Archive for the ‘Cancer’ Category

If you’re grilling meat this Memorial Day, you should seriously consider stocking up on Guinness.

Grilling meat is a warm-weather tradition in America, especially on Memorial Day weekend. It’s also an ancient human tradition, uniting friends and family around food and fire as long as our species has existed. Unfortunately, it also unites us around chemicals that can cause cancer.

Warnings like that can make it seem like scientists ruin everything — they already took sitting, late-night snacks and fireworks from us. But science works both ways, and now it has found at least a partial solution for this carnivore’s conundrum. According to a recent study, published in the Journal of Agricultural and Food Chemistry, the secret to safer grilling has been under our noses all along.

Beer is a common ingredient at backyard cookouts, usually as a beverage. But research suggests marinating meat with beer, particularly dark beer, can curb the creation of polycyclic aromatic hydrocarbons (PAHs). These carcinogenic chemicals form as fat and juices drip from meat onto flames or embers, which then send smoky PAHs wafting up to coat the surface of our food.

PAHs can exist in more than 100 different combinations, some of which are found in known toxic cocktails like cigarette smoke and car exhaust. These chemicals have caused tumors, birth defects and reproductive problems in lab animals, according to the U.S. EPA, but the same effects have not been seen in humans. The National Cancer Institute says PAHs “become capable of damaging DNA only after they are metabolized by specific enzymes in the body.” Nonetheless, health concerns raised in a 2002 report have led the European Union to set safety standards for PAHs in food.

Previous studies have shown that beer, wine, tea and rosemary marinades can reduce carcinogens in cooked meat, but until now little was known about how various beer styles affect this phenomenon. And according to the recent study, the kind of beer seems to make a pretty significant difference.

To reach that conclusion, the researchers marinated pork for four hours in one of three beer types: regular pilsner, non-alcoholic pilsner or black beer. They then grilled the pork to well-done on a charcoal grill and tested its PAH levels. Black beer had the most dramatic effect, reducing eight major PAHs to less than half the amount found in unmarinated grilled pork. (The researchers chose eight PAHs that are identified by the EU as “suitable indicators for carcinogenic potency of PAHs in food.”)

The two pilsners also showed an “inhibitory effect” on PAHs, but not as much. The regular pilsner suppressed PAHs by 13 percent, and the non-alcoholic variety went slightly further with 25 percent.

“Thus, the intake of beer-marinated meat can be a suitable mitigation strategy,” the researchers say.

The study’s authors aren’t sure why beer marinade has this effect, or why dark beer fights PAHs better than pilsner does. It isn’t the alcohol, since non-alcoholic pilsner nearly doubled the PAH suppression of its boozier relative. They suspect it might be antioxidant compounds in beer, especially darker beers, since antioxidants could restrict the movement of free radicals that are required for PAH formation. More research will be needed to know for sure, but this theory could help explain why antioxidant-rich red wine, green tea and rosemary extracts also keep carcinogens in check.

Whatever you use, the American Institute for Cancer Research already recommends marinating meat for at least 30 minutes to limit both PAHs and heterocyclic amines (HCAs), another type of chemical compound that can damage DNA. It also suggests grilling fish and poultry more often than red meat or processed meats like hot dogs, which can increase the risk for certain cancers. Reducing temperature, time on the grill and smoke exposure are other options for limiting cancer risk.

And while it can’t take the place of a juicy, beer-marinated pork chop, there’s also another, even more surefire way to cut back your risk: Save some room on the grill for fruits, vegetables and mushrooms.

http://www.mnn.com/food/healthy-eating/blogs/how-dark-beer-can-make-grilled-meat-less-carcinogenic

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Researchers at the Karolinska Institute, Sweden, say guidelines that advise people to stay out of the sun unless wearing sunscreen may be harmful, particularly in northern countries which have long, cold winters.

Exposure to ultraviolet radiation from sunlight is often cited as a cause of skin melanoma (malignant tumour of melanocytes) and avoiding overexposure to the sun to prevent all types of skin cancer is recommended by health authorities.

