Jim Allison confronts cancer, critics with immunotherapy.

Decked out in black tie, Jim Allison stood on the red carpet in Silicon Valley. It was unfamiliar territory for the small-town boy from South Texas who had become a scientist and spent his research career on what many considered a lost cause, the study of the immune system’s cancer-fighting potential.

But he always believed that’s where the action would be, and now here was Facebook CEO Mark Zuckerberg saying Allison’s breakthrough “will change lives for generations to come.” For that, late-night television host Conan O’Brien handed him the 2014 Breakthrough Prize in Life Sciences, which includes a $3 million check.

Allison had become a rock star.

There had been something fiercely independent in him since high school, where he battled teachers over creationism.

There had been an extraordinary run of cancer deaths in his family, not least his 45-year-old mom, which convinced him that there had to be better treatment than radiation and chemotherapy.

And there had been that wild, creative streak that once led to him blowing a harmonica with country music legend Willie Nelson.

Whatever the source of his genius, Allison, chairman of immunology at the University of Texas M.D. Anderson Cancer Center, is credited with one of the most important breakthroughs in cancer history, the discovery that finally frees the immune system to attack tumors – a dramatic departure from the existing models of treating the disease.

Allison did it – made the discovery, then translated it into a drug – in a climate that wasn’t exactly welcoming.

The achievement has recently won Allison a raft of awards that M.D. Anderson President Dr. Ron DePinho thinks will culminate in the Nobel Prize. “By creating this brilliant approach that treats the immune system rather than the tumor, Jim Allison opened a completely new avenue for treating cancers that’s the most exciting and promising area of cancer research today,” DePinho says.

Bearded and scraggly haired, the 65-year-old Allison insists he never set out to cure cancer. Rather, he describes his motivation as “the selfish desire to be the first person on the planet to know something.”

“It can be hard to go against the system,” Allison says, “but sometimes you have to do it for progress to be made.”

Six months before his red carpet moment in Mountain View, Allison found himself arriving late to Chicago’s famed Arie Crown Theater, site of an immunotherapy session at the American Society of Clinical Oncology’s 49th annual meeting.

For years, he’d been going to such gatherings. Historically, they’d been sparsely attended, the result of a series of flops that changed the idea of enlisting the immune system to fight cancer from the field’s Holy Grail to a forgotten stepchild.

But here were 4,000 doctors who’d come from around the world to hear how the immune system was saving the lives of patients whose cancers historically meant a death sentence. They had come because of a flash of brilliance by Allison that deciphered which molecules on the surface of T cells function as catalysts – and which one functions as the brake.

Jim Allison's work with immunotherapy is considered a breakthrough against cancer. Photo: Craig Hartley, For The Chronicle

Family cancers
Allison was 11 years old when his mother died.

She’d been seriously sick with lymphoma for some time, but he had no idea how seriously when his father called him to her bedside, stopping him from heading to the local swimming pool with some buddies. She died as he held her hand.

Allison remembers walking out of the house and wandering aimlessly, trying to comprehend things. No one ever told him much about his mother’s illness, certainly not that she had cancer. That only came later.

The family cancers would keep coming. He lost an uncle to melanoma, another to lung cancer. Years later, his brother would die of prostate cancer.

It was all a motivating force, he says, but emphasizes he never considered curing cancer his purpose.

“If I had, I’d never have found the immune system’s brake,” says Allison, who was diagnosed with prostate cancer and successfully treated by prostatectomy in 2005.

“Because of my family history, I always had in the back of my mind that if my research uncovered something that might help, I’d make the leap,” he says. “But I always knew the key was figuring out how things work, finding the right button to push.”

The hardest thing to accept was that his breakthrough didn’t come soon enough to save his brother, who had ignored joint pain, only to learn it was advanced prostate cancer.

Allison was at his brother’s side, too, when he died in 2005, holding his hand.

Important revelation

At 16, Allison graduated from high school and went to University of Texas-Austin, where he quickly lost interest in going on to medical school, soured, first, by all the memorization it would require, then by the realization that doctors have an inordinate amount of responsibility.

“As a scientist you make mistakes all the time – that’s how you learn,” Allison says. “But a physician has to be right all the time. I prefer the scientist’s life – get an idea, devise an experiment, learn if it checks out. You only have to be right sometimes.”

