Can Faith in God Help Alleviate Depression?

Story at-a-glance

• Modern, unhealthy lifestyles predispose you to non-alcoholic fatty liver disease which may lead to liver cancer. Recent research suggests that regular exercise reduces the risk of developing liver cancer
• Previous research has shown that breast and colon cancer patients who exercise regularly have half the recurrence rate than non-exercisers, and the cumulative evidence strongly indicates that exercise really should be part of standard cancer care
• Many recent studies have shown that exercise provides a level of protection against stress-related disorders and depression, and recent research demonstrates that these protective benefits are induced even if the exercise is forced as a mandatory part of a program, such as doctor’s orders, school curriculum or military service
• Mounting evidence shows that our healthcare and clinical guidelines are based in large part on fraudulent studies that report untruthful results in order to accommodate the interests of corporations. In one review, scientists could NOT replicate 47 of the 53 published studies—all of which were considered important and valuable for the future of cancer treatments

 

Can faith in a higher power help you overcome mental illness, the most common of which is depression? To find out, researchers at McLean hospital, a psychiatric institution affiliated with Harvard Medical School, asked 159 patients with prominent symptoms of depression how strongly they believed in a god.¹

They also asked how credible the patients thought their treatment was, and how effective they believed it would be in relieving their symptoms. The patients’ symptoms were assessed when admitted, and again upon release from the program.

Of the participants, 71 percent reported believing in a god or a higher power to some extent. Those whose belief in a god was stronger, regardless of the god or religious affiliation (including non-affiliation), were twice as likely to respond well to the treatment and experiencing better outcomes, such as:

• Lessening of depression
• Reductions in self-harm
• Increases in psychological well-being (peace of mind, ability to have fun, general satisfaction)

As reported by The Atlantic:²

“The researchers point out that people who believed in a god, or were affiliated with a religion, were also more likely to believe their psychiatric treatment was credible and to expect positive results.

It may be, they write, that ‘the tendency to have faith in conventional social constructs’ can be generalized both to religion and the medical establishment. Since other studies have shown that faith in a given treatment is an important predictor of its effectiveness, that could help explain the association with improved outcomes found here.”

The Stigma of Mental Illness Within the Church

The recent suicide of 27-year-old Matthew Warren,³ youngest son of Pastor Rick Warren, founder of the mega-church Saddleback Valley Community Church in California, brought mental illness back into view for many within the confines of religion.

NPR⁴ recently featured an interview with journalist and Evangelical Christian Christine Scheller on the sometimes complicated relationship between faith and mental illness. Scheller also lost her son to suicide five years ago.

While the stigma of mental illness does not cling to all denominations, some churches can tend to marginalize mental health problems and view them as issues that are best approached by reading the bible or praying.

In Scheller’s experience, the anti-psychiatry rhetoric used in some churches can delay much-needed treatment. When it became clear that Scheller’s younger son also suffered with depression, she decided to ignore the advice of the church, opting instead to seek professional help for her son.

“[S]tigma about mental illness is not unique to the evangelical community. We have our own particular ways in which it’s stigmatized, but it’s a pervasive problem,” she says.

Depressive Thinking Can Go Viral

In related research published in the journal Clinical Psychological Science, researchers suggest that certain types of depressive thinking can “go viral,” spreading to others living in close proximity. As reported in Time Magazine:⁶

“Although many people see depression as a chemical imbalance in the brain, scientists say social context and the way you see yourself and the world can be critical in causing and sustaining the illness… ‘Thinking styles are a really important factor in risk for depression,’ says the study’s lead author Gerald Haeffel, associate professor of clinical psychology at Notre Dame University. ‘How one thinks about life stress and negative moods is one of the best predictors that we have of future depression.’”

The two thinking styles explored in the study were:

• Rumination; constant brooding or worrying about what might go wrong
• Hopelessness

Both of these thinking styles have previously been linked to depression. But whereas the first places your focus on your negative mood, the other reflects on your lack of self worth and the consequences of an event. Says lead researcher Haeffel:

“For example, a person who feels hopeless might lose a job and see it as a personal failure and a sign that he will never be employable again. A more resilient person might blame the economy or see the situation as an opportunity to get a better position.”

The latter, hopelessness, was not found to be contagious, but rumination was. A suggested reason for this is because hopelessness centers around your own thoughts and deeply embedded beliefs about yourself, and so therefore may be less likely to have a major influence on the way others think about themselves and their lives. Ruminating and constant brooding, however, which focuses on all the bad things that might happen and sees the worst in every situation, is a mode that is more easily spread and mirrored by others.

“Interestingly, depression symptoms themselves were not contagious: simply having a roommate with symptoms of the disorder did not increase risk of developing the mental illness. But those who picked up a ruminative style of thinking from their roommates during the first three months of school had more than double the number of depressive symptoms of those who either weren’t exposed to this perspective or didn’t adopt the rumination three months later. And the risk was magnified if they experienced high levels of stress,” Time reports.

Positive Thinking Is Contagious Too!

Fortunately, the study also found that healthier modes of thinking were equally contagious, with the capacity to make a roommate adopt a more optimistic outlook as well. More than likely, you didn’t need a study to take notice of this. Most people will at some point or another have encountered someone in their life that either made you feel more positive or negative, simply by spending time with them.

A question they could not answer, however, was what the determining factor was that decided which roommate would adopt a thinking style more closely mirroring that of the other. Why are some people’s thinking styles more likely to dominate, rather than be influenced?

“Such information could enhance the current findings and contribute to new ways of treating and preventing depression,”Time writes. “The results suggest that depressive thinking styles can still be influenced during young adulthood — so this risk factor can be minimized even if it has already developed during high school or earlier. Targeting ruminative thinking might also enhance therapy.

“The therapist could assess if people in the patient’s life are modeling and providing adaptive cognitive feedback about stress and negative life events,” says Haeffel. “The therapist could then provide those with negative thinking styles with information about the contagion effect along with training that would help them identify negative thought patterns and provide examples of more adaptive ways of thinking.”

The Slow Opening Up to ‘Spiritual Science’

In 1993, only three of the United States’ 125 medical schools offered any sort of course work exploring the area of spirituality and medicine. Today, over 90 of these medical schools have formal courses where they explore randomized controlled studies and the effects of spiritual practices on longevity and health outcomes—a sure sign that what was once considered taboo is beginning to receive the discussion and serious investigation it deserves. Dr. Larry Dossey has written 11 books primarily focused on consciousness, spirituality, and the impact of spirituality on your health, including the book Healing Words: The Power of Prayer and the Practice of Medicine.

“I think we’re opening up,” Dossey said when I interviewed him, three years ago. “I’m sure you remember, about 40 years ago when meditation burst upon the scene in medicine, it was put down. It was called California Woo woo. Nobody wanted to have anything to do with it. But now nobody raises an eye about meditation and yoga, even in medicine. We’re in the same place with spirituality that we were with meditation about 20 years ago. People know you can’t ignore it. The correlation between spiritual practice and health outcomes is just too strong.

For example, the data shows that people who follow some sort of spiritual path in their life live on average seven to 13 years longer than people who do not follow a spiritual practice… We have a huge spectrum of data that shows, I think compellingly, that your thoughts really matter when it comes to getting well.”

