these cells show extra copies of the probes compared to normal cells. The Mayo research team found that the combination of cytology and FISH raised the detection rate of bile duct and pancreatic cancer from 20 percent to 43 percent. "Bile duct and pancreatic cancers are very difficult to diagnose," says Lewis Roberts, M.B.Ch.B., Ph.D., Mayo Clinic gastroenterologist and the study's senior author.

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Study finds association between hepatitis B and pancreatic cancer

A new study has shown that evidence of past hepatitis B infection was twice as common in people with pancreatic cancer than in healthy controls. This study is the first to report an association between past exposure to the hepatitis B virus and pancreatic cancer, but researchers cautioned that more studies are necessary to evaluate the nature of the link. "While our findings indicate that past exposure to hepatitis B is associated with the development of pancreatic cancer, more research is needed to determine whether this relationship is one of cause and effect," said lead author Manal M. Hassan, MD, PhD, assistant professor at The University of Texas M. D. Anderson Cancer Center. "If these findings can be confirmed by other studies, hepatitis B could be another risk factor for pancreatic cancer that is readily modifiable with treatment, and even preventable with a vaccine." In this study, Dr. Hassan and her colleagues compared evidence of hepatitis B and C infection (as determined by blood tests assessing antibodies to these viruses) between 476 patients with pancreatic cancer and 879 matched healthy individuals. Evidence of past exposure to hepatitis B was found in 7.6 percent of patients with pancreatic cancer versus 3.2 percent of controls. The association between hepatitis B exposure and pancreatic cancer remained statistically significant even after controlling for other risk factors, such as smoking. People with both diabetes (an established risk factor for pancreatic cancer) and hepatitis B exposure had a 7-fold increase in pancreatic cancer risk, compared to controls. No association was observed between hepatitis C exposure and pancreatic cancer. The authors noted that past studies have reported the presence of hepatitis B antigens in pancreatic fluids; others have identified impaired pancreatic function in people with chronic hepatitis B infection. These findings suggest that the hepatitis B virus may cause inflammation or DNA damage in the pancreas, which could increase cancer risk. The researchers also indicated that there may be an increased risk of liver failure after chemotherapy treatment among patients with pancreatic cancer who have a history of hepatitis B infection. Dr. Hassan noted that if their findings are confirmed, oncologists may want to consider checking the hepatitis B status of their patients with pancreatic cancer before beginning chemotherapy.

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Pancreatic cancer linked to herbicides

A new study links two weed killers with pancreatic cancer in pesticide applicators and their spouses. The authors--most of whom work for the National Cancer Institute--note that they are the first to link this particular malignancy with the farm chemicals, pendimethalin and EPTC.

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Mayo Clinic Researchers Formulate Treatment Combination Lethal To Pancreatic Cancer Cells

A combination of two targeted therapies packs a powerful punch to kill pancreatic cancer cells in the laboratory, Mayo Clinic cancer researchers report. With further testing of these drugs that are from classes of pharmaceuticals already used in patients, the Mayo research may lead to new treatment opportunities for patients with pancreatic cancer, which is extremely difficult to treat.

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An herbal extract inhibits the development of pancreatic cancer

An herb recently found to kill pancreatic cancer cells also appears to inhibit development of pancreatic cancer as a result of its anti-inflammatory properties, according to researchers from the Kimmel Cancer Center at Jefferson. The data were presented at the AACR 100th Annual Meeting 2009 in Denver. (Abstract 494) Thymoquinone, the major constituent of the oil extract from a Middle Eastern herbal seed called Nigella sativa, exhibited anti-inflammatory properties that reduced the release of inflammatory mediators in pancreatic cancer cells, according to Hwyda Arafat, M.D., Ph.D., associate professor of Surgery at the Jefferson Medical College of Thomas Jefferson University and a member of the Jefferson Pancreatic, Biliary & Related Cancers Center. Nigella sativa seeds and oil are used in traditional medicine by many Middle Eastern and Asian countries. It helps treat a broad array of diseases, including some immune and inflammatory disorders, Dr. Arafat said. Previous studies have also shown it to have anti-cancer effects on prostate and colon cancers. Based upon their previously published findings that thymoquinone inhibits histone deacetylases (HDACs), Dr. Arafat and her colleagues compared the anti-inflammatory properties of thymoquinone and trichostatin A, an HDAC inhibitor that has previously shown to ameliorate inflammation-associated cancers. The researchers used pancreatic ductal adenocarcinoma (PDA) cells, some of which were pretreated with the cytokine TNF-alpha to induce inflammation. Thymoquinone almost completely abolished the expression of several inflammatory cytokines, including TNF-alpha, interleukin-1beta, interleukin-8, Cox-2 and MCP-1, an effect that was more superior to the effect of trichostatin A. The herb also inhibited the activation and synthesis of NF-kappaB, a transcription factor that has been implicated in inflammation-associated cancer. Activation of NF-kappaB has been observed in pancreatic cancer and may be a factor in pancreatic cancer's resistance to chemotherapeutic agents. When animal models of pancreatic cancer were treated with thymoquinone, 67 percent of the tumors were significantly shrunken, and the levels of proinflammatory cytokines in the tumors were significantly reduced.

