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From Medicineworld.org: Pancreatic Cancer News Blog

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March 15, 2011, 10:22 PM CT

Malaria drug for pancreatic cancer?

Malaria drug for pancreatic cancer?

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

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

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

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

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January 21, 2011, 8:32 PM CT

Genetic code for form of pancreatic cancer

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

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

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

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

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June 24, 2010, 10:54 PM CT

Treatment of pancreatic adenocarcinoma

Treatment of pancreatic adenocarcinoma
Pancreatic ductal adenocarcinoma (PDAC) is a highly cancerous digestive tumor with a very poor prognosis. Hypoxia-inducible transcription factor-1α (HIF-1α) is involved in cancerous progression in a number of solid tumors, including PDAC, upregulation of HIF-1α accelerates PDAC progression, but the exact regulatory mechanisms of HIF-1αin PDAC has not been unequivocally addressed. Recently, an increasing number of studies reported that toll-like receptors (TLRs) were upregulated in epithelial malignancies and involved in tumor progression, but whether TLRs, such as TLR4, is expressed on PDAC cells remains unknown. In immune-related cells, TLR signal pathway may induce expression of HIF-1α, but it is also still unclear whether there exists some association between TLR4 and HIF-1α in tumor microenviroment, such as PDAC.

A research article to be published on June 21, 2010 in the World Journal of Gastroenterology addresses this question. The research team led by He-Shui Wu, MD, from Department of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, used real time polymerase chain reaction and immunohistochemistry, to detect TLR4, NF-κB p65 and HIF-1α expression in 65 cases of PDAC tissues and 38 cases of corresponding adjacent tissues.........

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June 4, 2010, 6:30 AM CT

Is that cyst Pancreatic Cancer?

Is that cyst Pancreatic Cancer?
Working with scientists from the University of Michigan and Indiana University, Van Andel Research Institute (VARI) researchers have developed a method that could be used to predict whether pancreatic cysts are non-malignant or are precursors to invasive cancer.

More pancreatic cysts are being detected due to the widespread use of high resolution abdominal imaging. These advances in early detection, when coupled with the new findings, could result in fewer deaths from pancreas cancer, which struck more than 42,000 Americans in 2009 and killed more than 35,000, as per the National Cancer Institute.

"Because of the difficulty in detecting pancreas cancer in its early stages, most cancers are advanced at the time of diagnosis and recur after removal of the tumor," said VARI Senior Scientific Investigator Brian Haab, Ph.D., first author of a study reported in the recent issue of Annals of Surgery. "The best hope for a long-term cure appears to be the detection and removal of these pre-malignant cysts".

"Dr. Haab and colleagues have sought to address a very challenging clinical management problem regarding cystic lesions of the pancreas," said Peter J. Allen, MD, FACS, a doctor and researcher specializing in pancreatic, liver, and stomach cancer at Memorial Sloan-Kettering Cancer Center. "As the use of cross-sectional imaging increases, clinicians are seeing increased numbers of patients with these lesions and it will become imperative to sort out non-malignant from pre-cancerous." .........

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March 24, 2010, 12:10 AM CT

Chemotherapy plus synthetic compound for pancreatic cancers

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".........

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February 8, 2010, 7:37 AM CT

Soft drink consumption and pancreatic cancer

Soft drink consumption and  pancreatic cancer
Consuming two or more soft drinks per week increased the risk of developing pancreatic cancer by nearly twofold compared to individuals who did not consume soft drinks, according to a report in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.

Although relatively rare, pancreatic cancer remains one of the most deadly, and only 5 percent of people who are diagnosed are alive five years later.

Mark Pereira, Ph.D., senior author on the study and associate professor in the School of Public Health at the University of Minnesota, said people who consume soft drinks on a regular basis, defined as primarily carbonated sugar-sweetened beverages, tend to have a poor behavioral profile overall.

However, the effect of these drinks on pancreatic cancer may be unique.

"The high levels of sugar in soft drinks may be increasing the level of insulin in the body, which we think contributes to pancreatic cancer cell growth," said Pereira.

For the current study, Pereira and colleagues followed 60,524 men and women in the Singapore Chinese Health Study for 14 years. During that time, there were 140 pancreatic cancer cases. Those who consumed two or more soft drinks per week (averaging five per week) had an 87 percent increased risk compared with individuals who did not.........

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January 29, 2010, 8:10 AM CT

How pancreatic cancer able to defeat drugs

How pancreatic cancer able to defeat drugs
Scientists at the Moores Cancer Center at the University of California, San Diego, have found one reason that pancreas cancer tumors are so difficult to treat with drugs. They have shown how a molecular switch steps up pancreas cancer cell survival as well as resistance to a standard chemotherapy drug, and have identified alternate routes cancer cells take to avoid the effects of the treatment.

The findings, by a group led by Andrew M. Lowy, MD, professor of surgery and chief of surgical oncology at the UCSD School of Medicine and the Moores UCSD Cancer Center, are reported online and will appear February 1 in the journal Cancer Research The study provides new insights into pancreas cancer development and new potential drug targets and therapy strategies against the disease.