Most ancient cultures knew this, and there are few lines dividing spirituality; the mind, and medicine in these cultures. Ironically, modern science now allows us to rediscover these ancient truths, which fell by the wayside with the advent of medical science and its narrow focus on individual parts as opposed to investigating the connections within the whole. Going back to where we started, David Rosmarin, the lead researcher of the featured study in which those with a stronger faith in God experienced far better treatment outcomes for their depression, said:

“Given the prevalence of religious belief in the United States — more than 90 percent of the population — these findings are important in that they highlight the clinical implications of spiritual life. I hope that this work will lead to larger studies and increased funding in order to help as many people as possible.”

The Rise of Energy Psychology

Many people avoid energy psychology as they believe it is an alternative form of New Age spirituality, yet nothing could be further from the truth. It is merely an advanced tool that can effectively address some of the psychological short circuiting that occurs in emotional illnesses. It is not any competition at all with any religion but merely an effective resource you can use with whatever spiritual belief you have.

My favorite technique for this is the Emotional Freedom Technique (EFT), which is the largest and most popular version of energy psychology.

EFT was developed in the 1990s by Gary Craig, a Stanford engineering graduate specializing in healing and self-improvement. It’s akin to acupuncture, which is based on the concept that a vital energy flows through your body along invisible pathways known as meridians. EFT stimulates different energy meridian points in your body by tapping them with your fingertips, while simultaneously using custom-made verbal affirmations. This can be done alone or under the supervision of a qualified therapist.⁷By doing so, you help your body eliminate emotional “scarring” and reprogram the way your body responds to emotional stressors.

While the following video will teach you how to do EFT, it is VERY important to realize that self-treatment for serious mental health issues is NOT recommended. For serious or complex issues, you need someone to guide you through the process as there is an incredible art to this process and it typically takes years of training to develop the skill to tap on deep-seated, significant issues.

Research Backs the Use of EFT for Depression

I have been a fan of energy psychology for many years, having witnessed its effectiveness in my medical practice and in my own personal life. However, studies have been few and far between as science has been trying to “catch up” with clinical experience. That has finally started to change. Several studies have been published in the last few years, showing just how safe and effective EFT really is.

For example, the following three studies show remarkable progress in a very short amount of time for people with a history of trauma:

1. A 2009 study⁸ of 16 institutionalized adolescent boys with histories of physical or psychological abuse showed substantially decreased intensity of traumatic memories after just ONE session of EFT.
2. An EFT study⁹ involving 30 moderately to severely depressed college students was conducted. The depressed students were given four 90-minute EFT sessions. Students who received EFT showed significantly less depression than the control group when evaluated three weeks later.
3. In a study of 100 veterans with severe PTSD¹⁰ (Iraq Vets Stress Project),¹¹ after just six one-hour EFT sessions, 90 percent of the veterans had such a reduction in symptoms that they no longer met the clinical criteria for PTSD; 60 percent no longer met PTSD criteria after only three EFT sessions. At the three-month follow-up, the gains remained stable, suggesting lasting and potentially permanent resolution of the problem.

Source: .mercola.com

 

New findings rejuvenate age-old drug development field.

On the internet, antiaging therapies abound. Longevity clinics peddle supplements and growth hormones. They advertise vitamin cocktails and antioxidant-rich diets. They offer chelation therapy. People who’ve tried such treatments talk glowingly of renewed vigor and rejuvenation. But none of these therapies have been shown definitively to make people live longer or dramatically improve health. Some can even cause harm.

The scientific literature contains even more experimental age-fighting therapies that have yet to fulfill their promise. That doesn’t mean the quest has been in vain, however. Over the past two decades, researchers have identified several pathways that seem to play a key part in longevity. The hope is that these pathways will lead to new drug treatments that slow the aging process and ward off age-related diseases such as cancer and Alzheimer’s.

But bringing therapies from the lab to the clinic won’t be easy. Here, Nature Medicine looks at the three of the most talked-about lines of investigation among scientists in the aging community.

Counting calories

Perhaps the surest path to longevity in lab models involves calorie restriction. Cutting calories seems to lengthen lifespans for protozoa, yeast, flies, worms, fish and mice. However, the data in primates are mixed. A 20-year study by researchers at the Wisconsin National Primate Research Center in Madison showed that calorie restriction could extend the lives of rhesus monkeys¹. But cutting calories failed to provide any survival benefit to monkeys in a 25-year study conducted at the US National Institute on Aging (NIA) Laboratory of Experimental Gerontology in Dickerson, Maryland². Why that might be isn’t entirely clear.

Demonstrating that calorie restriction extends age in humans will be even more difficult, considering the length and cost of such a trial. So, researchers have instead looked at the effects of calorie restriction on health outcomes that have been linked to aging, including body temperature, metabolic rate, inflammatory markers and insulin resistance. In 2007, the NIA funded three laboratories to look into some of these markers. The two-year study, which included 220 nonobese participants and wrapped up last year, compared a typical diet with one that curbed calories by 25%.

Trial results were scheduled to be released late last month (after Nature Medicine went to press) at the annual Experimental Biology meeting in Boston. The trial investigators, including Eric Ravussin, an obesity researcher at the Pennington Biomedical Research Center in Baton Rouge, Louisiana, declined to provide specifics ahead of time, although Ravussin says: “We reproduced a lot of the observations shown with caloric restriction in rodents.”

Rich Miller, associate director for research at the University of Michigan’s Geriatrics Center in Ann Arbor, sees no reason why calorie restriction shouldn’t extend longevity in humans, but it still may not be a feasible antiaging approach. In a world filled with a plethora of finger-licking combinations of fat, salt and sugar, few people would choose to cut their caloric intake by a quarter. Nonetheless, caloric restriction research has helped point researchers toward promising molecular pathways.

Sirtuins in the spotlight

One such mediator of caloric restriction is a family of proteins called sirtuins. Just over a decade ago, Leonard Guarente and his colleagues at the Massachusetts Institute of Technology in Cambridge showed that calorie restriction extends the lifespan of yeast, but the effect wasn’t present in mutants that lacked one of the sirtuin proteins, Sir2 (ref. 3). Guarente’s lab had already linked Sir2 to longevity in yeast, and this new research suggested a mechanism.

A media frenzy erupted in 2006 when a team led by one of Guarante’s former trainees, David Sinclair, a molecular biologist at Harvard Medical School in Boston, reported that a chemical found in red wine, known as resveratrol, appeared to make overweight mice live longer by activating SIRT1, the mammalian equivalent of Sir2 (ref. 4). The idea that swilling red wine might be the path to longer life was tantalizing, but Sinclair’s research soon came under fire. Some questioned whether the mouse model his team used was appropriate. Others couldn’t replicate parts of Sinclair’s results.

Sinclair published a rebuttal to the naysayers earlier this year in which his team outlined a proposed molecular pathway through which resveratrol acts⁵. Yet, even if resveratrol does in fact activate SIRT1, it does not seem to help healthy mice that aren’t obese live longer, according to two studies that supplemented standard mouse chow with varying doses of resveratrol beginning at 12 months of age^6, 7. “We tried two different doses at three different labs,” says David Harrison from the Jackson Laboratory in Bar Harbor, Maine, who led one of the studies as part of the NIA-funded Interventions Testing Program (ITP). “There was absolutely no hint of an effect.”