After completing his undergraduate studies and doctorate, Allison went to Scripps Clinic and Research Foundation near San Diego for his postdoctoral fellowship.

Some of his most lasting memories there didn’t involve science.

Allison describes himself as “always kind of doodling on the harmonica,” but it was during those postdoc nights that he became more serious. For a couple of years he played regularly with Clay Blaker and the Texas Honky Tonk Band.

He’d wangled an invitation to a party Willie Nelson’s label threw to celebrate the “Red Headed Stranger” album going platinum, and when Nelson asked Allison if he knew anywhere he could pick some music the next night, Allison didn’t hesitate to volunteer it was talent night at the Stingaree bar where he played.

Allison would join Nelson onstage there for “Blue Eyes Crying in the Rain.”

Music or science?

For all his love of music, Allison had no illusions. Asked by Blaker to accompany the band when it left Southern California to play Texas clubs, he opted to keep his day job.

He returned to Texas a year after completing his Scripps Clinic fellowship. He showed up at M.D. Anderson’s new science campus and procured a biochemist job.

By then, the mid-’70s, Allison already was keenly aware of cancer immunotherapy’s checkered history.

It was all the rage for a time, but when early mice experiments didn’t show benefits, immunotherapy fell out of favor.

“It had such a bad rap,” Allison says. “People would say to me, ‘Don’t do tumor immunology, it’ll ruin your reputation.’ “

In the ensuing years, cancer immunotherapy made some strides, but they were frequently undermined by hype, sometimes by the scientists themselves. Allison believed none of them really knew what they were doing. He set out to be the one who did.

He’d become fascinated following an undergraduate experiment he conducted that showed mice cured of leukemia had acquired an immune response that rejected his attempts to inject new tumors. He’d become even more interested as he learned of the immune system’s complexity, the communication and coordination it calls upon to recognize and eliminate any pathogen, all without causing damage to healthy tissue.

Fascinated by T cells

Allison was most interested in T cells, the immune system’s little-understood soldiers that “do all the killing.”

He wondered what about cancer disarms them. Why do they so efficiently attack virus-infected cells but not get the necessary signals to attack tumors?

In the next decade, Allison’s work laid important basic science groundwork. He identified, first, the T cells’ ignition switch, a receptor that has to recognize proteins on tumor cells, then the gas pedal, a co-stimulatory molecule necessary to activate the T cells. They would provide key insights that helped facilitate the big discovery still to come.

In that time, UC Berkeley came recruiting. He dithered for two years, but finally decided it was time to make the move. It took a former adviser telling him if he passed the job up, he’d put up his feet 10 years later thinking he could have been a contender.

By the ’90s, the race was on.

Numerous immunology labs were looking for molecular signals to rally T cells into action, and nothing looked so promising as CTLA-4. A newly discovered protein that protrudes from T cells’ surface, CTLA-4 turned out to resemble the structure of the “gas pedal” Allison described, so it seemed logical that it was an activation signal.

But when he tried binding molecules with CTLA-4 as he had done with the “gas pedal” protein, he got an opposite effect: It inhibited T-cell proliferation. Could it be a brake, not a gas pedal?

So while most everyone else was looking for evidence that CTLA-4 turned on the immune system, Allison designed a study based on the novel hypothesis that CTLA-4 turned it off: He implanted mice with cancer cells and treated some with an antibody that blocked CTLA-4 – in essence, taking the brake off the immune system.

Allison was astounded by the initial data his research fellow showed him at the end of November 1995: While all the untreated mice had died, 90 percent of the cancers of the treated mice had disappeared. Allison wanted to reproduce the results immediately, but there was a problem: His fellow was headed off to a European vacation, and Berkeley would soon be closing for Christmas.

Impatient, Allison instructed the fellow to inject tumors into a new bunch of mice, including a control group that didn’t get the antibody. He’d come in during the break and monitor the mice himself, unaware which was the control group and which got the treatment, a truly blinded study.

Gradual progress
Allison took the measurements every other day during December and, for a short while, the results were the source of despair. All the tumors were continuing to grow. But at about the third week, things began to change. In half of the mice, the cancers first stopped growing, then started shrinking, then disappeared.

