Metastasis of pancreatic cancer in action

PHILADELPHIA - Ben Stanger, MD, PhD, assistant professor of Medicine in the Division of Gastroenterology at the Perelman School of Medicine, University of Pennsylvania, and Andrew Rhim, MD, a Gastroenterology Fellow in the Stanger lab, discovered that pancreatic cancer cells in an animal model begin to spread before clinically obvious tumor tissue is detected. What's more, they showed that inflammation enhances cancer progression in part by facilitating a cellular transformation that leads to entry of cancer cells into the circulation. They report their findings this week in Cell.

Metastasis has been difficult to study because it involves a series of unpredictable events. To capture these events, the team developed a sensitive method to tag and track pancreatic epithelial cells in a mouse model of pancreatic cancer. Tagged cells invaded and entered the bloodstream unexpectedly early, before overt malignancy could be detected by rigorous analysis of tissue slides.
Pancreatic cancer is among the most lethal of cancers, with no real treatments, and at the time of diagnosis up to three-quarters of patients have metastatic disease, says Stanger. Little is known about how pancreatic cancer cells spread, "What leads to this are rare events that are hard to catch in tissues. Small numbers of cells break off tumors and move, but how can we find them?"
These wandering cells are associated with a phenomenon called the epithelial-to-mesenchymal transition (EMT). This change in cell motility is an important process during the development of embryos. But when the transition is aberrantly reactivated in adults it can have dire physiological consequences, leading to cancer metastasis as well as other disease processes. Epithelial cells form a covering or lining of a body surface and are the type of cell from which most solid tumors arise. However, when a molecular switch is turned off or absent, epithelial cells acquire characteristics of another cell type, called mesenchymal cells, and gain the ability to migrate and move away from the primary tumor site.
Using a mouse model of pancreatic cancer developed at Penn in 2005, the team delivered mutations in an oncogene and a tumor suppressor protein, K-ras and p53 respectively, in the pancreas. A green marker was also induced in the embryos' still-forming pancreas. At about one to two months, the juvenile mice developed pre-malignant lesions, and at about four to five months full blown pancreatic cancer.
During this time, the mouse pancreatic epithelial cells lost their epithelial characteristics and became more like mesenchymal cells, blending in and making their way to the bloodstream. True epithelial cells are sticky, keeping linings tightly connected, but these imposter epithelial cells changed identity, becoming less sticky.
With the green stain, the researchers were able to detect the transition from epithelial cell to mesenchymal cell in a tissue slide, showing many green cells that had undergone EMT. "We are now able to see what was before before unseeable – the pancreas cells that have taken on a disguise," says Stanger.
What spurs the EMT in first place? The team surmised that it was inflammation, so they blocked inflammation with an immunosuppressant, and at about eight to ten weeks, the green cells undergoing EMT disappeared. Conversely, when they induced pancreatitis- associated inflammation, the EMT green cells increased.
In trying to relate these findings to metastasis, they looked for green EMT cells outside of the pancreas and found them in the blood and distinct tissues such as the liver at eight to ten weeks of age, long before a pathologist would recognize it as cancer.
"These results provide new insight into the earliest events of cellular invasion and suggest that inflammation enhances cancer progression by giving cells increased access to the bloodstream," says Stanger.
The team plans to use the methodology used in this study to enhance the detection of spreading cells in human patients at an early timepoint, when therapy could have a greater impact.
Both the development of the pancreatic cancer mouse model and Dr. Stanger's current work were partially funded by research grants from the Pancreatic Cancer Action Network. "We are highly encouraged by Dr. Stanger's recent results," said Lynn Matrisian, PhD, vice president of Scientific and Medical Affairs at the Pancreatic Cancer Action Network. "A deeper understanding of the disease biology, and in particular metastasis, will move us closer to our goal of doubling the survival rate of pancreatic cancer by the year 2020."

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This work was also supported by the National Institutes of Health (NIDDK088945; NIDDK007066; NCI134292; NCI138907; NCI117969; NIDDK083355; NIDDK083111), the National Pancreas Foundation, the American Association for Cancer Research, the Pennsylvania Department of Health, and the Pew Charitable Trust.
Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4 billion enterprise.
Penn's Perelman School of Medicine is currently ranked #2 in U.S. News & World Report's survey of research-oriented medical schools and among the top 10 schools for primary care. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $507.6 million awarded in the 2010 fiscal year.
The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top 10 hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital – the nation's first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.
Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2010, Penn Medicine provided $788 million to benefit our community.

