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Gene Discovery May Improve Pancreatic Cancer Diagnosis, Treatment
 TUESDAY, May 1 (HealthDay News) -- Scientists say they can use small bits of genetic material called microRNA to spot key differences between chronic pancreatitis and pancreatic cancer, aiding in earlier diagnosis for the lethal malignancy.
The researchers say doctors might also someday use microRNA to help predict the survival of patients with pancreatic cancer.
The report is especially important, because pancreatic cancer is one of the most lethal cancers known, eventually killing almost all of the 33,000 Americans it affects each year.
The problem is that pancreatic tumors often grow very large without outward symptoms, leading to late diagnoses and poor patient outcomes.
But "microRNA can help in the diagnosis," said lead researcher Dr. Mark Bloomston, a professor of surgery at Ohio State University, Columbus. "It could also, potentially have some prognostic implications," he added.
His team published its findings in the May 2 Journal of the American Medical Association.
"MicroRNA are small genes that regulate other genes and cells," Bloomston explained. "The role of microRNA has already been explored in other cancers, such as leukemia, breast and lung cancer, and stomach and colon cancer. MicroRNAs are important in normal physiology in the development of the human body, so it is only fitting that they have a role in cancer," he said.
The Ohio expert noted that in the pancreas, microRNA takes on a different form in normal versus cancerous tissue. It is also altered in inflammatory conditions, such as chronic pancreatitis.
According to Bloomston, diagnosing pancreatic cancer is never simple, even when doctors have a biopsy tissue sample to evaluate. "However, looking at how microRNA differs between cancer and normal tissue could help in making an accurate diagnosis," he said.
In the study, the Ohio team performed experiments to identify the patterns of microRNA in pancreatic cancer, attempting to differentiate pancreatic cancer from benign pancreatic tissue.
The researchers also looked at pancreatic cancer cells from 65 patients and compared them with cells from 42 patients with pancreatitis.
"We found a group of microRNAs that distinguish between pancreatic cancers and the normal pancreas and also distinguish them from chronic pancreatitis," Bloomston said.
The researchers looked at cancer tissue from patients who survived for more than 24 months and compared it to those who died in less than 24 months.
"A two-year cut-off in pancreatic cancer is a milestone, because most patients recur or die within two years of their diagnosis," Bloomston said. "We were able to get a small subset of these microRNA genes that could differentiate long-term from short-term survivors," he said.
Bloomston believes that once they better understand how microRNA works in cancers, it might even be possible to target these tiny genes to treat the disease.
One expert cautioned that, although this discovery is exciting in terms of its potential application to diagnosis and treatment, it will be years before it reaches clinical application.
"It's a really long path from discovering something to translating that into something that happens to you in the doctor's office," said Dr. Scott A. Waldman, professor and chairman of pharmacology and experimental therapeutics at Thomas Jefferson University, Philadelphia, and the co-author of an accompanying journal editorial.
However, Waldman does believe the finding will have broad implications for treating many cancers.
"This is a multilevel discovery," he said. "This discovery reveals an underappreciated level of biological regulation. The researchers also identify how these microRNAs can be used for potential diagnostics and indication of survival," he said.
"Knowing who is less likely to survive will enable us to direct treatment to those patients and hopefully improve their survival," Waldman said. "In addition, when we find out what those microRNAs are regulating, they become targets for intervention," he added.
More information
For more information on pancreatic cancer, visit the American Cancer Society  .
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Imaging Technique Could Help Fight Metastatic Cancers
FRIDAY, April 27 (HealthDay News) -- A new imaging technique that measures diffusion of water through tumors may help guide the treatment of advanced prostate cancer that's spread to the bones, says a study by researchers at the University of Michigan Comprehensive Cancer Center.
This technique, called a functional diffusion map, uses an MRI scan and special software to monitor the movement of water through tumor cells over the course of treatment. As tumor cells die, this diffusion of water increases, the researchers explain.
In the study, the Michigan team tested the technique in mice with metastatic prostate cancer.
Mice that received chemotherapy showed progressive changes over the three weeks of treatment, while mice that did not receive chemotherapy had little or no change in water diffusion.
When the researchers removed the tumors from the mice, they found that the functional diffusion map had accurately measured tumor response to treatment. The study was published in the April 15 issue of Cancer Research.
The findings suggest that the functional diffusion map could provide an early assessment of tumor response to treatment, the scientists said. This could help patients avoid wasting time on a treatment that isn't working before they switch to an alternative therapy.
Currently, there is no way to detect bone tumor response to therapy, study author Brian D. Ross, a professor of radiology and biological chemistry at the U-M Medical School and co-director of the Molecular Imaging Program at the U-M Comprehensive Cancer Center, said in a prepared statement.