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Stanford study prevents pancreatic tumor growth in mice by inhibiting key protein

Researchers at Stanford University School of Medicine have identified a protein critical for the growth of pancreatic cancer. Blocking the expression of the protein slowed or prevented tumor growth in mice and made cultured cancer cells vulnerable to the conditions of low oxygen that occur in solid tumors. "This research clearly shows that inhibiting the protein inhibits the tumor's ability to grow," said cancer biologist Amato Giaccia, PhD. "Ultimately, we'd like to be able to specifically knock out the expression of this protein in pancreatic tumors in humans." Pancreatic cancer is a highly aggressive and deadly disease that accounts for more than 30,000 deaths in the United States annually, and current therapies are largely ineffective. "Right now, we have very little to offer these patients," said Giaccia. He is the Jack, Lulu and Sam Willson Professor and professor of radiation oncology and the senior author of the research, which will be published Feb. 1 in the journal Cancer Research. Giaccia is also a member of the Stanford Cancer Center. The researchers studied a protein called connective tissue growth factor, or CTGF. Also known as CCN2, the protein is involved in the abnormal growth of connective tissue in response to injury or disease. It was also thought to be involved in pancreatic tumor progression, although the exact role it played was unknown. Giaccia and his collaborators found that human pancreatic cancer cells expressing high levels of CCN2 grew robustly when injected under the skin of mice. In fact, in the developing tumor these cells soon out-competed others that expressed lower levels of the protein. Conversely, pancreatic cancer cells in which CCN2 expression was suppressed were either less likely or unable to form tumors when injected into mice.The researchers observed similar effects when the cancer cells were injected directly into the animals' pancreases. Cancer cells expressing high levels of CCN2 formed tumors that grew more rapidly and metastasized more aggressively than did those expressing lower levels, and the mice died sooner than others injected with cancer cells expressing less CCN2.

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Eating burned meat increases risk of pancreatic cancer

People who regularly eat very well-done red meat that is burned or charred may increase their risk of pancreatic cancer by almost 60 percent, according to a study by a University of Minnesota cancer researcher. “We found that those who preferred very well-done steak were almost 60 percent more likely to get pancreatic cancer as those who ate steak less well-done or did not eat steak,” Anderson said. “Furthermore, when we looked at amount of consumption with doneness preferences, we found that those with the highest intake of very well-done meat had a 70 percent higher risk for pancreatic cancer over those with lowest consumption.”

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Popular diabetes treatment could trigger pancreatitis, pancreatic cancer

A drug widely used to treat Type 2 diabetes may have unintended effects on the pancreas that could lead to a form of low-grade pancreatitis in some patients and a greater risk of pancreatic cancer in long-term users, UCLA researchers have found. In a study published in the online edition of the journal Diabetes, researchers from the Larry L. Hillblom Islet Research Center at UCLA found that sitagliptin, sold in pill form as Januvia, caused abnormalities in the pancreas that are recognized as risk factors for pancreatitis and, with time, pancreatic cancer in humans. Januvia is marketed by Merck & Co. Inc. Sitagliptin is a member of a new class of drugs that enhance the actions of the gut hormone known as glucagon-like peptide 1 (GLP-1), which has been shown to be effective in lowering blood sugar in people with Type 2 diabetes. The study is available at http://diabetes.diabetesjournals.org/cgi/content/abstract/db09-0058v1. "Type 2 diabetes is a lifelong disease — people often take the same drugs for many years, so any adverse effect that could over time increase the risk for pancreatic cancer would be a concern," said Dr. Peter Butler, director of the Hillblom Center and the study's lead investigator. "A concern here is that the unwanted effects of this drug on the pancreas would likely not be detected in humans unless the pancreas was removed and examined." An observed connection between Byetta, a drug used to treat Type 2 diabetes that is related to Januvia in its intended actions, and pancreatitis has already been reported, prompting a Food and Drug Administration warning. Amylin Corp., which markets Byetta, has suggested that since there is no known mechanism linking the cases of pancreatitis with Byetta, the association might be chance. The UCLA study suggests that there may indeed be a link between drugs that enhance the actions of GLP-1 and pancreatitis — by increasing the rate of formation of cells that line the pancreatic ducts.