Protein complex plays role in suppressing pancreatic tumors, study shows

BY KRISTA CONGER

Steve Fisch

Jonathan Pollack and Hunter Shain (left) led a team that discovered a protein complex suppressed the growth of pancreatic tumors.

A well-known protein complex responsible for controlling how DNA is expressed plays a previously unsuspected role in preventing pancreatic cancer, according to researchers at the Stanford University School of Medicine.

Technological advances in the way researchers can compare normal and tumor DNA showed that the gene for at least one subunit of the multi-subunit SWI/SNF protein complex was either deleted, mutated or rearranged in about a third of the 70 human pancreatic cancers that the Stanford team examined. Additionally, the researchers found that restoring the expression of one of the missing genes slowed the growth of pancreatic cancer cells in the laboratory and caused them to enter an arresting state called senescence.

“This is really strong genetic evidence that this complex plays a role in pancreatic cancer,” said associate professor of pathology Jonathan Pollack, MD, PhD, “and it suggests the influence of the SWI/SNF complex is on par with that of other well-known tumor suppressors, such as p53.”

Pollack is the senior author of the research, published online Jan. 9 in the Proceedings of the National Academy of Sciences. Graduate student Hunter Shain is the first author.

The tumor-suppressing role of the SWI/SNF complex had not been previously discovered because the disabling changes were spread among five of the complex’s protein subunits. In other words, one person’s pancreatic cancer might have a mutation or deletion in one protein subunit, while another’s could have a change in a different subunit. Considered individually, each variation occurs relatively infrequently.

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Shain and Pollack used a technique called array comparative genomic hybridization, or CGH, to pinpoint places in the genome that differed among normal and cancerous pancreatic epithelial cells. The procedure relies on the ability of single-stranded DNA to seek out and bind to its mirror image. By comparing the relative amounts of tumor and normal DNA that bind to a panel of reference sequences, the researchers can tell whether the cancer cell contains amplifications or deletions of genetic material in specific regions throughout the genome. These copy-number variations often occur in genes or regions important in regulating uncontrolled cell growth.

The researchers examined about 70 different pancreatic cancers, including specimens provided by their co-authors at the Sol Goldman Pancreatic Cancer Research Center at the Johns Hopkins University School of Medicine. Forty-eight of the cancers were primary samples from human patients that had been coaxed to grow in immune-deficient mice; 22 had been maintained as laboratory-grown cancer cell lines. Shain used high-density arrays of reference DNA sequences for the CGH, which allowed him to identify amplified or deleted regions at a much higher resolution than previously possible — narrowing the areas of interest to just a few thousand nucleotides rather than larger stretches of DNA.

When the researchers looked at the results of the array CGH analysis, they found many genes known to be involved in pancreatic cancer, and also some new candidates. In particular, they noticed that the genes for individual subunits of the SWI/SNF complex were altered in about 5 to 10 percent of the cancer samples — an interesting finding, but not prevalent enough to spark further immediate investigation under normal circumstances. However, when considered together, Shain and Pollack realized that more than a third of the cancer samples contained a deletion, mutation or rearrangement in the gene for at least one of the five subunits.

“Our intention was to identify new genes involved in pancreatic cancer,” said Pollack. “The discovery that SWI/SNF plays a role was exciting because we never would have found it any other way. It really validates the use of genome-wide analysis.”

The researchers then experimented with artificially increasing the expression of the gene for one of the subunits in cancer cells in which it was deleted. They found that, in the laboratory, these pancreatic cancer cells engineered to re-express the missing protein slowed their growth and even began to senesce, or enter a permanently arrested state, rather than dividing uncontrollably.

The involvement of SWI/SNF in pancreatic cancer is both exciting and challenging because of its global effect on gene expression. DNA is normally packaged tightly around bundles of protein called histones, and the combination of DNA and proteins is called chromatin. SWI/SNF works by repositioning histones on DNA to make it available for transcription factors that govern DNA’s use as a template for the synthesis of RNA, which goes on to serve as a template for the proteins to do the work of the cell.

“We’re becoming more and more aware that chromatin modification and remodeling play an important role in cancer,” said Pollack, pointing out that several other recent studies have also zeroed in on proteins controlling the architecture of the genome. “What we’d like to learn now is specifically how altering this particular complex affects cancer progression. The major effect is likely to be through changes in the expression of genes.”