About 500,000 people in the United States develop metastatic prostate or breast cancers that spread to the bone, he said.
More information
The U.S. National Cancer Institute has more about metastatic cancer.
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Scientists Spot Mechanism Behind Lung Cancer Drug Resistance
 THURSDAY, April 26 (HealthDay News) -- Scientists have discovered a key means by which some lung cancer tumors become resistant to drugs such as Iressa and Tarceva.
The finding could lead to better combination drug treatments, the researchers report.
"We wanted to find out why tumors become resistant to certain drugs," explained senior researcher Dr. Pasi A. Janne, an assistant professor of medicine at Harvard Medical School. "While patients respond to drugs like Iressa and Tarceva, the majority of patients become resistant to them. The cancers figure out a way to grow in the presence of these drugs."
His team reported its findings in the April 26 online edition of Science.
Doctors often resort to drugs such as Iressa (gefitinib) and Tarceva (erlotinib) to treat advanced non-small-cell lung cancer. These agents work by blocking epidermal growth factor receptor (EGFR), a molecule lying on the surface of cancer cells.
Tumors that respond to these EGFR inhibitors shrink rapidly and dramatically, but in time they can become resistant and start growing again.
In about half of the cases, a mutation in the EGFR gene interferes with the ability of the drug to bind to the receptor. Once this happens, these drugs cease to work.
However, in many other cases the cause of resistance remains unknown.
Investigating that issue, Janne's team experimented with lung cancer cells resistant to Iressa.
They found that a mutation in a second gene can also cause the drug to stop working. "We identified a single mutation in another gene that occurred in the drug-resistant cells," Janne said. "This is the MET oncogene. And we have a specific drug that targets this gene."
Analysis of samples from patients whose tumors became resistant after initially responding to Iressa showed that the MET mutation was present in samples from four of 18 patients.
"When we treated the resistant cells with a MET inhibitor, it completely restored the effectiveness of Iressa," Janne said. "We found the same MET mutation in about 20 percent of lung cancer patients."
This is a wholly new mechanism for lung cancer drug resistance, Janne said, and it is also "a mechanism that we can target with a specific drug. This is a potentially new and important therapy for these individuals." he said. According to Janne, similar mechanisms may also be at work in other cancers.
The Harvard group is working on ways to combine treatment with currently available EGFR inhibitors and MET inhibitors that are currently in clinical trials. They also want to study more drug-resistant samples, to get a better idea of how often this resistance mechanism occurs.
One expert views the finding as another indication of cancer's complexity.
"This shows the complexity of treating a rapidly changing tumor type," said Michael Melner, a scientific program director at the American Cancer Society. "The mutation of the MET gene is only one explanation out of many for the resistance of the tumors."
Drug combinations appear more and more necessary for treating many cancers, Melner added. "This is another study that points to things being more complex than we think they are. Clearly, combinations of drugs are going to be necessary to treat multiple cancer types. And this is just another indication of that," he said.
More information
For more information on lung cancer, visit the U.S. National Cancer Institute.
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Cancer Patients at High Risk of Drug Interactions
WEDNESDAY, April 18 (HealthDay News) -- Because they often take several medications at the same time, cancer patients are at high risk for adverse drug interactions, Canadian researchers report.
These adverse events can result in the inactivation of cancer-fighting drugs and can also cause severe harm or even death, the team reported in the April 18 issue of the Journal of the National Cancer Institute.
Many cancer patients take drugs to treat their cancer, along with drugs to treat the side effects of cancer therapies and secondary illnesses, noted researchers at the Princess Margaret Hospital in Toronto.
They had 405 cancer patients fill out a questionnaire about all the medications they'd taken in the previous four weeks. The researchers then used a drug interaction software program to analyze the data and to identify potential drug interactions, ranking them by severity.
The study found that nearly a third of the patients were exposed to at least one potential drug interaction and that there were 276 drug combinations with the potential to interact.
About 77 percent of the interactions were of moderate severity (risk of serious health problems), and about nine percent were of major severity (risk of death). The researchers also found that about eight percent of patients received duplicate medications.
The drugs that most commonly interacted with cancer medications were warfarin (used to prevent blood clots), anti-hypertension drugs, aspirin and anticonvulsants.
"We suggest that patients at high risk ... be routinely screened for potential drug interactions. The development of medication databases and computerized physician medication order entry linked to screening electronic programs could help health professionals to identify dangerous drug combinations and monitor prescriptions of agents with high risks of interactions," the study authors wrote.
More information
The U.S. Food and Drug Administration has more about drug interactions.
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