Sinclair admits that resveratrol is not very potent. “I do believe that we can do better,” he says. Sirtris Pharmaceuticals, a company Sinclair helped found in 2006 that was purchased by the UK drug giant GlaxoSmithKline two years later, has already developed several compounds designed to modulate SIRT1 that are structurally distinct from resveratrol. The lead candidate, SRT2104, has been tested in a phase 1 trial and seems to be safe⁸. Whether it will also prove effective in people still remains to be seen.

Rapamycin on trial

Although resveratrol failed to have an effect in normal mice, another immune-suppressing drug called rapamycin emerged victorious from the ITP. “To everyone’s delight, it had a big effect, the biggest effect of any of the compounds we’ve tested so far,” Harrison says. Administering rapamycin to mice in their food starting at nine months of age increased median survival by at least two months on average in males and about twice that in females⁷. Similar age extensions were seen in mice exposed to rapamycin from 20 months of age⁹. If rapamycin worked as well in humans as it did in these mice, “it would give us about ten more years of healthy lifespan,” Harrison says.

However, the effects weren’t all positive. The mice that received rapamycin had more severe cataracts and greater testicular damage than the control mice¹⁰. The drug, which is currently approved to prevent rejection in organ transplant recipients, also tends to increase the risk of infectious diseases and diabetes in people. So, physicians are reluctant to give rapamycin or any of its many mimics, known as rapalogs, to otherwise healthy individuals.

A study published last year by Joseph Baur, of the University of Pennsylvania Perelman School of Medicine in Philadelphia, and David Sabatini, of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, suggests there may be a way to separate the good effects from some of the bad. Rapamycin inhibits the protein mTOR, short for mammalian target of rapamycin, which exists as part of two separate complexes, mTORC1 and mTORC2. Rapamycin’s beneficial effects appear to be due to inhibition of mTORC1. However, Baur’s and Sabatini’s research suggests that the drug also disrupts mTORC2, and that this disruption may explain the insulin resistance seen in mice¹¹. A compound that targets only mTORC1 might have fewer side effects.

New leases on life

Aging researchers continue to test other potential life-extending compounds with demonstrated safety profiles. For example, Harrison and his ITP colleagues recently gave mice green tea extract, a component of the spice turmeric, a triglyceride commonly found in coconut oil and other health supplements with purported longevity benefits that are known to be safe in people, but they didn’t see any effect on life span in the animals¹². Now on the researchers’ plate is metformin, a drug used to treat type 2 diabetes. At an aging conference in San Antonio last year, Rafael de Cabo and his colleagues from the NIA reported that a low dose of metformin extended the lifespan of mice. A high dose, however, was toxic.

Developing an antiaging pill with absolutely no side effects may simply be unrealistic, notes Matt Kaeberlein, an aging researcher at the University of Washington in Seattle. “There are reasons why these mutations that slow aging are generally not selected for in nature,” he says. “They have costs associated with them.” How hefty those costs might be and whether society will be willing to pay them remains a question for the ages.

Source:Nature

 

 

 

Majority of children readmitted to hospital following transplant.

Nearly two-thirds of children receiving stem cell transplants returned to the hospital within six months for treatment of unexplained fevers, infections or other problems, according to a study performed at Dana-Farber/Children’s Hospital Cancer Center in Boston. Children who received donor cells were twice as likely to be readmitted as children who received their own stem cells.

“No one had ever looked at these data in children,” said Leslie E. Lehmann, MD, clinical director of pediatric stem cell transplantation at Dana-Farber/Children’s Hospital Cancer Center (DF/CHCC). “This is very important information and will allow us to counsel families appropriately, as well as try to devise interventions that reduce the rate of readmissions.”

The study by Lehmann and Harvard Medical School student David Shulman is being presented at the 26th annual meeting of the American Society of Pediatric Hematology Oncology in Miami, April 24-27.

A record review of 129 children from 2008 to 2011 revealed that 64 percent had at least one hospital readmission within 180 days of transplant. The source of the donor cells was a key predictor: 79 percent of patients receiving transplants from a related or unrelated donor were readmitted compared to 38 percent who received their own cells (autologous transplant). The mean number of readmissions was 2.4, indicating that for some children, discharge after transplant is just the beginning of a long process characterized by repeated hospital stays.

Fever without a documented source of infection accounted for 39 percent of the readmissions; 24 percent were for infections and 15 percent for gastrointestinal problems.

“Most of the patients went on to be successfully treated and ultimately did very well,” commented Lehmann.

“We hope these findings can eventually lead to identifying a group of low-risk children who could be managed at local hospitals rather than transplant centers, reducing costs and inconvenience to families.”

Lehmann said the goal is to identify which patients could be safely treated without requiring an admission to the hospital.

Source: Dana-Farber/Children’s Hospital Cancer Center

 

Sleeping pills could actually IMPROVE your memory, claims controversial new research.

 

• Researchers claim that the zolpidem in some sleeping pills enhances the brain’s ability to build-up memories
• They say the findings could help in the development of treatments for Alzheimer’s and dementia
• Contradicts previous research which found the drug may actually CAUSE memory loss

 

 

 

Taking sleeping tablets could help improve your memory, according to controversial new research.

 

A team of researchers claim to have discovered the mechanism that enables the brain to build-up memories – and say they found that a commonly prescribed sleeping tablet containing zolpidem enhances this process.

 

They hope the discovery could lead to new sleep therapies that could improve memory for ageing adults and those with dementia, Alzheimer’s and schizophrenia.

 

The findings contradict a wealth of previous research that has suggested that sleeping pills can have devastating effects on health, including memory.

 

The new research claims to have demonstrated, for the first time, the critical role that sleep spindles play in consolidating memory in the hippocampus.

 

Sleep spindles are bursts of brain activity that last for a second or less during sleep.

 

Earlier research found a link between sleep spindles and the consolidation of memories that depend on the hippocampus, the part of the brain that is involved in memory forming, organising, and storing.

 

The research team say they showed that the drugs could significantly improve that process, far more than sleep alone.

 

Lead author of the study, Dr Sara Mednick, a psychologist from the University of California Riverside, said: ‘We found that a very common sleep drug can be used to increase memory.

 

‘This is the first study to show you can manipulate sleep to improve memory.

 

‘It suggests sleep drugs could be a powerful tool to tailor sleep to particular memory disorders.’

 

But previous research has suggested that sleeping pills taken by more than a million Britons significantly increase the risk of dementia.

 

Pensioners who used benzodiazepines – which include temazepam and diazepam – are 50 per cent more likely to succumb to the devastating illness, a Harvard University study found.

 

They work by changing the way messages are transmitted to the brain, which induces a calming effect but scientists believe that at the same time they may be interfering with chemicals in the brain known as neurotransmitters, which may be causing dementia.

 

The new study tested normal sleepers, who were given varying doses of sleeping pills and placebos, allowing several days between doses to allow the drugs to leave their bodies.

 

Researchers monitored their sleep, measured sleepiness and mood after napping, and used several tests to evaluate their memory.

 

They found that zolpidem significantly increased the density of sleep spindles and improved verbal memory consolidation.

