Important steps toward developing a blood test to catch pancreatic cancer early

 

Pancreatic cancer is the fourth most common cause of cancer-related death in the United States and has a 5-year survival rate of only 6 percent, which is the lowest rate of all types of cancer according to the American Cancer Society. This low survival rate is partially attributed to the difficulty in detecting pancreatic cancer at an early stage. According to a new 'proof of principle' study published in Aug. 27 issue of Cancer Prevention Research, Moffitt Cancer Center researchers hope to improve pancreatic cancer survival rates by identifying markers in the blood that can pinpoint patients with premalignant pancreatic lesions called intraductal papillary mucinous neoplasms (IPMNs). "One promising strategy to reduce the number of people affected by pancreatic cancer is to identify and treat premalignant pancreatic lesions," said first author Jennifer Permuth-Wey, Ph.D., M.S., assistant member in the Departments of Cancer Epidemiology and Gastrointestinal Oncology at Moffitt. "IPMNs are established precursor lesions to pancreatic cancer that account for approximately half of all asymptomatic pancreatic cysts incidentally detected by computerized tomography (CT) scans or magnetic resonance imaging (MRI) in the U.S. each year." IPMNs can be characterized as either low- or high-risk for the development of pancreatic cancer; however, the only way to accurately characterize the severity of IPMNs is by their surgical removal that is in itself associated with a risk of complications, such as long-term diabetes and death. Alternatively, not removing the IPMN(s) could lead to a missed opportunity to prevent high-risk lesions from developing into invasive pancreatic cancer. Moffitt researchers want to develop a fast, cost-effective blood test that can accurately differentiate low-risk IPMNs that can be monitored from high-risk IPMNs that need to be surgically removed by studying microRNAs (miRNAs), a class of small molecules that regulate key genes involved in the development and progression of cancer. "Using new digital technology, we compared the expression patterns of miRNAs in the blood and discovered a set of 30 miRNAs that differentiated between IPMN patients and healthy volunteers. We also identified five miRNAs that could distinguish between high-risk IPMNs and low-risk IPMNs," said senior author Mokenge Malafa, M.D, F.A.C.S., department chair and program leader for Moffitt's Gastrointestinal Oncology Program. "We are excited about our preliminary findings, but much more research is needed before such a blood test could be made available in the clinical setting." "The hope is that in the not-so-distant future a miRNA-based blood test can be used in conjunction with imaging features and other factors to aid the medical team in accurately predicting disease severity of IPMNs and other pancreatic cysts at the time of diagnosis or follow-up so that more informed personalized medical management decisions can be made," explained Permuth-Wey. The authors believe that the incorporation of such a blood test into routine clinical practice could provide a prime opportunity for intervention during the pre-cancerous phase before the development of pancreatic malignancy. Through funding from the State of Florida and the newly established Florida Academic Cancer Center Alliance, Moffitt researchers plan to further their research on IPMNs by partnering with researchers from the University of Florida Health Cancer Center and the University of Miami/Sylvester Comprehensive Cancer Center. This new partnership, called the Florida Pancreas Collaborative, represents the first state-wide multi-cancer center collaboration dedicated to conducting research on IPMNs with the ultimate goal of promoting the prevention and early detection of pancreatic cancer. "Considering that Florida ranks second in the number of pancreatic cancer deaths that occur each year and the fact that pancreatic cancer is projected to surpass breast, prostate, and colorectal cancer and become the second leading cause of cancer deaths by 2030, we are thrilled that our state is committed to investing in pancreatic cancer research now," said Permuth-Wey. "Early detection and screening are the most effective ways for 'at-risk' individuals to minimize the potential for developing pancreatic cancer," said Malafa. Screening and diagnostic procedures for pancreatic cysts and other gastrointestinal conditions can be performed at Moffitt's state-of-the-art endoscopy clinic. This research was made possible by patients who were treated at Moffitt and generously donated blood and tissue samples to the Total Cancer Care® Program and was supported in part by grants from the American Cancer Society (93-032-16) and the National Cancer Institute. Story Source: The above post is reprinted from materials provided by Moffitt Cancer Center.Note: Materials may be edited for content and length. Moffitt Cancer Center. "Important steps toward developing a blood test to catch pancreatic cancer early." ScienceDaily. ScienceDaily, 28 August 2015. <www.sciencedaily.com/releases/2015/08/150828102339.htm>.