"To understand how to treat pancreas cancer tumors, we need to better understand their circuitry and behavior," Lowy said.

Pancreas cancer is a especially deadly cancer, fast-moving and difficult to detect early. It's estimated that more than 35,000 people died from pancreas cancer last year in the United States.

RON is a signaling protein known as a tyrosine kinase, essentially a switch that turns on various activities in cells. Prior work in Lowy's lab showed that RON is overexpressed in a majority of premalignant and pancreas cancer cells, and could also help cells resist dying. The scientists wanted to find out what role, if any, RON played in pancreas cancer development and progression.........

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November 2, 2009, 8:52 AM CT

Hepatitis B does not increase pancreatic cancer risk

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".........

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September 24, 2009, 6:57 AM CT

Progress in Pancreatic cancer treatment

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

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

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

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

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August 2, 2009, 11:01 PM CT

metformin reduces risk of pancreatic cancer

metformin reduces risk of pancreatic cancer
Taking the most commonly-prescribed anti-diabetic drug, metformin, reduces an individual's risk of developing pancreas cancer by 62 percent, as per research from The University of Texas M. D. Anderson Cancer Center, reported in the Aug. 1 issue of Gastroenterology

"This is the first epidemiological study of metformin in the cancer population, and it offers an exciting direction for future chemoprevention research for a disease greatly in need of both therapy and prevention strategies," said Donghui Li, Ph.D., professor in M. D. Anderson's Department of Gastrointestinal Medical Oncology.

An oral medication, metformin is the most usually prescribed drug for type 2 diabetes. As per Li, more than 35 million prescriptions for the drug are filled annually, and it's most often given to type 2 diabetic patients who are obese and/or have insulin resistance.

"Metformin works by increasing the cellular sensitivity to insulin and decreasing its level circulating in diabetics. Insulin also seems to have a growth-promoting effect in cancer," said Li, the study's senior author. "Metformin activates the AMP kinase, which is a cellular engery sensor. Recent publications have described that AMP kinase also plays an important role in the development of cancer by controlling cell division and growth."........

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July 27, 2009, 11:04 PM CT

Smoking increases risk of metastatic pancreatic cancer

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.........

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April 20, 2009, 5:08 AM CT

Herbal extra to against pancreatic cancer

Herbal extra to against pancreatic cancer
An herb recently found to kill pancreas cancer cells also appears to inhibit development of pancreas cancer as a result of its anti-inflammatory properties, as per scientists 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 pancreas cancer cells, as per 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 a number of Middle Eastern and Asian countries. It helps treat a broad array of diseases, including some immune and inflammatory disorders, Dr. Arafat said. Prior 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.........

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April 6, 2009, 9:25 PM CT

Finding pancreatic cancer early

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

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

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

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

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February 25, 2009, 4:55 AM CT

Determining Risk for Pancreatic Cancer

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

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

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

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

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

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

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January 15, 2009, 7:15 PM CT

Genes and pancreatic cancer

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.........

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January 14, 2009, 6:31 AM CT

New gene to predict outcome in pancreatic cancer

New gene to predict outcome in pancreatic cancer
Variations in mismatch repair genes can help predict therapy response and prognosis in patients with pancreas cancer, as per research from The University of Texas M. D. Anderson Cancer Center presented today in advance of the American Society of Clinical Oncology (ASCO) Gastrointestinal Cancers Symposium.

In the study, single nucleotide polymorphisms (SNPs) in genes involved in DNA mismatch repair were linked to response to gemcitabine (Gemzar)-based preoperative chemoradiation, tumor resectability (the likelihood of removing the entire tumor), and overall survival.

"Gemcitabine is a major chemotherapeutic agent used to treat pancreas cancer, but we don't understand why some patients respond and most patients do not," said Donghui Li, Ph.D., the study's main author and professor in M. D. Anderson's Department of Gastrointestinal Medical Oncology. "There has been no biomarker for pancreas cancer used in the clinic to predict response. Our research interest has been to determine whether genetic variation in DNA repair can be a predictor of therapy response or a prognosis factor for patient survival".

DNA repair is a complicated process, Li noted, with various mechanisms responsible for identifying and correcting different types of DNA damage. Mismatch repair genes correct mistakes in DNA replication or trigger cell death (apoptosis) if repair is not possible. Ensuring cell death is critical to preventing the runaway cell division that occurs in cancerous tumors.........

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January 14, 2009, 6:29 AM CT

Hepatitis C May Increase Pancreatic Cancer Risk

Hepatitis C May Increase Pancreatic Cancer Risk
A newly released study shows that infection with hepatitis C virus (HCV) increases a person's risk for a highly fatal cancer of the biliary tree, the bile carrying pathway between the liver and pancreas. This finding is in the recent issue of Hepatology, a journal published by John Wiley & Sons on behalf of the American Association for the Study of Liver Diseases (AASLD). The article is also available online at Wiley Interscience (www.interscience.wiley.com).