The researchers are now working to pinpoint exactly which genes are important to drive the growth of human pancreatic cells by artificially overexpressing or blocking the expression of genes coding for various SWI/SNF subunits.

In addition to Shain and Pollack, other Stanford researchers involved in the study include graduate student Craig Giacomini and former pathology resident Karen Matsukuma, MD, PhD.

The research was supported by the National Cancer Institute and the Lustgarten Foundation.
Information about Stanford’s Department of Pathology, which also supported the work, is available at http://pathology.stanford.edu/.

Reduce the risk of pancreatic cancer

Results of a new study suggest that eating more fiber may reduce the risk of pancreatic cancer by as much as 60%. Not all types of fiber were found to provide the same protective effects, however.

Not all fiber protects against cancer

Pancreatic cancer is one of the most lethal forms of cancer and one for which there is scant information about the effects of diet. This new study, which reportedly is the first to explore the impact of different types of fiber on the risk of pancreatic cancer, was conducted by a research team in Italy.

The study involved 326 patients with pancreatic cancer and 652 cancer free individuals. All the participants had completed questionnaires about their dietary intake.
The investigative team observed the following:

• The greatest intakes of soluble fiber were associated with a 60% reduced risk of pancreatic cancer. Soluble fiber is the type that absorbs water and slows down the digestive process. Food sources include apples, beans, citrus fruit, barley, and oats.
• Intake of insoluble fiber was linked to a 50% reduced risk. Insoluble fiber increases stool bulk and helps prevent constipation. Food sources include vegetables, nuts, and whole grains. It’s helpful to note that fruits, vegetables, grains, and legumes (beans) typically contain both soluble and insoluble fiber, although individual foods frequently favor one or the other type.
• Intake of lignin and cellulose may reduce risk of pancreatic cancer by 50 to 60%. Lignin is a component of fiber and is insoluble in water. Food sources include wheat and root vegetables. Cellulose also is a component of fiber and is the main factor in the cell walls of plants. Legumes, apple skin, nuts, and cabbage contain large amounts of cellulose.
• Fruit fiber reduced the risk of pancreatic cancer by 50%, but grain fiber had no protective effect

Other studies have examined the role of diet in pancreatic cancer. A new study published in Public Health Nutrition, for example, noted that protection against the risk of pancreatic cancer “has been associated with the regular consumption of wholegrain cereals and derived products.”

Another study, published in the Journal of the National Cancer Institute, reported on the possible role of folate in pancreatic cancer. The investigators followed 81,922 men and women and their dietary habits and reported that “Our results suggest that increased intake of folate from food sources, but not from supplements, may be associated with a reduced risk of pancreatic cancer.”

The National Cancer Institute estimates that nearly 44,000 people will be diagnosed with pancreatic cancer in 2012, and that more than 37,000 people will die of the disease. Researchers continue to look for ways to prevent and treat this deadly disease, and eating more fiber may be one such way to reduce the risk of pancreatic cancer.

SOURCES:
Bidoli E, Pelucchi C, Zucchetto A et al. Fiber intake and pancreatic cancer risk: a case-control study. Annals Oncology 2012; 23(1): 264-68
Gil A, Ortega RM, Maldonado J. Wholegrain cereals and bread: a duet of the Mediterranean diet for the prevention of chronic diseases. Public Health Nutr 2011 Dec; 14(12): 2316-22
Larsson SC, Hakansson N, Giovannucci E. Wolk A. Folate intake and pancreatic cancer incidence: a prospective study of Swedish women and men. J Natl Cancer Inst 2006 Mar 15; 98(6): 407-13
National Cancer Institute

Saying Goodbye to a Friend in Denver.

Denver's Lustgarten Foundation Research Walk Committee extends our deepest sympathies to the Sandoval Family on their recent loss.

To quote Ken Salazar ... "We have lost a friend, leader and visionary today."

Secretary Ken Salazar and Paul Sandoval crossing the finish line last fall at
Denver's 2011 Lustgarten Pancreatic Cancer Research Walk. 

Team Sandoval at the 2011 Denver's Lustgarten Pancreatic Cancer Research Walk. 

Longtime Denver political activist Paul Sandoval passes away from pancreatic cancer

Denver Post - by Lynn Bartels

Paul Sandoval, a wheeler-and-dealer who mapped out the careers of numerous politicians in an office at his tamale shop, has lost the biggest campaign of his life.

Known as the godfather of Colorado politics, the former Democratic state senator advised everyone from governors to U.S. senators on issues big and small, from bilingual education to pollster strategy.