 

Dr Mednick said: ‘Zolpidem enhanced sleep spindles in healthy adults producing exceptional memory performance beyond that seen with sleep alone or sleep with the comparison drug.

 

‘The results set the stage for targeted treatment of memory impairments as well as the possibility of exceptional memory improvement above that of a normal sleep period.’

 

Dr Mednick also hopes to study the impact of zolpidem on older adults who experience poor memory because individuals with Alzheimer’s, dementia and schizophrenia are known experience decreases in sleep spindles.

 

Dr Mednick, who began studying sleep in the early 2000s, says sleep is a very new field of research and its importance is generally not taught in medical schools.

 

‘We know very little about it,’ she said.

 

‘We do know that it affects behaviour, and we know that sleep is integral to a lot of disorders with memory problems.

 

‘We need to integrate sleep into medical diagnoses and treatment strategies. This research opens up a lot of possibilities.’

 

Source: http://www.dailymail.co.uk

 

 

 

Quitting smoking ‘cuts heart risk despite weight gain’.

Stopping smoking cuts the risk of heart disease even if it leads to significant weight gain, a US study says.

Researchers writing in the Journal of the American Medical Association say the prospect of weight gain makes some smokers reluctant to stop.

But they say quitting has a “positive effect on cardiovascular risk“.

The health gains from giving up were most marked in people who did not have diabetes, but people with the condition were still said to have benefited.

 “Start Quote

If you’re keen to quit smoking but worried about putting on weight, using smoking cessation aids such as inhalators, gum, or lozenges may help you resist the temptation to reach for comfort food in the place of a cigarette”

Doireann Maddock of the British Heart Association

Obesity is a risk factor in heart disease, leading past research to examine whether weight gain might cancel out some of the benefits of quitting smoking.

Studies suggest people who stop smoking gain on average 6-13lb (2.7-5.9kg) over the first six months.

The JAMA research looked at the smoking habits and heart health of more than 3,000 people between 1981 and 2011.

Former smokers who had stayed away from tobacco for more than four years had a 54% lower risk of heart and artery disease than smokers.

Recent quitters who had stopped smoking for up to four years experienced almost the same benefit with a 53% lower relative risk.

This was despite recent quitters typically gaining 5-10lb over a period of four years, and long-term quitters 1-2lb.

Dr James Meigs, one of the authors of the study at Harvard Medical School, said: “We can now say without question that stopping smoking has a very positive effect on cardiovascular risk for patients with and without diabetes, even if they experience moderate weight gain.”

Doireann Maddock, senior cardiac nurse at the British Heart Foundation said weight gain should not deter smokers from quitting.

“If you’re keen to quit smoking but worried about putting on weight, using smoking cessation aids such as inhalators, gum, or lozenges may help you resist the temptation to reach for comfort food in the place of a cigarette.”

Source:BBC

 

 

Cherries May Prevent Gout Flares.

Patients with gout were less likely to report acute attacks after 2 days of eating cherries or imbibing cherry extract than during periods after no cherry intake, according to data reported in Arthritis & Rheumatism by Yuqing Zhang, DSci, and colleagues from Boston University School of Medicine in Massachusetts.

Dr. Zhang, who is professor of medicine and epidemiology at Boston University School of Medicine, told Medscape Medical News that cherry intake during a 2-day period was associated with a 35% lower risk for gout attacks and that cherry extract intake was associated with a 45% lower risk.

Risk for gout attacks was reduced by 75% when cherry intake was combined with allopurinol use. Dr. Zhang said, “We found that if subjects took allopurinol alone, it reduced the risk of gout attack by 53%; if subjects took cherry alone, it reduced the risk by 32%; if they took both, the risk of gout attack was reduced by 75%.”

These associations were discovered in a case-crossover study of 633 individuals with physician-diagnosed gout who were prospectively recruited and followed online for 1 year. When a participant reported a gout attack, the researchers asked about the onset date of the gout attack, symptoms and signs, medications, and potential risk factors (including daily intake of cherries and cherry extract) during the 2 days before the attack. Patients served as their own controls, so the same information was assessed for 2-day control periods not associated with gout attacks. A cherry serving was defined as one-half cup or 10 to 12 cherries.

Participants had a mean age of 54 years; 88% were white and 78% were male. Of patients with some form of cherry intake, 35% ate fresh cherries, 2% ingested cherry extract, and 5% consumed both fresh cherry fruit and cherry extract. Researchers documented 1247 gout attacks during the 1-year follow-up period, with 92% occurring in the joint at the base of the big toe.

Factors associated with increased serum uric acid levels, such as increased alcohol consumption and purine intake, or use of diuretics, were associated with increased risk for recurrent gout attacks.

“Our findings indicate that consuming cherries or cherry extract lowers the risk of gout attack,” Dr. Zhang said in a press release. “The gout flare risk continued to decrease with increasing cherry consumption, up to three servings over two days.” Further cherry intake was not associated with additional benefit.

“However, the protective effect of cherry intake persisted after taking into account patients’ sex; body mass (obesity); purine intake; and use of alcohol, diuretics, and antigout medications,” according to the release.

The authors speculate that cherries may decrease serum uric acid levels by increasing glomerular filtration or reducing tubular reabsorption. They also note that cherries and cherry extract contain high levels of anthocyanins, which possess anti-inflammatory properties.

Dr. Zhang told Medscape Medical News, “While our study findings are promising, randomized clinical trials should be conducted to confirm whether cherry products could provide a nonpharmacological preventive option against grout attacks. Until then we would not advocate on the basis of the current findings that individuals who suffer from gout abandon standard therapies and opt for cherry extract products as an alternative.”

In an accompanying editorial, Allan Gelber, MD, from Johns Hopkins University School of Medicine in Baltimore, Maryland, and Daniel Solomon, MD, from Brigham and Women’s Hospital and Harvard University Medical School in Boston, write that the findings are promising but reiterates the need for randomized clinical trials to confirm that consumption of cherry products could prevent gout attacks.

Dr. Gelber told Medscape Medical News, “For the patient who asks his/her doctor ‘Doc, what can I do, myself, to decrease my chance of developing another gout attack, above and beyond the medications you have prescribed for me?’ our response would include that one of the options is dietary modification. Previously, physician recommendations included advocating for moderation in alcohol consumption, weight reduction, and decreasing high-purine foods from the diet…but now there are new data supporting a beneficial role in eating cherries to reduce one’s risk for recurrent gout attacks.”

Dr. Gelber noted that the most definitive support for the recommendation to eat cherries as a strategy to reduce gout risk would come from a randomized clinical trial. “Just as with new medications that come down the pipeline, dietary interventions ought also be subject to the rigor of a clinical trial. Such a study could be undertaken. There is logistical challenge to undertaking such a trial since cherry fruit is broadly available. But, in a controlled setting, such a trial would be feasible,” he said.

Source: Mescape.com

 

 

 

Role of exercise in cancer patients.

Mounting evidence shows that exercise can not only help cancer patients get well but also help keep their cancer from recurring. Yet, few oncologists tell their patients to engage in exercise beyond their simple daily, normal activities.

And many cancer patients are reluctant to exercise, or even discuss it with their oncologist.