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Optical techniques show continued promise in detecting pancreatic cancer

Optical technology developed by a Northwestern University professor of biomedical engineering has been shown to be effective in detecting the presence of pancreatic cancer through analysis of neighboring tissue in the duodenum, according to clinical trial results published in the journal Disease Markers. The promising new technology -- which researchers hope could help raise the extremely low survival rate of pancreatic cancer patients by aiding early detection -- uses novel light-scattering techniques to analyze extremely subtle changes in the cells of the duodenum, part of the small intestine neighboring the pancreas. The cells are obtained through a minimally invasive endoscopy. The study shows that cells that appear normal using traditional microscopy techniques do show signs of abnormality when examined using the Northwestern technique, which provides cell analysis on the much smaller nanoscale. The technology was developed by Vadim Backman, professor of biomedical engineering at the McCormick School of Engineering and Applied Science at Northwestern, and Vladimir Turzhitsky, a graduate student in Backman's lab. Clinical trials have been conducted in collaboration with Hemant Roy, M.D., director of gastroenterology research at NorthShore University HealthSystem, and Randall Brand, M.D., a gastroenterologist at the University of Pittsburgh Medical Center. In the study of 203 patients, the technique accurately discriminated with 95 percent sensitivity between healthy patients and those with differing stages of the disease. (Only 5 percent of patients were found to have been diagnosed with false negatives after testing.) The specificity of the testing group was 71 percent. These results confirm those of an earlier study of 51 patients published in August 2007 in the journal Clinical Cancer Research.The larger number of patients in the more recent study allowed researchers to calculate the "area under the receiver operator characteristic" (AUROC), which is an analysis of the accuracy of the test in distinguishing healthy samples from diseased samples. While the sensitivity and specificity of tests may vary based on the threshold set by researchers for diagnosis, the AUROC measures the overall efficacy of the diagnostic technique. The analysis showed an 85 percent AUROC for the Northwestern method. (Clinically sound tests typically have an AUROC greater than 70 percent.)The study in Disease Markers also reports promising results in detecting mucinous cyst lesions, which are a precursor to cancer. If confirmed in further clinical trials, this approach may lead to a method for early diagnosis.

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UC Davis researchers discover Achilles' heel in pancreatic cancer

UC Davis Cancer Center researchers have discovered a metabolic deficiency in pancreatic cancer cells that can be used to slow the progress of the deadliest of all cancers. Published in the October issue of the International Journal of Cancer, study results indicate that pancreatic cancer cells cannot produce the amino acid arginine, which plays an essential role in cell division, immune function and hormone regulation. By depleting arginine levels in cell cultures and animal models, the team was able to significantly reduce pancreatic cancer-cell proliferation. "There have been few significant advances in 15 years of testing available chemotherapy to treat pancreatic cancer," said Richard Bold, chief of surgical oncology at UC Davis and senior author of the study. "The lack of progress is particularly frustrating because most patients are diagnosed after the disease has spread to other organs, eliminating surgery as an option. We have to turn back to basic science to come up with new treatments." Bold explained that average survival time for those diagnosed with pancreatic cancer is just four-and-a-half months, although chemotherapy can extend that prognosis up to six months.

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The effective chemoradiotherapy method for pancreatic cancer

In the present study, the retrospective analysis of chemoradiotherapy for locally advanced pancreatic cancer was performed, utilizing gemcitabine as a radiation sensitizer administered twice weekly at a dose of 40 mg/m2. The median survival was 15.0 months and the overall 1-year survival rate was 60%, while the median progression- free survival was 8 months. Patients developing liver metastases had worse prognosis. We might need another strategy for the chemoradiotherapy for those patients.

