Day: 01/16/2011

Daily Aspirin Linked to Steep Drop in Cancer Risk

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MONDAY, Dec. 6 — Long-term use of a daily low-dose aspirin dramatically cuts the risk of dying from a wide array of cancers, a new investigation reveals.

Specifically, a British research team unearthed evidence that a low-dose aspirin (75 milligrams) taken daily for at least five years brings about a 10 percent to 60 percent drop in fatalities depending on the type of cancer.

The finding stems from a fresh analysis of eight studies involving more than 25,500 patients, which had originally been conducted to examine the protective potential of a low-dose aspirin regimen on cardiovascular disease.

The current observations follow prior research conducted by the same study team, which reported in October that a long-term regimen of low-dose aspirin appears to shave the risk of dying from colorectal cancer by a third.

“These findings provide the first proof in man that aspirin reduces deaths due to several common cancers,” the study team noted in a news release.

But the study’s lead author, Prof. Peter Rothwell from John Radcliffe Hospital and the University of Oxford, stressed that “these results do not mean that all adults should immediately start taking aspirin.”

“They do demonstrate major new benefits that have not previously been factored into guideline recommendations,” he added, noting that “previous guidelines have rightly cautioned that in healthy middle-aged people, the small risk of bleeding on aspirin partly offsets the benefit from prevention of strokes and heart attacks.”

“But the reductions in deaths due to several common cancers will now alter this balance for many people,” Rothwell suggested.

Rothwell and his colleagues published their findings Dec. 7 in the online edition of The Lancet.

The research involved in the current review had been conducted for an average period of four to eight years. The patients (some of whom had been given a low-dose aspirin regimen, while others were not) were tracked for up to 20 years after.

The authors determined that while the studies were still underway, overall cancer death risk plummeted by 21 percent among those taking low-dose aspirin. But the long-term benefits on some specific cancers began to show five years after the studies ended.

At five years out, death due to gastrointestinal cancers had sunk by 54 percent among those patients taking low-dose aspirin.

The protective impact of low-dose aspirin on stomach and colorectal cancer death was not seen until 10 years out, and for prostate cancer, the benefits first appeared 15 years down the road.

Twenty years after first beginning a low-dose aspirin program, death risk dropped by 10 percent among prostate cancer patients; 30 percent among lung cancer patients (although only those with adenocarcinomas, the type typically seen in nonsmokers); 40 percent among colorectal cancer patients; and 60 percent among esophageal cancer patients.

The potential impact of aspirin on pancreatic, stomach and brain cancer death rates was more problematic to gauge, the authors noted, due to the relative paucity of deaths from those specific diseases.

They also found that higher doses of aspirin did not appear to boost the protective benefit. And while neither gender nor smoking history appeared to affect the impact of low-dose aspirin, age definitely did: the 20-year risk of death went down more dramatically among older patients.

And while cautioning that more research is necessary to build on this “proof of principle,” the authors suggested that people who embark on a long-term, low-dose aspirin regimen in their late 40s and 50s are probably the ones who stand to benefit the most.

Dr. Alan Arslan, an assistant professor in the departments of obstetrics and gynecology and environmental medicine at NYU Langone Medical Center in New York City, described the findings as “very significant.”

“[This] is the largest study to show that people who take aspirin for a long period of time have a reduced risk of death from many cancers, especially gastrointestinal cancers,” he noted.

“The take-home message for patients is that if someone is taking low-dose or regular aspirin, it may put them at a reduced risk of death from cancer,” Arslan added. “However, if someone is not already taking aspirin they should talk with their physician before starting. Aspirin has risks of side effects, including bleeding and stroke.”