Last year in February doctors diagnosed Sandoval with pancreatic cancer, and told him he likely had six months left to live.

His wife, Paula, said he died about about 2:30 this afternoon. He was 67.

"He died very peacefully," she said.

In recent weeks, he had been on a portable hospital bed in his living room. Among the visitors he received

PHOTOS: PAUL SANDOVAL

• Slideshow: More images from Paul Sandoval's life and times.

on Friday was Ken Salazar, U.S. Secretary of the Interior. Paula Sandoval said her husband understood Salazar but was unable to speak much with him because he was so weak.

"We have lost a friend, leader and visionary today," Salazar said in a statement.

"In his life, Paul Sandoval gave voice to fellow citizens who wanted better schools, safer communities and a chance to pursue the American dream. I will never forget his passion for public service, his heart, and the love he showed for his friends, neighbors and family. He is a role model and a hero."

It was at Sandoval's tamale shop, La Casita, in 1997 that the pair drew Salazar's future on a restaurant napkin: Salazar would run for state attorney general in 1998. He held that post until being elected U.S. senator in 2004.

Gov. John Hickenlooper said Sandoval was "beloved by many Coloradans."

"Many a great conversation took place and many tamales eaten in the backroom of Paul's restaurant," he said in a statement.

"While his family and friends were his passion, he loved a good political fight. He was a man with a deep reservoir of humility and compassion and an amazing sense of humor.

"Our hearts go out to his wife, Paula, and his entire family. Helen and I will miss him beyond measure."

Paul John Sandoval was born June 29, 1944, in Denver on a stretch of Mariposa Street that would become Interstate 25. He was the ninth of Jerry and Camilla Sandoval's 11 children. Two siblings died in childhood.

Before he could speak much English, Sandoval could say "Denver Post — 5 cents" and he hustled alongside his brothers to sell newspapers. His brother, Joe, a former educator with Denver Public Schools, recalled last year that they once had to track down a delinquent customer at a bar.

"Paul said, 'What about my interest?' The guy said, 'Here's your quarter interest.' I had never even heard that term 'interest' before," Joe said. "Paul's been a wheeler and dealer all his life."

The boys grew up surrounded by politics. Their dad and uncle founded the meatpackers union, and Sandoval learned at an early age it was about the person, not the party.

"Paul and my dad used to stay up all hours of the night waiting for election results," Joe said. "I couldn't handle it; I had to go to bed. But Paul became a political junkie."

By eighth grade, Sandoval was delivering groceries for the Gem Market in northeast Denver. A few blocks away, a tall kid named Wellington Webb had the same job at Goodrich Grocery.

In the 1970s they served together in the legislature and and in 1991 Sandoval helped Webb become Denver's first back mayor.

In addition to his wife Paula, a former state senator and Denver City Council member, Sandoval is survived by four daughters from his previous marriage: Kendra, Cris, Andrea, and Amanda; and a son, Brett Sterkel, from an earlier relationship.

Read more:Paul Sandoval, longtime Colorado Democratic activist, dead at age of 67 - The Denver Posthttp://www.denverpost.com/breakingnews/ci_20470407/paul-sandoval-longtime-colorado-democratic-activist-dead-67#ixzz1t0jwgsxI

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Pancreatic cancer vaccine underway

UK Scientists are testing a new vaccine for treating pancreatic cancer in more than 1000 patients suffering from advanced forms of the disease.

TeloVac, which is now being tested in 53 UK hospitals, would not protect individuals against infectious diseases or cancer but would help the immune system to recognize and kill malignant cells in patients with pancreas tumor.

Researchers at TeloVac trial, who are using the new vaccine in combination with chemotherapy, hope the shot would boost the effects of the treatment by stimulating the immune system to fight the disease.

The vaccine, also named GV1001, contains small sections of telomerase -- a protein that is over-produced by cancer cells. The injection of the vaccine, therefore, presents the immune system with telomerase, helping T-cells to recognize and target the cancer cells more effectively.

Previous smaller studies have shown that patients who received the vaccine in addition to chemotherapy lived in average three months longer than those who had only undergone chemotherapy.

“"The problem is tumors are clever and are able to turn the immune cells into traitors which help to guard the tumor,” said Professor John Neoptolemos from Royal Liverpool University Hospital, who is helping to co-ordinate the trial. “The vaccine takes away the masking effect of the tumor.”