A recent study¹ by the Mayo Clinic investigated exercise habits among cancer patients and their clinicians’ roles in providing related counseling, and found that:

“Participants overwhelmingly cited usual daily activities as their source of ‘exercise.’ Symptoms, particularly treatment-related, discouraged participation, with fear of harm being a significant concern only among younger women. Exercise was recognized as important for physical and mental well-being, but seldom as a means to mitigate symptoms.

…Although respondents preferred to receive guidance from their oncologist, none reported receiving more than general encouragement to ‘stay active.’ A lack of direction was typically accepted as a sanction of their current activity levels. Participants appeared less receptive to guidance from ancillary health professionals.”

An Important Conversation You’d Be Wise to Have With Your Oncologist

Fear that exercise might be harmful appears to be largely unfounded, though it’s certainly understandable. It can be difficult to be enthusiastic about exercise if you struggle with nausea, fatigue, and other detrimental side effects from the treatment. However, it may be helpful to focus on the benefits you can reap from exercise. For example, research has shown that exercising during and after cancer treatment can:

• Reduce your risk of dying from cancer
• Reduce your risk of cancer recurrence
• Boost energy and minimize the side effects of conventional cancer treatment (see additional listing below)

The fact that most oncologists overlook this vital aspect of their patients’ care is highly unfortunate, especially considering how most patients defer to their recommendations. However, it’s not unexpected. Conventional doctors are trained to prescribe drugs, not exercise.

Ideally, they’d prescribe exercise in the same manner drugs are prescribed – in specific “doses” and intervals. To do this properly, oncologists would be wise to develop relationships with personal trainers, and prescribe training sessions for their patients. If you have cancer, I would highly recommend discussing exercise with your oncologist, and/or work with a trained fitness professional who can help you devise a safe and effective regimen.

Exercise Needs to Be Part of Standard Cancer Care

A recent report issued by the British organization Macmillan Cancer Support² argues that exercise really should be part of standard cancer care. It recommends that all patients getting cancer treatment should be told to engage in moderate-intensity exercise for two and a half hours every week, stating that the advice to rest and take it easy after treatment is an outdated view.

According to Ciaran Devane, chief executive of Macmillan Cancer Support:⁴

“Cancer patients would be shocked if they knew just how much of a benefit physical activity could have on their recovery and long term health, in some cases reducing their chances of having to go through the grueling ordeal of treatment all over again…”

Indeed, the reduction in risk for recurrence is quite impressive. Previous research has shown that breast and colon cancer patients who exercise regularly have half the recurrence rate than non-exercisers.⁵ Macmillan Cancer Support also notes that exercise can help you to mitigate some of the common side effects of conventional cancer treatment, including:

Reduce fatigue and improve your energy levels	Manage stress, anxiety, low mood or depression	Improve bone health
Improve heart health (some chemotherapy drugs and radiotherapy can cause heart problems later in life)	Build muscle strength, relieve pain and improve range of movement	Maintain a healthy weight
Sleep better	Improve your appetite	Prevent constipation

How Exercise Can Improve Cancer Outcome

This topic is near and dear to my heart, as I went to medical school in large part because I wanted to use exercise as a therapeutic tool to help people get healthier. I strongly believe that without fitness, it is virtually impossible to achieve optimal health. Lack of exercise can also severely hamper your recuperative efforts once disease has set in.

A 2005 study⁶ by researchers at Harvard Medical School found that breast cancer patients who exercise moderately for three to five hours a week cut their odds of dying from cancer by about half, compared to sedentary patients. In fact, any amount of weekly exercise increased a patient’s odds of surviving breast cancer. This benefit remained constant regardless of whether women were diagnosed early on or after their cancer had spread.

Similarly, researchers investigating the impact of physical activity on cancer recurrence and survival in patients with stage III colon cancer found those who were more active cut their risk of recurrence in half.⁷

One of the primary reasons exercise works to lower your cancer risk is because it drives your insulin levels down, and controlling your insulin levels is one of the most powerful ways to reduce your cancer risks. It’s also been suggested that apoptosis (programmed cell death) is triggered by exercise, causing cancer cells to die. This theory was demonstrated in two studies published in 2006. In one, mice who used running wheels developed fewer and smaller skin tumors.⁸ The second study found that exercise reduced the number and size of intestinal polyps.⁹

The studies also found that the number of tumors decreased along with body fat, which may be an additional factor. This is because exercise helps lower your estrogen levels, which explains why exercise appears to be particularly potent against breast cancer.

If you’re male, be aware that athletes have lower levels of circulating testosterone than non-athletes, and similar to the association between estrogen levels and breast cancer in women, testosterone is known to influence the development of prostate cancer in men. Strength training may be of particular benefit. In one 2009 study¹⁰, men who regularly worked out with weights and had the highest muscle strength were between 30 percent and 40 percent less likely to lose their life to a deadly tumor.

Other research has shown:

• Exercising moderately for six hours a week may reduce colorectal cancer mortality¹¹
• Three hours per week of moderate-intensity physical activity may lower risk of prostate cancer mortality by about 30 percent¹², and lower the rate of disease progression by 57 percent¹³

Of course, exercise also improves the circulation of immune cells in your blood, whose job it is to neutralize pathogens throughout your body. The better these cells circulate, the more efficient your immune system is at locating and defending against viruses and diseases, including cancer, trying to attack your body.

Exercise Tips for Cancer Patients

I would strongly recommend you read up on my Peak Fitness program, which includes high-intensity exercises that can reduce your exercise time while actually improving your benefits.

Now, if you have cancer or any other chronic disease, you will of course need to tailor your exercise routine to your individual circumstances, taking into account your fitness level and current health. Often, you will be able to take part in a regular exercise program – one that involves a variety of exercises like strength training, core-building, stretching, aerobic and anaerobic – with very little changes necessary. However, at times you may find you need to exercise at a lower intensity, or for shorter durations.

Always listen to your body and if you feel you need a break, take time to rest. But even exercising for just a few minutes a day is better than not exercising at all, and you’ll likely find that your stamina increases and you’re able to complete more challenging workouts with each passing day. In the event you are suffering from a very weakened immune system, you may want to exercise at home instead of visiting a public gym. But remember that exercise will ultimately help to boost your immune system, so it’s very important to continue with your program, even if you suffer from chronic illness or cancer.

Intense Workouts May Also Be Safe for Heart Patients

Another group of people often discouraged from exercise are those suffering with heart problems, but even here the mindset is starting to change. In an about-face in the way patients recovering from heart attacks or heart surgery are typically treated, a new study¹⁴ suggests high-intensity workouts may in fact be a safe choice. The study followed 4,800 Norwegian heart patients who did aerobics. Only three cardiac arrests occurred in over 170,000 hours of intensive exercise in these patients.

According to Reuters:¹⁵

“The number was too small to say for sure that high impact workouts are just as safe as moderate ones, but they show the overall risk of exercise bringing on cardiac arrest is fairly low, according to the authors. There is plenty of evidence that the harder people work out, the more benefit they gain in cardiovascular function, said Oeivind Rognmo, a researcher at the Norwegian University of Science and Technology in Trondheim and lead author of the study…”

The participants completed both moderate- and high-intensity workouts, spending a combined total of 129,456 hours working out at moderate intensity and 46,364 hours at high intensity. Moderate intensity workouts included an hour of walking, or other exercises resulting in exertion at 60-70 percent of maximum heart rate. The high-intensity workouts consisted of four-minute-intervals (cycling, running, or cross country skiing), pushing their heart rate up to 85-95 percent of maximum, followed by four-minute-long rest periods.