Three-protein biomarker raises possibility of a urine test for pancreatic cancer

 

Scientists have uncovered a new biomarker that suggests a urine test for pancreatic cancer could one day become a reality (Credit: Pancreatic Cancer Research Fund) With a lack of clear symptoms even when the disease is well progressed, more than 80 percent of pancreatic cancer diagnoses come after the cancer has already spread. This has led some researchers to look beyond blood to urine testing, which is a less complex fluid. Among those is a team at the Queen Mary University of London, which has uncovered a three-protein biomarker in the urine of pancreatic cancer sufferers, suggesting a less invasive, early stage test may be on the way. At just three percent, the five-year survival rate for pancreatic cancer is lower than any form of common cancer. Because it is difficult to detect, sufferers are often diagnosed after it has already spread which rules out surgical removal of the tumor, the only current method of treatment. Adding to the complexity are the difficulties in distinguishing between pancreatic cancer and the inflammatory condition known as chronic pancreatitis. But the Queen Mary researchers say they have made progress in addressing both problems. The scientists gathered a total of 488 urine samples. 192 came from patients with pancreatic cancer, 92 from those with chronic pancreatitis, 87 from healthy volunteers and another 117 from patients with benign and malignant liver and gall bladder conditions. They tallied around 1,500 proteins in the urine samples, but zeroed in on three in particular for a closer look: LYVE1, REG1A and TFF1. The pancreatic cancer sufferers had higher levels of all three proteins than the healthy patients. And in a discovery that could help separate them from those with chronic pancreatitis, the latter group displayed significantly lower levels of these proteins. The researchers say that the combined three-protein signature can help detect stage one and two pancreatic cancer with more than 90 percent accuracy. Stage two detection carries a survival rate of 20 percent, while stage one can see survival rates of up to 60 percent. "This is a biomarker panel with good specificity and sensitivity and we’re hopeful that a simple, inexpensive test can be developed and be in clinical use within the next few years," says lead researcher Dr Tatjana Crnogorac-Jurcevic. From here, the team aims to carry out further tests on people from high risk groups which includes those with obesity, a family history of pancreatic cancer, heavy smokers and people over 50 with new-onset diabetes. They are also hopeful of collecting ongoing samples from volunteers over the next five to ten years. Studying samples of those who went on to develop pancreatic cancer could allow them to establish if the three-protein biomarker is present during the latency period. This refers to the time after the genetic changes take place that cause the cancer develop and before the clinical presentation. The research was published in the journal Clinical Cancer Research. Source: Queen Mary University of London

Early sign of pancreatic cancer identified by researchers

 

September 28, 2014

Dana-Farber Cancer Institute

A sign of the early development of pancreatic cancer - an upsurge in certain amino acids that occurs before the disease is diagnosed and symptoms appear has been identified by a team of researchers. Although the increase isn’t large enough to be the basis of a new test for early detection of the disease, the findings will help researchers better understand how pancreatic cancer affects the rest of the body.

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Scientists at Dana-Farber Cancer Institute, the Massachusetts Institute of Technology, and other institutions have discovered a sign of the early development of pancreatic cancer – an upsurge in certain amino acids that occurs before the disease is diagnosed and symptoms appear. The research is being published online today by the journal Nature Medicine.

Although the increase isn’t large enough to be the basis of a new test for early detection of the disease, the findings will help researchers better understand how pancreatic cancer affects the rest of the body, particularly how it can trigger the sometimes deadly muscle-wasting disease known as cachexia.

“Most people with pancreatic ductal adenocarcinoma (PDAC) [by far the most common form of pancreatic cancer] are diagnosed after the disease has reached an advanced stage, and many die within a year of diagnosis,” said Brian Wolpin, MD, MPH, of Dana-Farber, co-senior author of the new study with Matthew Vander Heiden, MD, PhD, of MIT and Dana-Farber. “Detecting the disease earlier in its development may improve our ability to treat it successfully. In this study, we asked whether PDAC produces metabolic changes – changes in the way the body uses energy and nutrients – that can be detected before the disease is diagnosed.”

The researchers utilized blood samples collected years earlier from 1,500 people participating in large health-tracking studies. They analyzed the samples for more than 100 different metabolites – substances produced by the metabolic process – and compared the results from participants who had gone on to develop pancreatic cancer and those who had not.