More than 4 million Americans are infected with HCV, which causes chronic hepatitis, cirrhosis and liver cancer. However, the associations between the virus and other potentially-related cancers are less clear.

To better understand the associations between HCV and these cancers, scientists led by Hashem El-Serag of Baylor College of Medicine, conducted a retrospective cohort study of more than 718,000 U.S. veterans who were treated at Veterans Affairs medical facilities between October 1, 1988 and September 30, 2004. Among them, 146,394 were infected with HCV and 572,293 were not. Uninfected subjects were matched to infected ones by sex, age and type and date of visit.

The scientists followed the subjects for an average of 2.3 years to determine the incidence these cancers. They observed that "risk for biliary tree cancer in the HCV-infected cohort, eventhough low (4 per 100,000 person-years), was more than double that in the HCV-uninfected cohort".........

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November 25, 2008, 9:41 PM CT

Radiation Before Surgery Improves Pancreatic Cancer Outcomes

Radiation Before Surgery Improves Pancreatic Cancer Outcomes
Pancreas cancer is one of the deadliest and most difficult to treat cancers. Now, in a major step forward, scientists at NewYork-Presbyterian Hospital/Weill Cornell Medical Center have shown that administering radiation treatment previous to surgery nearly doubles survival in pancreas cancer patients with operable tumors.

"Patients who received pre-surgical (neoadjuvant) radiation had almost double the overall survival compared with similar patients who didn't undergo radiation, and survived significantly longer than patients who received radiation after the tumor was removed," says the study's senior author, Dr. David Sherr, assistant professor of clinical radiation oncology at Weill Cornell Medical College, and a radiation oncologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.

The findings appear in the Nov. 15 issue of the International Journal of Radiation Oncology, Biology and Physics.

Pancreas cancer remains the fifth deadliest malignancy in the United States, killing more than 32,000 Americans each year. It is typically not detected until it is already at an advanced stage when cure is rarely possible. In fact, the five-year survival rate for pancreas cancer has been stalled at just 5 percent for the past 25 years.

Because pancreatic tumors have often spread or have directly invaded critical structures by the time they are detected, just 15 to 20 percent of patients are deemed suitable candidates for surgical removal (resection) of the tumor. And while post-operative radiotherapy has long been used to sterilize residual cancer cells that may not have been removed by surgery, the notion of using radiation before resection has been a controversial one.........

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October 29, 2008, 8:52 PM CT

New pancreas tumor registry

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.........

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September 29, 2008, 10:19 PM CT

Hepatitis B exposure and pancreatic cancer

Hepatitis B exposure and pancreatic cancer
Manal Hassan, M.D., Ph.D.

Credit: M. D. Anderson Cancer Center

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.

"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.........

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September 25, 2008, 11:01 PM CT

Prevention and treatment of pancreatic cancer

Prevention and treatment of pancreatic cancer
A number of gastrointestinal tumors, including pancreas cancer, have been shown to overexpress the EGFR. The overexpression of EGFR correlates with rapidly progressive disease and poor prognosis. Targeting EGFR pathway as a potential therapeutic strategy for pancreas cancer has been developed. Erlotinib is a small molecule tyrosine kinase inhibitor that efficiently blocks EGFR. Preliminary results of phase III trial in pancreas cancer revealed an improvement in survival with the addition of erlotinib. Treatment with anti-EGFR agents is used as a potential therapeutic strategy for pancreas cancer, but the mechanisms are still not precisely understood.

This article was published on September 21, 2008 in the World Journal of Gastroenterology The research team from Department of Gastroenterology, Affiliated First People's Hospital, Shanghai Jiao Tong University, China studied the effects of erlotinib on six different pancreas cancer cell lines. How erlotinib exhibits its antineoplastic activity in vivo needs to be further elucidated.

In this study authors revealed the efficacy of erlotinib, as a single agent, on pancreas cancer cells growth in vitro, and in vivo study using a nude mice xenograft model and the mechanisms involved were also explored. Erlotinib repressed BxPC-3 cell growth in a dose-dependent manner, triggered G1 arrest and induced cell apoptosis,and suppressed capillary formation of endothelium in vitro. In vivo, erlotinib treated mice demonstrated a reduced tumor volume and weight as compared with control. The relationship between EGFR and angiogenesis has also been investigated using tube formation assay in vitro and immunohistochemical analysis of tumor-associated blood vessels in vivo. These findings provide evidence for the inhibitive activity of erlotinib in pancreas cancer cells. Inhibition of EGFR may be a promising adjuvant in chemotherapeutic strategy in the therapy of the dismal disease. The results also demonstrate that EGFR signaling pathway is an important target in pancreas cancer.........

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Did you know?
A gene therapy that prevents tumour cells from growing in mice could one day offer hope to sufferers of hard-to-treat pancreas cancer, new research suggests.Pancreas cancer is the fifth-leading cause of cancer deaths in the West and is virtually untreatable - only 3% of patients are alive five years after diagnosis. Most die within six months of diagnosis, since symptoms do not commonly appear until the cancer is very advanced.

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