But the new study, which followed nearly 30000 women over 20 years, suggests that women who stay out of the sun are at increased risk of melanomas and are twice as likely to die from any cause, including cancer.

It is thought that a lack of vitamin D may be to blame. Vitamin D is created in the body through exposure to sunshine and a deficiency is known to increase the risk of diabetes, TB, multiple sclerosis and rickets.

Previous studies showed that vitamin D can increase survival rates for women with breast cancer while deficiencies can signal prostate cancer in men.

The study looked at 29518 Swedish women who were recruited from 1990 to 1992 and asked to monitor their sunbathing habits.

After 20 years there had been 2545 deaths and it was found that women who never sunbathed were twice as likely to have died from any cause.

Women who sunbathed in the mild Swedish summer were also 10% less likely to die from skin cancer, although those who sunbathed abroad in sunnier countries were twice as likely to die from melanoma.

Yinka Ebo, senior health information officer at Cancer Research UK, said striking a balance was important.

“The reasons behind higher death rates in women with lower sun exposure are unexplained . overexposure to UV radiation from the sun or sunbeds is the main cause of skin cancer.”

http://www.timeslive.co.za/thetimes/2014/05/09/avoiding-sunshine-could-kill-you-study-finds

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

Swiss scientists broke a four-decade-long informal ban on LSD research yesterday when they announced the results of a study in which cancer patients received the drug to curb their anxiety about death.

The study, which was published in the Journal of Nervous and Mental Disease, looked at the safety and efficacy of LSD when used in combination with talk therapy. The researchers used the semisynthetic psychedelic drug to facilitate discussions about the cancer patients’ fears of dying. The patients who took LSD, most of whom were terminally ill, experienced 10-hour-long supervised “trips.” One patient described the trips to The New York Times as a “mystical experience,” where “the major part was pure distress at all the memories I had successfully forgotten for decades.”

These periods of distress are regarded as therapeutically valuable because they allow patients to address their memories and the emotions they evoke. The patients underwent 30 such trips over the course of two months.

A year after the sessions ceased, the patients who had received a full dose of LSD — 200 micrograms — experienced a 20 percent improvement in their anxiety levels. That was not the case for the group who received a lower dose, however, as their anxiety symptoms actually increased. They were later allowed to try the full dose after the trial had ended.

Because of the small number of study participants, the researchers are reluctant to make any conclusive statements about the LSD treatment’s effectiveness. Indeed, the results were not statistically significant. But the fact that the study took place at all bodes well for psychedelic drug research, as the drug caused no serious side effects. Rick Doblin, executive director of the Multidisciplinary Association for Psychedelic Studies, a foundation that has funded many of these studies, thinks that revisiting LSD-based treatments is worthwhile. “We want to break these substances out of the mold of the counterculture,” Doblin told The New York Times, “and bring them back to the lab as part of a psychedelic renaissance.”

http://www.theverge.com/2014/3/5/5473828/lsd-drug-therapy-first-time-in-40-years

Thanks to Jody Troupe for bringing this to the attention of the It’s Interesting community.

lab to lcinic
The research team is building a smaller portable version of the laboratory’s cancer detection system. Source: Milind Rajadhyaksha, Ph. D., Memorial Sloan-Kettering Cancer Center, New York, NY.

Residual%20Cancer%20Margins

A common surgery for non-melanoma skin cancer, known as Mohs surgery, typically achieves excellent results but can be a long process, as the surgeon successively removes the area of concern until the surrounding tissue is free of cancer. To determine whether further tissue removal is necessary, the borders of the lesion must be processed in a laboratory to check for residual cancer tissue — a process that takes 20 – 45 minutes and is often repeated numerous times. Now, National Insititute of Biomedical Imaging and Bioengineering (NIBIB)-funded researchers have developed a microscopic technique to analyze removed tissue rapidly right in the clinic — dramatically reducing the length, inefficiency, and expense of this procedure.