“We found that higher levels of branched chain amino acids were present in people who went on to develop pancreatic cancer compared to those who did not develop the disease,” Wolpin said. (Branched chain amino acids are one family of amino acids, the building blocks of proteins.) The amount of time that would elapse before those individuals were diagnosed with pancreatic cancer ranged from two to 25 years, although the highest risk was in the several years before diagnosis, the researchers found.

“These findings led us to hypothesize that the increase in branched chain amino acids is due to the presence of an early pancreatic tumor,” Wolpin remarked. This theory was confirmed in laboratory experiments performed by Vander Heiden’s group at the Koch Institute for Integrative Cancer Research at MIT. Their experiments showed that mice with newly formed pancreatic tumors had above-normal blood levels of these amino acids.

The researchers found the increase was due to a breakdown of muscle tissue, which caused branched amino acids to be released into the bloodstream. This process is similar to what occurs in patients with cancer cachexia. “What was surprising about our results was that it appears the breakdown of muscle protein begins much earlier in the disease process than previously appreciated,” noted Vander Heiden.

The findings provide an important lead to scientists studying how pancreatic tumors interact with patients’ normal tissues, the authors say. According to Vander Heiden, this work provides a glimpse into how pancreatic cancer changes the way the rest of the body handles nutrients. “This work has the potential to spur progress in detecting pancreatic tumors earlier and identifying new treatment strategies for those with the disease,” he remarks.

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Story Source:

The above story is based on materials provided by Dana-Farber Cancer Institute. Note: Materials may be edited for content and length.

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Journal Reference:

1. Jared R Mayers, Chen Wu, Clary B Clish, Peter Kraft, Margaret E Torrence, Brian P Fiske, Chen Yuan, Ying Bao, Mary K Townsend, Shelley S Tworoger, Shawn M Davidson, Thales Papagiannakopoulos, Annan Yang, Talya L Dayton, Shuji Ogino, Meir J Stampfer, Edward L Giovannucci, Zhi Rong Qian, Douglas A Rubinson, Jing Ma, Howard D Sesso, John M Gaziano, Barbara B Cochrane, Simin Liu, Jean Wactawski-Wende, JoAnn E Manson, Michael N Pollak, Alec C Kimmelman, Amanda Souza, Kerry Pierce, Thomas J Wang, Robert E Gerszten, Charles S Fuchs, Matthew G Vander Heiden, Brian M Wolpin. Elevation of circulating branched-chain amino acids is an early event in human pancreatic adenocarcinoma development. Nature Medicine, 2014; DOI: 10.1038/nm.3686

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Short nanotubes target pancreatic cancer

 

June 5, 2014

Rice University

Short, customized carbon nanotubes have the potential to deliver drugs to pancreatic cancer cells and destroy them from within, according to researchers. Pristine nanotubes produced through a new process can be modified to carry drugs to tumors through gaps in blood-vessel walls that larger particles cannot fit through. The nanotubes may then target and infiltrate the cancerous cells' nuclei, where the drugs can be released through sonication -- that is, by shaking them.

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Short, customized carbon nanotubes have the potential to deliver drugs to pancreatic cancer cells and destroy them from within, according to researchers at Rice University and the University of Texas MD Anderson Cancer Center.

Pristine nanotubes produced through a new process developed at Rice can be modified to carry drugs to tumors through gaps in blood-vessel walls that larger particles cannot fit through.

The nanotubes may then target and infiltrate the cancerous cells' nuclei, where the drugs can be released through sonication -- that is, by shaking them.

The research led by Rice chemist Andrew Barron was reported in the Royal Society of Chemistry's Journal of Materials Chemistry B.

Most pancreatic cancer patients die within a year of diagnosis and have a five-year survival rate of 6 percent, partially because there is no method for early detection, according to the American Cancer Society. Tumors are often inoperable and pancreatic cancer cells are also difficult to reach with chemotherapy, said co-author Jason Fleming, a professor of surgical oncology at MD Anderson.

"These findings are encouraging because they offer a potential delivery solution for pancreatic cancer patients whose tumors resist standard chemotherapy," Fleming said. "There are molecular and biological barriers to efficient delivery of chemotherapy to pancreatic cancer tumors, and these nanotubes might be able to make some of those irrelevant."

Rice scientists made nanotubes pure enough to modify for the purpose and small enough to squeeze through the body's defenses, Barron said. The researchers knew from previous work that nanotubes could be modified -- a process called functionalization -- to carry chemotherapy agents and release them at a controlled rate through sonication.

"This time, we were trying to work out how long the tubes should be and the extent of functionalization to maximize uptake by the cells," Barron said.