During the more than 129,000 combined hours of moderate exercise, one person died from cardiac arrest. And during over 46,000 combined hours of high-intensity workouts, two suffered cardiac arrest during or within an hour of exercise, but both survived. According to the lead author:¹⁶

“We found that both types of intensities were associated with low event rates… I think (high-intensity training) should be considered for patients with coronary heart disease.”

Remember to Listen to Your Body

One of the key principles I teach and believe in is to listen to your body. This applies no matter what your current state of health is. If your body will not allow you to exercise, either due to pain or worsening of your underlying condition, then you have no practical option but to honor your body’s signals and exercise less.

Even though your body desperately needs the exercise to improve, you will only get worse if you violate your current limitations. So you may have to start with as little as just minutes a day. That’s okay. As your body gradually improves so will your tolerance to exercise, and you’d be wise to do as much as your body will allow in order to achieve a high level of health.

Additional Strategies to Help Prevent Cancer

While exercise is an important facet of cancer prevention and treatment, it’s certainly not the only one. I believe the vast majority of all cancers could be prevented by strictly applying the healthy lifestyle recommendations below:

• Avoid sugar, especially fructose. All forms of sugar are detrimental to health in general and promote cancer. Fructose, however, is clearly one of the most harmful and should be avoided as much as possible.
• Optimize your vitamin D. Vitamin D influences virtually every cell in your body and is one of nature’s most potent cancer fighters. Vitamin D is actually able to enter cancer cells and trigger apoptosis (cell death). If you have cancer, your vitamin D level should be between 70 and 100 ng/ml. Vitamin D works synergistically with every cancer treatment I’m aware of, with no adverse effects. I suggest you try watching my one-hour free lecture on vitamin D to learn more.
• Avoid charring your meats. Charcoal or flame broiled meat is linked with increased breast cancer risk. Acrylamide – a carcinogen created when starchy foods are baked, roasted or fried – has been found to increase cancer risk as well.
• Avoid unfermented soy products. Unfermented soy is high in plant estrogens, or phytoestrogens, also known as isoflavones. In some studies, soy appears to work in concert with human estrogen to increase breast cell proliferation, which increases the chances for mutations and cancerous cells.
• Improve your insulin receptor sensitivity. The best way to do this is by avoiding sugar and grains and making sure you are exercising, especially with Peak Fitness.
• Maintain a healthy body weight. This will come naturally when you begin eating right for your nutritional type and exercising. It’s important to lose excess body fat because fat produces estrogen.
• Drink a quart of organic green vegetable juice daily. Please review my juicing instructions for more detailed information.
• Get plenty of high quality animal-based omega-3 fats, such as krill oil. Omega-3 deficiency is a common underlying factor for cancer.
• Curcumin. This is the active ingredient in turmeric and in high concentrations can be very useful adjunct in the treatment of cancer. For example, it has demonstrated major therapeutic potential in preventing breast cancer metastasis.¹⁷ It’s important to know that curcumin is generally not absorbed that well, so I’ve provided several absorption tips here.
• Avoid drinking alcohol, or at least limit your alcoholic drinks to one per day.
• Avoid electromagnetic fields as much as possible. Even electric blankets can increase your cancer risk.
• Avoid synthetic hormone replacement therapy, especially if you have risk factors for breast cancer. Breast cancer is an estrogen-related cancer, and according to a study published in the Journal of the National Cancer Institute, breast cancer rates for women dropped in tandem with decreased use of hormone replacement therapy. (There are similar risks for younger women who use oral contraceptives. Birth control pills, which are also comprised of synthetic hormones, have been linked to cervical and breast cancers.)

If you are experiencing excessive menopausal symptoms, you may want to consider bioidentical hormone replacement therapy instead, which uses hormones that are molecularly identical to the ones your body produces and do not wreak havoc on your system. This is a much safer alternative.

• Avoid BPA, phthalates and other xenoestrogens. These are estrogen-like compounds that have been linked to increased breast cancer risk
• Make sure you’re not iodine deficient, as there’s compelling evidence linking iodine deficiency with certain forms of cancer. Dr. David Brownstein¹⁸, author of the book Iodine: Why You Need It, Why You Can’t Live Without It, is a proponent of iodine for breast cancer. It actually has potent anticancer properties and has been shown to cause cell death in breast and thyroid cancer cells.

The organization offers loads of helpful information about the benefits of exercise for cancer patients on their website, and also has a number of videos on the subject, available on their YouTube channel.

^{URL: http://www.youtube.com/watch?feature=player_embedded&v=mut3RTiVfD0}

 

^Source: Dr. Mercola

 

 

 

 

 

Building a Biobank to Explore Mysteries of the Genome.

GTEx is collecting multiple tissue samples from an estimated 1,000 individual donors for genetic research. (Image from the National Disease Research Interchange GTEx Team)

The architects of the biobank wanted nothing left to chance and everything well documented.

That’s why they developed 150 standard operating procedures to ensure that tissue samples were collected, processed, and stored in exactly the same way. And that’s why they are collecting data on the best temperatures for shipping the samples across the United States.

All that planning is paying off for the Genotype-Tissue Expression (GTEx) project, which will use the samples to investigate how genes are regulated in health and disease. Sponsored by the National Institutes of Health (NIH), the project has nearly 4,400 samples of “normal” human tissue from about 175 donors. By collecting many more samples, the project aims to be a resource for studying genetic variation and the regulation of genes in specific tissues.

“This project is an attempt to understand how normal genetic variation influences the expression of genes throughout the body,” said the study’s leader, Dr. Jeffery Struewing of the National Human Genome Research Institute. NCI and the National Institute of Mental Health are also playing lead roles in the effort.

Normal tissue—that is, tissue with no signs of disease—is not routinely collected for research. GTEx is the first large-scale project to collect high-quality samples of up to 32 tissue types from many individual donors.

During a pilot study that began last year, investigators with NCI’s cancer Human Biobank (caHUB) and their collaborators were responsible for acquiring and managing the biospecimens. On average, each organ and tissue donor has contributed 25 types of postmortem tissue, including heart, muscle, and skin. Surgical donors have also contributed tissues.

A Bigger Biobank

Based on the success of the pilot, the NIH Common Fund is scaling up GTEx, with a goal of reaching 1,000 donors in 3 years. This larger number of donors and samples will provide the statistical power that is needed to ask fundamental questions about the genome, the researchers said.

All cells in the human body contain essentially the same complement of genes, but these genes are activated, or expressed, differently in different types of cells. For the first time, GTEx will allow researchers to investigate how common genetic variants influence the regulation of gene expression using a set of reference tissues.

The relationship between genetic variants and gene regulation in different tissues is “a fascinating biology question, but it is also relevant in medicine,” said Dr. Barbara Stranger of Harvard Medical School and Brigham and Women’s Hospital, who studies genes and complex diseases but is not involved in GTEx.

“Healthy individuals will have some of the same regulatory processes as people with a complex disease,” Dr. Stranger continued. Understanding these processes could provide information about a variety of diseases.