With approximately 3.5 million new cases per year in the U.S., Mohs surgery is a fairly common procedure that many people undergo repeatedly as new skin cancers appear. It can take one to three hours, or even longer depending on the size and location of the lesion. The process is lengthy because after a section of tissue is removed, it must be frozen and stained so it can be examined to ensure the borders are clear of residual tumor. Although highly effective, the current practice is labor intensive for surgeons and assisting staff, as well as lengthy and stressful for patients. The time spent by surgical personnel and those analyzing the tissue in the lab increases the expense of the procedure, which has been estimated to cost $ 2-3 billion per year in the U.S.

NIBIB-supported researchers led by Milind Rajadhyaksha, Ph.D. at Memorial Sloan Kettering are using their expertise in optical imaging to improve this common procedure. Optical imaging is a technique that uses visible or near-infrared light to obtain detailed images of organs, tissues, and cells. The investigators developed a new pathological assessment technique called strip mosaicing confocal microscopy — a type of optical imaging — that can provide high resolution images during removal of basal cell and squamous cell carcinomas (non-melanoma skin cancers) and perhaps other tumors of the skin. The new technique uses a focused laser line that performs multiple scans of the tissue to obtain image “strips” that are then combined, like a mosaic, into a complete image of the excised tissue. The process takes only 90 seconds and eliminates the need to freeze and stain the tissue samples for analysis — a process that takes 20 to 45 minutes.

The new imaging technique was tested on 17 patients with 34 tissue samples. The overall image quality was excellent, with high resolution and contrast, providing for good visibility of the epidermis and dermis. Researchers compared the new technique against the Mohs approach with its frozen section processing. The new technique achieved a promising 94% in preliminary measures of sensitivity and specificity for detecting skin cancer margins, which is comparable to the “gold standard” Mohs procedure. These preliminary results demonstrated that the optical technique could potentially detect skin cancer margins with the same accuracy as the conventional frozen section technique.

The results of this study were obtained under laboratory conditions; a clinical trial is now being conducted to demonstrate the feasibility of using this technique in the clinical setting, the ultimate goal of the research group.

Steve Krosnick, M.D., NIBIB director for the Program for Image-Guided Interventions, explains the utility of the optical system: “The technology is particularly well-suited for Mohs-trained surgeons, who are experts at performing excisions and interpreting images of tissue samples removed during the Mohs procedure. Image quality, ability to make accurate interpretations, and time savings will be key parameters for adoption of the system in the clinical setting, and the current results are very encouraging.”

The research was conducted by a team consisting of two laboratories at Memorial Sloan-Kettering Cancer Center, New York, NY, as well as students from Bronx High School of Science, New York and Livingston High School, Livingston New Jersey. The work is published in the October 2013 issue of the British Journal of Dermatology.

http://www.nibib.nih.gov/news-events/newsroom/new-imaging-technique-speeds-removal-non-melanoma-skin-cancers

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

Ibm

Software that read tens of thousands of research papers and then predicted new discoveries about the workings of a protein that’s key to cancer could herald a faster approach to developing new drugs.

The software, developed in collaboration between IBM and Baylor College of Medicine, was set loose on more than 60,000 research papers that focused on p53, a protein involved in cell growth implicated in most cancers. By parsing sentences in the documents, the software could build an understanding of what is known about enzymes called kinases that act on p53 and regulate its behavior; these enzymes are common targets for cancer treatments. It then generated a list of other proteins mentioned in the literature that were probably undiscovered kinases, based on what it knew about those already identified. Most of its predictions tested so far have turned out to be correct.

“We have tested 10,” Olivier Lichtarge of Baylor said Tuesday. “Seven seem to be true kinases.” He presented preliminary results of his collaboration with IBM at a meeting on the topic of Cognitive Computing held at IBM’s Almaden research lab.

Lichtarge also described an earlier test of the software in which it was given access to research literature published prior to 2003 to see if it could predict p53 kinases that have been discovered since. The software found seven of the nine kinases discovered after 2003.