Several discoveries were key, he said. First, Rice graduate student, alumnus and co-author Alvin Orbaek purified the carbon nanotubes of iron catalysts necessary to their growth by flushing them with chlorine. "Leftover iron particles damage the tubes through oxidation," Barron said. "That makes subsequent use difficult."

The next step was to cut the nanotubes down to size. Very long nanotubes are floppy and hard to deal with, Barron said. Enrico Andreoli, a postdoctoral research associate in Barron's group and lead author of the paper, used a thermal process to chop them to an average length of 50 nanometers. (A human hair is about 100,000 nanometers wide.)

"Instead of ending up with a fluffy nanotube powder, we get something that looks like a hockey puck," Barron said. "It's not dense -- it looks like a spongy puck -- but you can cut it with a razor blade. You can weigh it and do accurate chemistry with it."

Barron's lab added polyethyleneimine (PEI) to the nanotube surfaces. In lab tests, the modified tubes were easily dispersed in liquid and able to pass through barriers into live cancer cells to infiltrate the nuclei. A small-molecule variant of PEI proved to be less toxic to cells than larger versions, Barron said.

"This research shows that the particles are small enough to get inside cells where you like them to be and that they may have an increased killing advantage -- but that's still unknown," Fleming said.

Fleming, whose work focuses on improving drug delivery for pancreatic cancer, cautioned that more research is required. "The next step will be to test this approach in mice that have allografts taken from human tumors," he said. "The architecture of these tumors will more closely resemble that of human pancreatic cancer."

Supportive tumor tissue surrounding cancer cells hinders, rather than helps, pancreatic cancer

 

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Fibrous tissue long suspected of making pancreatic cancer worse actually supports an immune attack that slows tumor progression but cannot overcome it, scientists at The University of Texas MD Anderson Cancer Center report in the journal Cancer Cell.

"This supportive tissue that's abundant in pancreatic cancer tumors is not a traitor as we thought but rather an ally that is fighting to the end. It's a losing battle with cancer cells, but progression is much faster without their constant resistance," said study senior author Raghu Kalluri, Ph.D., M.D., chair of Cancer Biology. "It's like having a car with weak yet functioning brakes vs. having one with no brakes."

The team's findings point to a potential new avenue for guiding treatment, including immunotherapy, and offer an explanation for the failure of a promising combination drug approach in clinical trials.

"Cancer is one form of tissue injury. When our defense system detects damaged cells it sends soldiers to contain and repair the damage," Kalluri said. "When it cannot remove the damaged cells and repair the injured area, our defensive fibrotic response tries to put a boundary around it, to contain it and prevent it from spreading."

Pancreas cancer is resistant to treatment and only about 7 percent of patients survive for five years. An estimated 46,420 new U.S. cases will be diagnosed in 2014 and 39,590 people will die of the disease.

Study results consistent with failed clinical trial

Kalluri and colleagues used genetically engineered mouse models that allowed depletion of tissue-repair cells called myofibroblasts in pancreatic cancer. Myofibroblasts compose a major portion of supportive tissue called stroma and also produce collagen, which serves as a scaffold for wound-healing and tissue regeneration. Up to 90 percent of a pancreas tumor can consist of fibrotic support tissue.

When the scientists depleted myofibroblast production in mice with either early or later-stage pancreatic ductal adenocarcinoma their tumors became much more invasive, aggressive and lethal.

"We did these experiments thinking that we would show the importance of myofibroblasts and fibrosis in pancreas cancer progression, but the results went completely against that hypothesis," Kalluri said.

Since myofibroblasts and collagen are thought to block chemotherapy, the team treated their myofibroblast-depleted mice with gemcitabine, the standard treatment for pancreas cancer. The drug did not have any effect on the disease course or improve survival.

These results track those of a major clinical trial that combined a myofibroblast-depleting drug called a hedgehog inhibitor with gemcitabine to treat pancreatic cancer patients. The trial was stopped in 2012 when an interim analysis showed the patients taking the combination had faster disease progression than the control group that took only gemcitabine, a surprising result.

"This paradigm-shifting study identifies the reason why the hedgehog-inhibitor trials failed," said co-author Anirban Maitra, M.D., professor of Pathology and scientific director of the Sheikh Ahmed Bin Zayed Al Nahyan Center for Pancreatic Cancer Research.

All solid tumors include some degree of fibrosis, Maitra said, but not as much as pancreas cancer.