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Shining light on pancreatic cancer

Using novel light-scattering techniques, researchers have found the first evidence that early stage pancreatic cancer causes subtle changes in part of the small intestine. The easily monitored marker may ultimately allow early detection for a disease notorious for having few obvious symptoms, the primary reason pancreatic cancer killed more than 33,000 Americans last year.

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Low levels of key protein may indicate pancreatic cancer risk

A protein that dwindles in response to obesity and a sedentary lifestyle may one day help doctors predict which people are at increased risk for pancreatic cancer, new research by Dana-Farber Cancer Institute and collaborating scientists indicates.

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Obesity and lack of exercise could enhance the risk of pancreatic cancer

Obesity and aversion to exercise have become hallmarks of modern society -- and a new study suggests that a blood protein linked to these lifestyle factors may be an indicator for an increased risk of developing pancreatic cancer. Researchers from the Dana Farber Cancer Institute report their findings in the Aug. 15 issue of Cancer Research, a journal of the American Association for Cancer Research.

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Birth records hold pancreatic cancer clue

Pregnancies in Jerusalem in the 1960s and 1970s may hold vital clues about how pancreatic cancer and diabetes are linked. According to research published in the online open access journal BMC Medicine, women with a history of gestational diabetes had a higher risk of developing pancreatic cancer later in life.

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Abnormal DNA repair genes may predict pancreatic cancer risk

Abnormalities in genes that repair mistakes in DNA replication may help identify people who are at high risk of developing pancreatic 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 lead 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 pancreatic cancer risk. In a case-control study of 734 patients with pancreatic 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 researchers looked for direct effects of the gene variants (also called single nucleotide polymorphisms) on pancreatic 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.

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Pancreatic cancer - What you need to know

Other adjustable risk factors for pancreatic cancer include diet high in red meat, obesity, diabetes mellitus, chronic pancreatitis, helicobacter pylori infection, occupational exposure to certain pesticide, dyes and some other chemicals.

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Berries and Onions Slash Pancreatic Cancer Risk By Up To 59 Percent

A high intake of the flavonols found in certain fruits and vegetables can decrease the risk of developing pancreatic cancer a quarter in non-smokers, and more than twice that in smokers.

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VCU Massey Cancer researchers find gene therapy that kills pancreatic cancer cells

Researchers at the Virginia Commonwealth University Massey Cancer Center and the VCU Institute of Molecular Medicine have published findings that implicate a new chemoprevention gene therapy for preventing and treating pancreatic cancer, one of the most lethal and treatment-resistant forms of cancer.

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IDO2 an active enzyme to target in pancreatic cancer

An enzyme that is overexpressed in pancreatic cancer cells may hold the key to successfully treating the disease with targeted immunotherapy, researchers from Thomas Jefferson University reported at the 2008 Annual Meeting of the Southern Surgical Association. Previous data show that a protein, indoleamine 2,3-dioxygenase (IDO), is overexpressed in pancreatic ductal adenocarcinomas, according to Jonathan R. Brody, Ph.D., an assistant professor in the Department of Surgery at Jefferson Medical College of Thomas Jefferson University in Philadelphia, and co-director of the Jefferson Center for Pancreas, Biliary and Related Cancers. The center is led by Charles J. Yeo, M.D., Samuel D. Gross Professor and chair of the Department of Surgery, who was also involved with the study.According to Dr. Brody, IDO is an enzyme that represses the immune system, thus protecting the cancer cells and helping them evade immune detection. The Jefferson researchers and their collaborators from the Lankenau Institute for Medical Research (LIMR) in Wynnewood, Pa., previously reported that the IDO inhibitor D-1-methyl-tryptophan (1-MT), preferentially targets a related protein, IDO2.

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Jefferson scientists find protein helps pancreatic cancer cells evade immune system and spread

A protein that helps prevent a woman's body from rejecting a fetus may also play an important role in enabling pancreatic cancer cells to evade detection by the immune system, allowing them to spread in the body. Researchers found that the metastatic pancreatic cancer cells in the lymph nodes produce enough of the protein, IDO, to wall-off the immune system's T-cells and recruit cells that suppress the immune response to the tumor.

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