“P53 biology is central to all kinds of disease,” says Lichtarge, and so it seemed to be the perfect way to show that software-generated discoveries might speed up research that leads to new treatments. He believes the results so far show that to be true, although the kinase-hunting experiments are yet to be reviewed and published in a scientific journal, and more lab tests are still planned to confirm the findings so far. “Kinases are typically discovered at a rate of one per year,” says Lichtarge. “The rate of discovery can be vastly accelerated.”

Lichtarge said that although the software was configured to look only for kinases, it also seems capable of identifying previously unidentified phosphatases, which are enzymes that reverse the action of kinases. It can also identify other types of protein that may interact with p53.

The Baylor collaboration is intended to test a way of extending a set of tools that IBM researchers already offer to pharmaceutical companies. Under the banner of accelerated discovery, text-analyzing tools are used to mine publications, patents, and molecular databases. For example, a company in search of a new malaria drug might use IBM’s tools to find molecules with characteristics that are similar to existing treatments. Because software can search more widely, it might turn up molecules in overlooked publications or patents that no human would otherwise find.

“We started working with Baylor to adapt those capabilities, and extend it to show this process can be leveraged to discover new things about p53 biology,” says Ying Chen, a researcher at IBM Research Almaden.

It typically takes between $500 million and $1 billion dollars to develop a new drug, and 90 percent of candidates that begin the journey don’t make it to market, says Chen. The cost of failed drugs is cited as one reason that some drugs command such high prices (see “A Tale of Two Drugs”).

Lawrence Hunter, director of the Center for Computational Pharmacology at the University of Colorado Denver, says that careful empirical confirmation is needed for claims that the software has made new discoveries. But he says that progress in this area is important, and that such tools are desperately needed.

The volume of research literature both old and new is now so large that even specialists can’t hope to read everything that might help them, says Hunter. Last year over one million new articles were added to the U.S. National Library of Medicine’s Medline database of biomedical research papers, which now contains 23 million items. Software can crunch through massive amounts of information and find vital clues in unexpected places. “Crucial bits of information are sometimes isolated facts that are only a minor point in an article but would be really important if you can find it,” he says.

Lichtarge believes that software like his could change the way scientists conduct and assess new research findings. Scientists currently rely in part on the reputation of the people, institutions, and journals involved, and the number of times a paper is cited by others.

Software that gleans meaning from all the information published within a field could offer a better way, says Lichtarge. “You might publish directly into the [software] and see how disruptive it is,” he says.

Hunter thinks that scientists might even use such tools at an earlier stage, having software come up with evidence for and against new hypotheses. “I think it would really help science go faster. We often waste a lot of time in the lab because we didn’t know every little thing in the literature,” he says.

http://www.technologyreview.com/news/520461/software-mines-science-papers-to-make-new-discoveries/

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

Camel

A research team from Saudi Arabia’s King Abdulaziz University has been making claims about discovering anti-cancer properties in camel urine for the last several years, and are now claiming they’ve shown good results in tests on healthy humans, though those results have yet to see publication. The researchers are seeking support from the Saudi Food and Drug authority, which oversees the nation’s clinical trials, to let them keep moving forward and testing the substance — which is extracted from camel urine — on patients suffering from cancer.

The team plan to release more data on their work at a conference later this month.

http://www.geekosystem.com/camel-urine-cancer-cure/

File photo of Watson receiving data encompassing his personal genome sequence in Houston

James Watson, co-discoverer of the double helix structure of DNA, lit into targets large and small. On government officials who oversee cancer research, he wrote in a paper published on Tuesday in the journal Open Biology, “We now have no general of influence, much less power … leading our country’s War on Cancer.”

On the $100 million U.S. project to determine the DNA changes that drive nine forms of cancer: It is “not likely to produce the truly breakthrough drugs that we now so desperately need,” Watson argued. On the idea that antioxidants such as those in colorful berries fight cancer: “The time has come to seriously ask whether antioxidant use much more likely causes than prevents cancer.”