If TeloVac passes the current trial successfully, it would be available for treating advanced forms of pancreatic cancer by the end of 2013. However, more studies would be underway to assess its effectiveness in preventing pancreatic cancer and treating patients suffering from earlier stages of the disease.

Scientists hope the method could work on other types of cancers as well and therefore have planned a trial on patients with lung tumor for later this year.

“We strongly believe this has the potential to overcome the limits of other current cancer vaccines and become part of the standard of care not only for pancreatic cancer but for various other types of cancers,” said Jay Sangjae Kim, the founder of GemVax, the Korean company developing the TeloVac vaccine.

“In other words, a truly 'universal' vaccine will be available in the near future,” he added.

Researchers ID promising pancreatic cancer screening marker

Proteins found in blood serum distinguish cancer from non-cancerous conditions, U-M study shows

ANN ARBOR, Mich. — Researchers at the University of Michigan Comprehensive Cancer Center have identified a protein that shows distinct changes in structure between pancreatic cancer, non-cancerous diseases and normal blood serum. The protein also changes from early stage pancreatic cancer to advanced disease.

The finding suggests a blood test could serve as a potential screening tool to detect pancreatic cancer – which has the worst prognosis of any cancer type – at an earlier, more treatable stage.

"One of the difficulties in screening for pancreatic cancer is distinguishing it from other conditions, such as diabetes or pancreatitis. There is not a good marker currently that can do that. Ultimately, we need to detect earlier stages of pancreatic cancer that can be operated on and treated. Once the cancer reaches advanced stages, it becomes difficult to treat," said senior study author David M. Lubman, Ph.D., Maude T. Lane Professor of Surgical Immunology at the U-M Medical School, and a U-M professor of surgery, pathology and chemistry.

In this study, published online in the Journal of Proteome Research, Lubman and colleagues looked at proteins in the blood, and identified one, haptoglobin, that is in fairly high abundance. Haptoglobin is a type of glycoprotein, a category of proteins that has complex chains of sugar groups attached to it. These sugar groups are highly regulated in normal cells but develop a different structure in cancer cells.

The study looked at a total of 31 blood serum samples. The samples were from disease-free controls, patients with chronic pancreatitis, patients with diabetes and patients with varying stages of pancreatic cancer.
Because haptoglobin appears in abundance in serum, it is easy to pull out and isolate from the blood serum with an antibody. The researchers could then look at the structure of the sugar groups from the haptoglobin in the serum using a mass spectrometer, which is a device that separates and identifies molecules based on their molecular weight. They found it was easy to see the changes in the structure of the sugar groups from serum samples of pancreatic cancer versus non-cancerous disease, with distinct changes in structure or the amount of each structure present for each stage of pancreatic cancer versus pancreatitis, diabetes or normal samples.
Researchers are continuing to refine the assay, and are looking to develop a method that would allow them to evaluate hundreds of samples at once. Eventually, they hope this would lead to a test in which patients submit blood samples through their local doctors' offices, which are then sent to centralized laboratories for processing.
"Screening for pancreatic cancer would not be done through the general population because it's a fairly rare cancer. Rather, a test like this could potentially be used to screen people who are in high risk groups – those with a family history of pancreatic cancer, people who are obese or smoke, and people who have long-term diabetes or pancreatitis," Lubman says.
Researchers believe that a similar test could be used for colon and liver cancer, although more work is needed to identify the best markers in those diseases.
The researchers will continue to refine the markers to allow them to better and more reliably distinguish early stage pancreatic cancer. They will also begin testing this approach in larger samples. This test is not available to patients at this time.
Pancreatic cancer statistics: 43,140 Americans will be diagnosed with pancreatic cancer this year and 36,800 will die from the disease, according to the American Cancer Society

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Additional authors: Zhenxin Lin, Diane M. Simeone, Michelle A. Anderson, Xiaolei Xie, Kerby A. Shedden and Mack T. Ruffin, all from U-M; and Randall E. Brand from University of Pittsburgh
Funding: National Cancer Institute, National Institutes of Health, U-M Gastrointestinal Specialized Program of Research Excellence (SPORE) grant
Disclosure: None
Reference: Journal of Proteome Research, doi: 10.1021/pr200102h
Resources:
U-M Cancer AnswerLine, 800-865-1125
U-M Comprehensive Cancer Center, www.mcancer.org
Clinical trials at U-M, www.UMClinicalStudies.org

Pancreatic Cancer Survival Improves By Over 60% With Combination Of Four Drugs

Patients with pancreatic cancer who take a combination of four chemotherapy medications were found to have 60% better average survival, French scientists reported in NEJM (New England Journal of Medicine). Despite having to endure several side effects, the scientists informed that the quality of life of the survivors was not badly affected.