Donors and Families

“No one really knew if this would work,” said Dr. Sherilyn Sawyer, who co-led the development of the GTEx biobank and until recently was part of NCI’s Office of Biorepositories and Biospecimen Research (OBBR). “So we’re ecstatic that the infrastructure we put in place through caHUB has resulted in the specimens that have produced an amazing collection of data.”

GTEx works with organizations involved in tissue and organ donation in several cities. When an organ or tissue donor who is eligible for GTEx passes away, one of these organizations contacts the deceased person’s family to ask permission to collect tissues from their loved one for the study.

“It’s a sensitive time, so care is taken,” said Anna M. Smith of the Frederick National Laboratory for Cancer Research, who works on ethical, legal, and regulatory affairs for GTEx. “It goes without saying that there would be no biobank without the donors and families.”

 

GTEx minimizes changes to tissue by using standard procedures to collect, process, and store the samples. (Image from the National Disease Research Interchange GTEx Team)

Once specimens are collected, they are preserved and shipped to the Van Andel Institute in Grand Rapids, MI, which is the central repository of materials. By collecting, processing, and storing the tissue samples in a controlled and uniform way, the researchers hope to maintain them in a nearly natural state and minimize alterations.

“The quality of the biospecimen is extraordinarily important,” said Dr. Sawyer. Collecting tissues with uniformly high RNA and DNA quality helps ensure that the information gained from analyzing the samples will “be as accurate to the biology of the tissues as possible,” she explained.

GTEx staff regularly scrutinize tissue samples to be sure that they are of high quality. “GTEx has a higher degree of quality-control management over the whole process than other projects we have done,” noted Dr. Scott Jewell, who directs the Program for Biospecimen Science at the Van Andel Institute.

Whether the same amount of quality control that went into GTEx will be required for all biobank projects is not yet known, Dr. Jewell added. But the lessons learned from GTEx could guide future efforts. Toward this end, researchers have released approximately 150 standard operating procedures related to biobanking.

Logistical Challenges

“This project turned out to be a hugely complex logistical challenge,” said Dr. Jim Vaught, deputy director of OBBR. But with these challenges have come opportunities to ask important questions about biobanking.

For example, no one knows the best temperatures for shipping biospecimens. The GTEx team developed shipping containers that have “data loggers” to record the temperature at every minute. These data could help reveal the optimal temperatures for shipping biospecimens.

A Universe of Data

The GTEx project will more than triple its pool of donors in the next 3 years. Success will depend on a robust and flexible information technology system, noted Charles Shive, director of software development at the Frederick National Laboratory for Cancer Research.

A web-based application developed by Shive and his colleagues allows project members with various levels of access to data to communicate and monitor the progress of specimen processing and data collection in real time. “We know where specimens are at all times in the GTEx pipeline,” said Shive.

Pathologists review images of all tissue samples to assess the quality of biospecimens. Using the web application, pathologists can add their comments to “the universe of data associated with each sample,” Shive said.

“Unless the research is done and the data are generated, no one is ever going to know the answers,” said Smith.

Another question GTEx could help answer is how long tissues remain scientifically useful after the blood flow to an organ has been cut off. During the pilot study, GTEx researchers at the Broad Institute, in Cambridge, MA, observed a drop-off in RNA quality that was linked to the interval between death and tissue collection. Degradation depends on the type of tissue and how much time has passed since blood flow to the tissue ceased, the researchers found.

“For some tissues, the RNA will stay good for many hours after blood flow to the organ stops,” said Dr. Wendy Winckler, co-leader of the Broad GTEx team, which conducts molecular studies, including RNA sequencing. “But in the pancreas and the spleen, for example, if you don’t get the tissue within a few hours [after death] you’re not going to get [useful RNA].”

Despite these challenges, the researchers are optimistic. “Getting biospecimens for any research project is a tremendous challenge,” said Dr. Kristin Ardlie, also a leader of the GTEx work at the Broad. “We’ve been surprised by how well the process has worked in this project.”

The Broad researchers deposit their data quarterly in the database of Genotypes and Phenotypes (dbGP). Investigators can apply for access to the data, which have been stripped of identifying information to protect the anonymity of the donors. In addition, the project plans to make extra samples available to researchers in 2013.

Many Questions to Explore

GTEx data will likely be used to interpret genome-wide association studies. In recent years, these studies have identified inherited genetic variants associated with common diseases. The variants, however, often map to regions of the genome that lack genes, raising questions among researchers about how the variants influence disease risk.

A logical explanation could be that these variants influence the regulation of genes and thereby increase (or decrease) the risk of disease.

“Many common variants associated with common human diseases may be more about affecting the regulation of gene expression than about changing protein structure,” said Dr. Nancy Cox of the University of Chicago, who is developing statistical tools for analyzing data generated by GTEx. “This is one reason we believe the GTEx project is so important.”

With samples of so many tissues, GTEx could also help researchers look at changes in gene expression throughout the body. “A disease process might not be limited to one particular cell type or tissue type,” said Dr. Stranger.

“People will be using data from this project for a long time and in different ways,” she added. “There are all kinds of people waiting to see the GTEx results.”

Watch the video on youtube: URL  http://www.youtube.com/watch?feature=player_embedded&v=MLlqYdu6jY4

 

Source: NCI

Lung Cancer Genome Surveys Find Many Potential Drug Targets.

Five new studies have identified genetic and epigenetic alterations in hundreds of lung tumors, including many changes that could be targeted by drugs that are already available or in clinical testing.

The reports, all published this month, included genomic information on more than 400 lung tumors. In addition to confirming genetic alterations previously tied to lung cancer, the studies identified other changes that may play a role in the disease. (Links to the study abstracts appear in the sidebar below.)

“These five papers are the first major salvo of genome-wide studies using all of the newest technologies to analyze a large number of lung cancers,” said Dr. John Minna, a clinician and lung cancer researcher at the University of Texas Southwestern Medical Center, who co-authored one of the studies.

Collectively, the studies covered the main forms of the disease—lung adenocarcinomas, squamous cell cancers of the lung, and small cell lung cancers.

Although preliminary, the findings could be used to develop molecular markers for identifying patients who are candidates for certain targeted drugs. At the same time, researchers in the lab can now evaluate the newly discovered changes to identify novel potential therapeutic targets.

“All of these studies say that lung cancers are genomically complex and genomically diverse,” said Dr. Matthew Meyerson of Harvard Medical School and the Dana-Farber Cancer Institute, who co-led several of the studies, including a large-scale analysis of squamous cell lung cancer by The Cancer Genome Atlas (TCGA) Research Network.

Some genes, Dr. Meyerson noted, were inactivated through different mechanisms in different tumors. He cautioned that little is known about alterations in DNA sequences that do not encode genes, which is most of the human genome.

Squamous Cell Tumors

The TCGA investigators sequenced the genomes or exomes (the protein-coding regions of DNA) of tumor samples from 178 patients with squamous cell lung cancer. In more than half of the tumors examined, the researchers found a change to a gene or a signaling pathway that is targeted by a drug that exists or is in development. The findings were reported in Nature on September 9.

“This gives us an enormous opportunity for progress in this disease,” said Dr. Meyerson.