That Watson’s impassioned plea came on the heels of the annual cancer report was coincidental. He worked on the paper for months, and it represents the culmination of decades of thinking about the subject. Watson, 84, taught a course on cancer at Harvard University in 1959, three years before he shared the Nobel Prize in medicine for his role in discovering the double helix, which opened the door to understanding the role of genetics in disease.

Other cancer luminaries gave Watson’s paper mixed reviews.

“There are a lot of interesting ideas in it, some of them sustainable by existing evidence, others that simply conflict with well-documented findings,” said one eminent cancer biologist who asked not to be identified so as not to offend Watson. “As is often the case, he’s stirring the pot, most likely in a very productive way.”

There is wide agreement, however, that current approaches are not yielding the progress they promised. Much of the decline in cancer mortality in the United States, for instance, reflects the fact that fewer people are smoking, not the benefits of clever new therapies.

“The great hope of the modern targeted approach was that with DNA sequencing we would be able to find what specific genes, when mutated, caused each cancer,” said molecular biologist Mark Ptashne of Memorial Sloan-Kettering Cancer Center in New York. The next step was to design a drug to block the runaway proliferation the mutation caused.

But almost none of the resulting treatments cures cancer. “These new therapies work for just a few months,” Watson told Reuters in a rare interview. “And we have nothing for major cancers such as the lung, colon and breast that have become metastatic.”

The main reason drugs that target genetic glitches are not cures is that cancer cells have a work-around. If one biochemical pathway to growth and proliferation is blocked by a drug such as AstraZeneca’s Iressa or Genentech’s Tarceva for non-small-cell lung cancer, said cancer biologist Robert Weinberg of MIT, the cancer cells activate a different, equally effective pathway.

That is why Watson advocates a different approach: targeting features that all cancer cells, especially those in metastatic cancers, have in common.

One such commonality is oxygen radicals. Those forms of oxygen rip apart other components of cells, such as DNA. That is why antioxidants, which have become near-ubiquitous additives in grocery foods from snack bars to soda, are thought to be healthful: they mop up damaging oxygen radicals.

That simple picture becomes more complicated, however, once cancer is present. Radiation therapy and many chemotherapies kill cancer cells by generating oxygen radicals, which trigger cell suicide. If a cancer patient is binging on berries and other antioxidants, it can actually keep therapies from working, Watson proposed.

“Everyone thought antioxidants were great,” he said. “But I’m saying they can prevent us from killing cancer cells.”

Research backs him up. A number of studies have shown that taking antioxidants such as vitamin E do not reduce the risk of cancer but can actually increase it, and can even shorten life. But drugs that block antioxidants – “anti-antioxidants” – might make even existing cancer drugs more effective.

Anything that keeps cancer cells full of oxygen radicals “is likely an important component of any effective treatment,” said cancer biologist Robert Benezra of Sloan-Kettering.

Watson’s anti-antioxidant stance includes one historical irony. The first high-profile proponent of eating lots of antioxidants (specifically, vitamin C) was biochemist Linus Pauling, who died in 1994 at age 93. Watson and his lab mate, Francis Crick, famously beat Pauling to the discovery of the double helix in 1953.

One elusive but promising target, Watson said, is a protein in cells called Myc. It controls more than 1,000 other molecules inside cells, including many involved in cancer. Studies suggest that turning off Myc causes cancer cells to self-destruct in a process called apoptosis.

“The notion that targeting Myc will cure cancer has been around for a long time,” said cancer biologist Hans-Guido Wendel of Sloan-Kettering. “Blocking production of Myc is an interesting line of investigation. I think there’s promise in that.”

Targeting Myc, however, has been a backwater of drug development. “Personalized medicine” that targets a patient’s specific cancer-causing mutation attracts the lion’s share of research dollars.

“The biggest obstacle” to a true war against cancer, Watson wrote, may be “the inherently conservative nature of today’s cancer research establishments.” As long as that’s so, “curing cancer will always be 10 or 20 years away.”

http://www.reuters.com/article/2013/01/09/us-usa-cancer-watson-idUSBRE90805N20130109