Pancreatic cancer has an extremely high death rate. For this reason, patients are more likely to willingly endure chemotherapy side effects in order to live a few months longer.

Of the approximately 43,000 people who are diagnosed with pancreatic cancer in the USA annually, 36,800 of them die from it. Pancreatic cancer represents only 2.5% of all cancer cases in America, but is the fourth leading cause of cancer death in the country. Fewer than 6% of patients survive for longer than five years after diagnosis.

Dr. Thierry Conroy of Nancy University and Centre Alexis Vautrin, Nancy, France, performed a Phase III trial - known as PRODIGE 4/ACCORD 11 - on 342 patients with pancreatic cancer. Half of them were randomly selected to receive FOLFIRINOX (made up of four drugs: oxaliplatin, irinotecan, leucovorin and fluorouracil), while the other half received Gemzar (gemcitabine), the first line drug used for pancreatic cancer therapy. They were all under seventy-six years of age and received their medications for six months.

The median survival time was:

• 6.8 months in the gemcitabine group. After six months 66% reported a significant decline in their quality of life.
• 11.1 months in the FOLFIRINOX group. After six months 31% reported a considerable decline in their quality of life.

Those in the FOLFIRINOX group experienced significantly more side effects, including diarrhea, weight loss, numbness in hands and feet, and pain. However, the patients felt the side effects were worth it and did not severely undermine their quality of life.

The researchers said that FOLFIRINOX therapy should only be used for patients aged less than 75 years, due to its high toxicity.

They wrote:

(FOLFIRINOX is now a first line option for metastatic pancreatic patients) who are younger than 76 years, and who have a good performance status ([Eastern Cooperative Oncology Group score (ECOG)] 0 or 1), no cardiac ischemia and normal or nearly normal bilirubin levels."

This study was financed by pharmaceutical company Amgen, the French government, and the French National League Against Cancer.

"FOLFIRINOX versus Gemcitabine for Metastatic Pancreatic Cancer"
Thierry Conroy, M.D., Françoise Desseigne, M.D., Marc Ychou, M.D., Ph.D., Olivier Bouché, M.D., Ph.D., Rosine Guimbaud, M.D., Ph.D., Yves Bécouarn, M.D., Antoine Adenis, M.D., Ph.D., Jean-Luc Raoul, M.D., Ph.D., Sophie Gourgou-Bourgade, M.Sc., Christelle de la Fouchardière, M.D., Jaafar Bennouna, M.D., Ph.D., Jean-Baptiste Bachet, M.D., Faiza Khemissa-Akouz, M.D., Denis Péré-Vergé, M.D., Catherine Delbaldo, M.D., Eric Assenat, M.D., Ph.D., Bruno Chauffert, M.D., Ph.D., Pierre Michel, M.D., Ph.D., Christine Montoto-Grillot, M.Chem., and Michel Ducreux, M.D., Ph.D.
N Engl J Med 2011; 364:1817-1825May 12, 2011

Written by Christian Nordqvist

View drug information on Gemzar.

Copyright: Medical News Today
http://www.medicalnewstoday.com/articles/225130.php

"Beating the Odds" Night Out

When:  Friday, April 27, 2012 | 7 -11 pm
Where:  Knights of Columbus
17 Willow St.,Westborough, MA


Tickets: $50 per person | Includes: $30,000 of "funny money" chips, 1 raffle ticket, buffet style hors d'oeuvres.  Purchase Tickets Now.

Join us for a fun filled evening of: Vegas Games - Roulette, Black Jack, Craps, Poker, LCR
3 Hole Putting Green
Music, Dancing, Hors D'oeuvres
Bidding on Silent Auction, Prizes
Cash Bar

There will be a wall of Honor to recognize loved ones affected by pancreatic cancer. 

Please note: Tickets are only available online for purchase. Tickets will NOT be sold at the door.

Pancreatic cancer vaccine in N.J. clinical trial renews hope for patients

  Friday, 06 April 2012 18:00

BY BOB HOLT

NEWJERSEYNEWSROOM.COM

More than 44,000 people are diagnosed with pancreatic cancer each year, and nearly three-quarters of them die within a year, according to statistics.
But a trial conducted at the Cancer Institute of New Jersey in New Brunswick has given renewed hopes in stabilizing a patient’s immunity.
“It’s a promising lead," Elizabeth Poplin from the Cancer Institute of New Jersey told CBS New York. “We’re giving them a vaccine into the pancreas and into their arm in the hopes of boosting their immunity to the cancer.”