The TCGA model integrates genomic data for squamous cell lung cancers with clinical information, when available, and with other tumor characteristics, such as gene expression, epigenetic changes to cells, and alterations in the number of gene copies.

“The framework for these five studies was built on a convergence of new technologies and the need to better understand the biology of lung cancers as it relates to new therapies for our patients,” said Dr. Paul Paik, who treats patients with lung cancer at Memorial Sloan-Kettering Cancer Center and was part of the clinical team involved in TCGA.

Small studies (for example, here and here) have provided hints that certain signaling pathways are important in squamous cell lung cancers, leading to new trials of targeted drugs. “Now, with the publication of the TCGA study, we know that squamous cell lung cancers have a myriad of potentially targetable changes,” Dr. Paik noted.

An unexpected finding was the presence of mutations in the EGFR gene in about 1 percent of squamous cell tumors. These tumors might respond to available drugs that block signals through the EGFR pathway.

The researchers also found evidence of genetic changes that may help lung cancer cells evade surveillance by the immune system.

The Five Studies

• Comprehensive Genomic Analysis Identifies SOX2 as a Frequently Amplified Gene in Small Cell Lung Cancer (Nature Genetics)
• Integrative Genome Analyses Identify Key Somatic Driver Mutations of Small Cell Lung Cancer (Nature Genetics)
• Comprehensive Genomic Characterization of Squamous Cell Lung Cancers (Nature)
• Genomic Landscape of Non-Small Cell Lung Cancer in Smokers and Never-Smokers (Cell)
• Mapping the Hallmarks of Lung Adenocarcinoma with Massively Parallel Sequencing (Cell)

Testing Lung Tumors

Any therapeutic targets to emerge from the new reports would need to be incorporated into molecular tests that can identify candidates for certain drugs. A leader in this work is the Lung Cancer Mutation Consortium, which has been building knowledge of the mutations associated with the disease and testing for these changes.

Many patients with lung adenocarcinomas have benefited from targeted drugs. Crizotinib (Xalkori), for instance, has elicited some dramatic responses in patients whose tumors harbor a particular gene fusion. Some medical centers now routinely test tumors before selecting treatment for patients with lung adenocarcinomas.

“If you look at lung cancer as a whole, the big therapeutic targets were first identified in adenocarcinomas,” Dr. Minna explained. “Now there are new targeted therapies that could make an impact on squamous cell lung cancer.”

At Memorial Sloan-Kettering, all patients with squamous cell lung cancer have their tumors tested for drug targets using various techniques, including DNA sequencing. Among 28 of these patients evaluated recently, more than 60 percent had tumors that contained a potential target.

Dr. Paik noted that his group will use the TCGA results to expand their testing. “In a sense, the future potential of this new work is being realized now,” he said. “That’s pretty exciting.”

Small Cell Lung Cancer

Two new reports describe genetic changes in small cell lung cancers, which tend to be aggressive and about which little has been known. The research teams conducted exome or whole-genome sequencing on a total of 82 samples of such tumors.

“This study gave us a host of new targets to explore,” said Dr. Charles Rudin of the Johns Hopkins Kimmel Cancer Center, who led one study. The next steps will be to validate which targets are driving the growth of tumors and are “druggable,” he added.

The researchers found that a gene called SOX2, which plays a role in normal development, may contribute to some small cell lung cancers, as well as other cancers, and could be targeted.

Small cell lung cancers have been challenging to study because most are not treated surgically, so tumor samples are rare. What’s more, these tumors have high rates of genetic mutations due to tobacco smoke, yet only some mutations are driving the disease, noted Dr. Roman Thomas of the University of Cologne in Germany, who led the other study.

Using statistical “filters,” his group found that genes involved in modifying histone proteins, which help package DNA within a cell, were frequently mutated in the disease.

“These cancers are extraordinarily complex, so as researchers our steps forward are incremental—but, still, they are steps,” Dr. Thomas noted. “No one would have imagined that lung cancer would be the prototypical disease for targeted medicine.”

Comparing Tumors in Smokers and Nonsmokers

Non-small cell lung cancers were the focus of two additional studies, which appeared in Cell. One group sequenced the exomes or genomes of 183 tumor samples, and the other conducted whole-genome sequencing of tumor tissues from 17 smokers and nonsmokers.

“We found a substantially lower number of mutations in the genomes of tumors from nonsmokers compared to the smokers,” said Dr. Ramaswamy Govindan of the Washington University School of Medicine in St. Louis, MO, who led the study. Five study participants who had never smoked had a mutation that could be targeted by an existing drug.

All these studies show how diverse and how complicated the cancer genome is. But we now have a panoramic view of the genomic landscape, and this is important for moving forward in this disease.

—Dr. Ramaswamy Govindan

In all, the study authors found 54 genes with potentially targetable alterations in the 17 patients.

“The days of large clinical trials for lung cancer are over,” Dr. Govindan said, noting that patients need to be selected for specific treatments based on the characteristics of their tumors. “We also need to develop clinical trials that move targeted therapies to earlier stages of lung cancer, where we have a better chance of a cure.”

Future clinical trials, he predicted, would look for relatively large effects of drugs in selected patients. Dr. Minna agreed, saying, “If the effects are not there, we will move on to the next target and the next drug.”

The new results are really a teaser for what’s coming. TCGA plans to sequence a total of 500 adenocarcinomas and 500 squamous cells tumors. These results could help shed light on issues such as epigenetic changes in lung cancer, mechanisms of drug resistance, and how tumors are influenced by the surrounding tumor microenvironment.

“All these studies published back to back show how diverse and how complicated the cancer genome is,” Dr. Govindan said. “But we now have a panoramic view of the genomic landscape, and this is important for moving forward in this disease.”

Dr. Minna added, “After treating thousands of patients with lung cancer and not doing too well, I am very excited about the new results.”

Source: NCI

The Golden Touch.

Most patients with ovarian cancer are diagnosed late, after tumor cells have already infiltrated the abdominal cavity and seeded multiple tumors on multiple organs – liver, spleen, intestines, and stomach. During the clinical portion of his MD/PhD program at Harvard Medical School, Alex Bagley saw that this cancer could benefit from a blend of his two interests, biology and engineering, and he saw the Koch Institute laboratory of Sangeeta Bhatia, MD, PhD, as a good place to blend them for his PhD research. Among Bhatia’s many projects, she designs multifunctional nanoparticles that can zoom to a tumor, detect changes in and around it, and improve the delivery of a therapeutic “payload.”

Bagley began working with gold nanorods, tiny particles that convert the energy from near-infrared light to heat. Delivering the golden nuggets to tumors and then exposing the tumors to that wavelength causes localized heating precisely at the disease sites. Lower levels of light cause blood vessels feeding the tumor to become more porous. That allows more drugs to enter the tumor, which enhances the therapeutic impact. Higher levels of light can directly kill tumor cells.

Conveniently, the vessels feeding tumors are more porous than normal blood vessels to begin with, while the tumor’s lymphatic drainage is blocked. In other words, the entrance is wide open but the exit is blocked. So when the nanoparticles are injected systemically, they naturally accumulate in tumors.

“Brilliant!” thought Bagley. “But how do we get the light into the deep abdominal cavity so that we can apply this technology to ovarian cancer?”

Source: MIT