The team's analysis of pancreatic tumors from 53 patients showed low levels of tumor myofibroblasts are associated with decreased survival.

Study findings are consistent with pathologic evidence that tumors with more fibrotic tissue more closely resemble normal pancreas tissue, indicating a better prognosis for patients, even though lab experiments indicated those tumors should be more aggressive, Maitra said.

"These findings also are likely to account for rather modest results in a phase I clinical trial of immunotherapy alone for pancreas cancer," Maitra said. "But it's not just a negative study, because it suggests what might work for these patients."

And what might work hinges on immune checkpoint blockade.

The immune system connection

To understand the cause of the swift progression, the team conducted gene expression profiling and RNA sequence analysis comparing control tumors to myofibroblast-depleted tumors.

Genes associated with tumor immunity were suppressed and fewer T cells and B cells infiltrated the myofibroblast-depleted tumors. The proportion of regulatory T cells, which suppress immune response, increased. They found greater expression of the immune checkpoint CTLA-4, which shuts down immune response.

The researchers then set up a new experiment using ipilimumab, a drug developed by co-author Jim Allison, Ph.D., chair of Immunology, that blocks CTLA-4, freeing T cells to attack tumors. Mice with depleted myofibroblasts who were treated with ipilimumab to stifle CTLA-4 had an average survival increase of 60% compared to untreated control mice and those with either depleted myofibroblasts or treated with ipilimumab alone.

These findings suggest that ipilimumab might work for patients with low levels of fibrosis in their tumors, Kalluri noted. Combining ipilimumab with a hedgehog inhibitor is likely to work better for those with high-fibrosis. The Kalluri laboratory is exploring these issues.

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Story Source:

The above story is based on materials provided by University of Texas M. D. Anderson Cancer Center. Note: Materials may be edited for content and length.

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Journal Reference:

1. Berna C. Özdemir, Tsvetelina Pentcheva-Hoang, Julienne L. Carstens, Xiaofeng Zheng, Chia-Chin Wu, Tyler R. Simpson, Hanane Laklai, Hikaru Sugimoto, Christoph Kahlert, Sergey V. Novitskiy, Ana De Jesus-Acosta, Padmanee Sharma, Pedram Heidari, Umar Mahmood, Lynda Chin, Harold L. Moses, Valerie M. Weaver, Anirban Maitra, James P. Allison, Valerie S. LeBleu, Raghu Kalluri. Depletion of Carcinoma-Associated Fibroblasts and Fibrosis Induces Immunosuppression and Accelerates Pancreas Cancer with Reduced Survival. Cancer Cell, 2014; DOI: 10.1016/j.ccr.2014.04.005

Some pancreatic cancer treatments may be going after wrong targets

 

May 22 / 2014

University of Michigan Health System

New research represents a significant change in the understanding of how pancreatic cancer grows – and how it might be defeated. Unlike other types of cancer, pancreatic cancer produces a lot of scar tissue and inflammation. For years, researchers believed that this scar tissue, called desmoplasia, helped the tumor grow, and they’ve designed treatments to attack this. But new research finds that when you eliminate desmoplasia, tumors grow even more quickly and aggressively. In the study, mice in which the desmoplasia was eliminated developed tumors earlier and died sooner.

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New research represents a significant change in the understanding of how pancreatic cancer grows – and how it might be defeated.

Unlike other types of cancer, pancreatic cancer produces a lot of scar tissue and inflammation. For years, researchers believed that this scar tissue, called desmoplasia, helped the tumor grow, and they’ve designed treatments to attack this.

But new research led by Andrew D. Rhim, M.D., from the University of Michigan Comprehensive Cancer Center, finds that when you eliminate desmoplasia, tumors grow even more quickly and aggressively. In the study, mice in which the desmoplasia was eliminated developed tumors earlier and died sooner.

“This flies in the face of 10 years of research,” says Rhim, assistant professor of gastroenterology at the U-M Medical School. “It turns out that desmoplasia is a lot more complex than previously thought. Components of this complex scar tissue may be the body’s natural defense against this cancer, acting as a barrier or fence to constrain cancer cells from growing and spreading. Researchers who have been trying to target desmoplasia to kill tumors may need to reevaluate their approach.”

Several drugs targeting desmoplasia are in clinical trials and one was recently stopped early because of poor results. “Our study explains why this didn’t work,” Rhim says.