Six patients with inoperable pancreatic cancer were tested, and the disease was “clinically stable” in four of them after a year. Injecting the vaccine directly into the pancreatic tumor seems to reawaken the body’s immunity toward the disease, Poplin said, according to NorthJersey.com.

When the investigation, sponsored by the National Cancer Institute, began two years ago, the vaccine was known as PANVAC, which contains genes that might stimulate that immune system.

“There has not been a significant breakthrough in the treatment of pancreatic cancer since an upgrade in chemotherapy in the mid 1990s,” Poplin said, according to a press release from CINJ.org. “When you talk about a disease that on average carries only a five-percent survival rate, the possibility of identifying better treatment and management options, especially by potentially utilizing the body’s own defenses, has become a challenge that my colleagues and I are committed to tackling.”

To be eligible for the clinical trial, patients had to have been diagnosed with inoperable pancreatic cancer that has not metastasized, and cannot have faced chemotherapy yet.

Lusgarten Walks -- You can make a difference

Help raise money for pancreatic cancer research ... join a Lustgarten Walk ...


Albany Pancreatic Cancer Reserach WalkAllentown Pancreatic Cancer Reserach Walk
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Westborough Westchester Pancreatic Cancer Reserach Walk/Run

Westlake Westchester Pancreatic Cancer Reserach Walk/Run

Harvard Medical School Adviser: More options for treating pancreatic cancer

QUESTION: I am a 55-year-old man who was recently diagnosed with pancreatic cancer. It is a neuroendocrine tumor. My doctor will be performing surgery in a couple of weeks and has discussed some new drugs that the Food and Drug Administration recently approved. Can you help me understand my diagnosis and the new drugs?

Answer: A cancer diagnosis can make a person feel very alone, but be assured you are not. About 44,000 Americans will be diagnosed with pancreatic cancer this year -- accounting for about 3% of all cancer diagnoses.

Neuroendocrine tumors and the more common type of pancreatic cancer start from different types of cells. They have different symptoms and are treated differently. People can lead relatively normal lives for several years with a neuroendocrine tumor, even if the disease has spread outside the pancreas.

There are two new FDA-approved drugs for pancreatic neuroendocrine tumors. They are sunitinib (Sutent) and everolimus (Afinitor). These new drugs disrupt molecular-level signaling within cancerous cells. They work in a much more targeted way than conventional chemotherapy. Cancer specialists see these two new drugs and drugs like them as the exciting new wave of cancer therapy.

Your doctor may have reviewed this information with you, but it may help to briefly describe the pancreas. It is a gland that's situated at the back of the abdomen, where it's close to and connected with many other structures in your body. The pancreas has two main functions: It produces digestive fluids and enzymes that are released into the small intestine, and it produces insulin and other hormones that are released into the bloodstream.

It is thought that the common type of pancreatic cancer comes from cells that produce digestive juices, while the neuroendocrine tumors arise from islet cells responsible for insulin and other hormones. This is the traditional view, but new evidence is suggesting that both types of cancer may originate from stem cells.
Your doctor has probably explained that your type of cancer can be removed surgically. Generally speaking, though, the operation is not performed if the cancer has spread beyond the pancreas itself. In that case, a surgical procedure does little to alter the course of the disease.

Up to 30% of pancreatic neuroendocrine tumors result in excess release of insulin or other hormones. If too much insulin is pumped out, blood sugar levels can plummet. Extra gastrin, a hormone that stimulates the stomach, can lead to stomach ulcers. Surplus glucagon can make blood sugar levels go up.
Now medications called somatostatin analogs are used to control hormone release. They may also slow the growth of the tumors.

Conventional chemotherapy is used to treat pancreatic neuroendocrine cancer after it has spread. It extends lifespan, but it doesn't cure the cancer.

The two new drugs sunitinib (Sutent) and everolimus (Afinitor) are exciting alternatives to conventional chemotherapy. Sunitinib inhibits an enzyme critical to a complex chain of chemical events -- a "signaling pathway." By doing so, it inhibits the spread of cancer cells.

Everolimus inhibits a different enzyme, mTOR, and a different pathway. The basic concept of zeroing in on a molecular-level target specific to cancer cells is the same.