PCA3: From basic molecular science to the clinical lab

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Prostate cancer is the second leading cause of cancer deaths in men in the United States. Use of the serum prostate specific antigen (PSA) test to screen men for prostate cancer since the late 1980s has improved the early detection of prostate cancer, however low specificity of the test translates to numerous false positive results and many unnecessary biopsies. New biomarkers to aid in prostate cancer diagnosis are emerging and prostate cancer gene 3 (PCA3) is one such marker. PCA3 is a noncoding RNA that is highly over-expressed in prostate cancer tissue compared to benign tissue. A non-invasive test for PCA3 was developed using whole urine collected after a digital rectal exam (DRE). Numerous clinical studies have demonstrated the utility of PCA3 for the diagnosis of prostate cancer and some studies suggest that PCA3 may also have prognostic value. The use of PCA3 in combination with serum PSA and other clinical information enhances the diagnostic accuracy of prostate cancer detection and will enable physicians to make more informed decisions with patients at risk for prostate cancer.

source: green journal

A Universal Marker for Tumor Cells?

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Cancer researchers have discovered a new genetic abnormality in tumor cells that sets them apart from normal cells. In mice and humans, cancer cells cranked out large amounts of a specific type of RNA that had been ignored until now. The discovery could shed light on how cancer develops, and it could give pathologists a new marker for detecting cancerous cells in a biopsy.

Postdoctoral researcher David Ting and colleagues in the lab of cancer geneticist Daniel Haber of Massachusetts General Hospital in Boston found their new marker by using a next-generation sequencing machine to measure the RNA molecules, or transcripts, that are encoded by a cancer cell’s DNA. Unlike traditional microarrays dotted with DNA probes that measure the activity of a subset of a cell’s 20,000 genes, this “digital” gene expression analysis tallied all RNA transcripts.

To the scientists’ surprise, a sizable fraction of the RNA transcripts in the first sample they tested—a mouse pancreatic tumor—were encoded by a type of DNA sequence called satellite repeats. These are short, repeated stretches of DNA that don’t code for proteins. Because satellite repeats weren’t considered important, microarrays don’t test for their expression, Haber says.

In eight of 10 mouse pancreatic tumors, the level of satellite transcripts was a stunning 40-fold higher than in normal mouse pancreatic cells, the team reports online today in Science. The findings were similar in human tumors: high levels of a particular satellite RNA in 15 of 15 human pancreatic cancers, as well as in a small sample of prostate, lung, kidney, and ovarian tumors when compared with normal human cells.

When Haber’s team stained this satellite RNA in pancreatic tissue that had been removed for biopsy, they showed that the cancer cells clearly stood out (see image), even in early stages of the disease. The marker could help improve cancer diagnosis, the researchers say. Often, doctors who suspect cancer in an organ will use a needle to collect a few cells and examine their shape. Although this test is less invasive than a surgical biopsy, it’s not as accurate—Ting says that only 60% to 80% of pancreatic samples obtained in this way are correctly diagnosed. Pathologist Ralph Hruban of the John Hopkins University School of Medicine in Baltimore, Medicine, who says the cell staining is “pretty impressive,” agrees that it could help with biopsies that are difficult to interpret.

Haber’s group hopes to use the marker to improve their circulating tumor cell (CTC) chip, a device that captures cancer cells floating in a sample of a patient’s blood. The method relies on protein markers to distinguish cancer cells from normal cells trapped by the chip, but no existing markers cut across cancer types. (Although cancer cells always carry mutations and abnormally expressed genes, until now no single genetic glitch distinguished cancer cells from normal cells.) “This seems to be so dramatically different,” Haber says. However, his group hasn’t yet worked out how to detect satellite RNA in the cells trapped by a CTC chip.

Down the road, the high levels of satellite expression could help reveal how cancer develops. “It’s surprising and it means something. But at this point we don’t know what it means,” says cancer biologist Tyler Jacks of the Massachusetts Institute of Technology in Cambridge. Haber’s group found that the high RNA levels correlate with the expression of certain genes involved in embryonic development—suggesting that cancer could be using normal developmental programs to evolve. But the researchers still need to figure out why the satellite RNA levels are so high and whether they contribute to cancer or are just a side effect of some other process.

source: science now