The researchers were able to arrive at this surprising conclusion by using a better mouse model. Previous models have used mice with compromised immune systems injected with human pancreatic cancer cells, producing tumors that don’t closely resemble human pancreatic cancer. The current model utilizes mice that are genetically engineered to express the two most common genetic mutations seen in pancreatic cancer. The mice developed cancer spontaneously, and the cancer closely resembled human pancreatic cancer.

Results of the study appear in Cancer Cell. The work represents a collaboration among teams at the University of Pennsylvania, Columbia University, Johns Hopkins University, Memorial Sloan Kettering Cancer Center and Mayo Clinic.

Using genetically engineered mice, the researchers blocked desmoplasia by knocking down the signaling pathway that produces it. They discovered that desmoplasia prevents the formation of blood vessels that fuel the tumor. When it’s suppressed, the blood vessels multiply, giving the cancer cells the fuel to grow. The researchers next wondered: What if you then target blood vessels with treatment?

What they found in this study was that a drug designed to attack blood vessels, called an angiogenesis inhibitor, significantly improved overall survival in the mice who had desmoplasia blocked. Angiogenesis inhibitors already exist on the market with approval from the U.S. Food and Drug Administration.

Another key finding of the study is that eliminating desmoplasia created tumors that resembled undifferentiated pancreatic cancer in humans. Undifferentiated tumors lack desmoplasia, have abundant blood vessels and grow and spread quickly. About 10 percent of pancreatic cancers in patients are undifferentiated.

This suggests that angiogenesis inhibitors may be effective in patients with undifferentiated tumors.

This study suggests that patients with highly aggressive, undifferentiated pancreatic cancer may be good candidates for treatment with an angiogenesis inhibitor, a drug that is already approved by the U.S. Food and Drug Administration for other cancers. Researchers are moving toward developing a clinical trial. Plans for such an approach are currently underway.

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Story Source:

The above story is based on materials provided by University of Michigan Health System. Note: Materials may be edited for content and length.

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Journal Reference:

1. Andrew D. Rhim, Paul E. Oberstein, Dafydd H. Thomas, Emily T. Mirek, Carmine F. Palermo, Stephen A. Sastra, Erin N. Dekleva, Tyler Saunders, Claudia P. Becerra, Ian W. Tattersall, C. Benedikt Westphalen, Jan Kitajewski, Maite G. Fernandez-Barrena, Martin E. Fernandez-Zapico, Christine Iacobuzio-Donahue, Kenneth P. Olive, Ben Z. Stanger. Stromal Elements Act to Restrain, Rather Than Support, Pancreatic Ductal Adenocarcinoma. Cancer Cell, 2014; DOI: 10.1016/j.ccr.2014.04.021

Bacteria in mouth may diagnose pancreatic cancer

 

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Patients with pancreatic cancer have a different and distinct profile of specific bacteria in their saliva compared to healthy controls and even patients with other cancers or pancreatic diseases, according to research presented today at the annual meeting of the American Society for Microbiology. These findings could form the basis for a test to diagnose the disease in its early stages.

"Our studies suggest that ratios of particular types of bacteria found in saliva may be indicative of pancreatic cancer," says Pedro Torres of San Diego State University who presented the research.

In the United States, approximately 40,000 people die every year due to pancreatic adenocarcinoma, making it the fourth leading cause of cancer related death. Patients diagnosed in the early stages of pancreatic cancer have a 5-year survival rate of 21.5%. Unfortunately symptoms do not appear until after the cancer has become untreatable in the vast majority of cases, says Torres.

In the study, Torres and his colleagues compared the diversity of saliva bacteria across 131 patients, 63 female and 68 male, being treated at the University of California, San Diego (UCSD) Moores Cancer Center. Of these patients, 14 had been diagnosed with pancreatic cancer, 13 with pancreatic disease, 22 with other forms of cancer and 10 disease free. Results showed that patients diagnosed with pancreatic cancer had higher levels of two particular oral bacteria, Leptotrichia and Campylobacter, when compared to any other healthy or diseased state including non-cancerous pancreatic disease. Those with pancreatic cancer also had lower levels of Streptococcus, Treponema and Veillonella.

"Our results suggest the presence of a consistently distinct microbial profile for pancreatic cancer," says Torres. "We may be able to detect pancreatic cancer at its early stages by taking individuals' saliva and looking at the ratios of these bacteria."

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Story Source:

The above story is based on materials provided by American Society for Microbiology. Note: Materials may be edited for content and length.