Research shows that sunitinib and everolimus can cut the growth of pancreatic neuroendocrine cancers in half. But these new medications do have side effects, including high blood pressure and low white blood cell counts.

The bottom line is that in this new era of targeted drugs, unusual cancers are becoming more treatable. A diagnosis of cancer is never welcome, but your diagnosis comes at a hopeful time.
Have a question? Send it to harvard_adviser@hms.harvard.edu

Happy Easter and Happy Passover from everyone on 

the Denver Lustgarten Walk Committee!  

Have a wonderful holiday weekend and

enjoy this fabulous Denver weather!

Healthy Vegan Options in Denver

Looking for vegan options to dine out in Denver?  This is a great resource ...

http://www.happycow.net/north_america/usa/colorado/denver/

5 Cancer-Fighting Foods You Should Be Eating

From Broccoli To Blueberries, Eat To Fight Breast Cancer

Kateri Wozny, Contributing writer

Women may think they are eating all the right foods to maintain a healthy lifestyle, but there are certain foods that can help lower the risk of the second-leading cause of cancer death among women: breast cancer.
Breast cancer causes more than 40,000 deaths per year and one in eight million women will experience breast cancer during their lifetime, according to the American Cancer Society.

Maybe you've seen women wearing a pink ribbon pin to symbolize their fight breast cancer, know of someone who has the disease or even know of someone who died from it.

Research studies have found cancer-fighting benefits in certain types of food. No food will prevent women from getting breast cancer, but experts say if women eat well and stick to a low-fat, healthy diet, it could lower the risk significantly.

Before you head out to your next grocery store visit, here's a list of breast cancer fighting foods to add to your diet.

Read the full article at ...

http://www.thedenverchannel.com/health/29436266/detail.html

Integrative Cancer Care in Colorado

Introducing Colorado Integrative Cancer Care, metro Denver’s only cancer treatment center that takes care of the whole you – mind, body, spirit – because we have hope for all of our patients.

Our scientific approach to treatment and the healing process integrates standard cancer care with mind-body techniques, including supplements and nutritional counseling, acupuncture, massage therapy, diet and exercise programs, and stress reduction.

We believe that cancer affects not just your body, but also your mind and spirit – and we take of all of it.

It’s just part of our prescription for hope.

To schedule an appointment please use our contact form. To learn more about our workshops please see the latest here.

Our Practice

We write to share with you the exciting news that we are joining Rocky Mountain Cancer Centers (RMCC) effective July 1, 2011.

As you might know, Dr. Diab practiced medicine at RMCC for over 10 years before joining the Medical Center of Aurora Clinic Services in 2010.

As the two of us formally become affiliated with RMCC, you will benefit in many ways.

We believe that fully integrative care is important, and we will continue to offer the complementary therapy services you’ve come to expect. RMCC currently offers some of these services, and the integrative program will expand to offer nutritional counseling, massage therapy, and traditional Chinese medicine, including acupuncture.

RMCC knows how to provide cancer care and hematology services like no other provider in Colorado. Oncology and hematology are all they do, and they have the resources and expertise to do them well.

As a member of the US Oncology network, RMCC is able to participate in a robust clinical trials program, which ensures patients have access to the latest treatments in all major cancer types. In addition, their Aurora cancer center recently installed a Novalis Tx., the most advanced tool for delivering radiation therapy currently available in Colorado.

To learn more about Rocky Mountain Cancer Centers, please visit their website at www.RockyMountainCancerCenters.com. Dr. Diab and Dr. Nallapareddy will continue to practice at the following locations:

1400 S. Potomac St. Ste. 215 Aurora, CO 80012

14100 E. Arapahoe Rd. Ste. 120 Ste. 120 Centennial, CO 80112

Please contact the scheduling coordinators at 303-418-7600 so we can work with you on your transition of medical records and arrange your appointments. Please fax the medical release form to 303-750-3137 or bring it to your next visit and we can begin your medical record transfer.

We believe this will be a positive change for everyone involved. If you have any questions, please do not hesitate to let us know.

Our Mission

The CICC staff will make every effort to:

• Treat our patients the way we like to be treated.
• Provide state of the art medical treatment.
• Be honest and caring at all times.
• Be an advocate for our patients.
• Keep an open mind about any issue.
• Provide emotional, spiritual, and social support.
• Advance cancer knowledge through scientific research.
• Address the unique individual needs of each patient.
• Keep family/significant others informed and involved.
• Value support and input of all health care staff and professionals.

http://drdiab.info/