In March 1996, the journal Science published Allison’s research: Blocking CTLA-4 enhances antitumor responses.

“Everyone thought I was crazy,” Allison says.

He took the finding and determined to apply it to cancer. He developed an antibody that worked great in mice, but for two years couldn’t find a company to fashion a human version. Most were still gun-shy about cancer immunotherapy because of the field’s past failures, and most were still convinced that the future of cancer treatment involved molecular targets on tumors, not the immune system itself.

Finally, a small New Jersey company named Medarex took the plunge, sublicensing the patent and manufacturing a drug called ipilimumab (ippy for short), the first of a new class of drugs called immune checkpoint inhibitors. The company would ultimately be acquired by Bristol-Myers Squibb for $2.4 billion.

Ippy was tested, successfully, in human patients for the first time in 2001, but results from its first large-scale trial weren’t good. There was little impact at 12 weeks, the point at which chemotherapy is assessed, so it was declared a failure. It took a second large trial for ippy’s prospects to gain momentum, after clinicians noticed some tumors that were unaffected at 12 weeks had shrunk; years later, some patients were thriving.

It turns out that the immune system sometimes took time to rev up, but once it did, its effects last, unlike other cancer therapies.

Patient’s turnaround

Sharon Belvin burst into tears in September 2006 when she was introduced to Allison.

Now employed at New York City’s Memorial Sloan Kettering Cancer Center – he’d left Berkeley in 2004 so he could work closely with doctors and make sure his discovery wasn’t mishandled – Allison had stopped by the office of Dr. Jedd Wolchok, his clinical partner. There was Belvin, the first patient he’d ever met who had received his drug.

She’d been diagnosed, at 22, with stage four melanoma, words she says are “impossible to hear and not think ‘death.’ ” In the next year, when nothing stopped the spread of Belvin’s cancer from her chest and lungs to her brain, Wolchok offered her ippy. Desperate, she jumped at the chance.

Infused through a vein every three weeks over three months, ippy quickly shrank Belvin’s tumors and had her walking again. A year later, the day Wolchok summoned Allison, she’d just gotten the news that she was in remission.

“That’s the reason you do this work,” says Allison, still moved by the memory. “It’s not about the awards, it’s about the difference made in people’s lives.”

Finally, FDA approval

It would take 10 years of trials involving 6,500 patients, but in 2011 the Food and Drug Administration finally approved ippy – brand name Yervoy – for melanoma. No previous treatment ever made a meaningful dent in the advanced disease’s five-year death rate of more than 95 percent, but the latest statistics show almost a quarter of all melanoma patients treated with ippy live at least three years, after which point none dies of the disease.

For a time, Allison loved living on Manhattan’s Upper East Side, enjoying Central Park and the Metropolitan Museum of Art. But the charm eventually wore off.

Dr. John Mendelsohn, then president of M.D. Anderson, began wooing him to Houston, promising that the famed cancer hospital could provide an even larger platform for Allison’s work. Mendelsohn retired in 2011 without making a formal offer, but DePinho, his successor, pushed hard to pick up the recruitment.

Allison accepted in late 2012, a year after the Cancer Prevention and Research Institute of Texas approved a $10 million grant for his recruitment. M.D. Anderson invested $30 million more to bolster its immunotherapy research capabilities, which enables Allison to design trials across a variety of tumor types, using ippy by itself or combining it – with other checkpoint inhibitors and with chemotherapy or targeted therapy.

It also provides Allison access to freshly removed tumors, which he can analyze to gauge ippy’s effect and understand how it works, as he did with mice.

On demand

These days Allison never finds himself bored. When not in his lab, he is wildly in demand on the lecture circuit, traveling constantly to evangelize about cancer immunotherapy’s promise.

The speaking engagements come not just because of Allison’s drug but because his discovery blasted open the door for cancer immunotherapy.

Scientists have since discovered eight other immune system brakes and developed a few corresponding pharmaceuticals now in clinical trials, one of which combined with Yervoy in the trial presented at the American Society of Clinical Oncology meeting in Chicago to bring advanced melanoma patients’ 1 1/2-year survival rate to 80 percent.

The National Institutes of Health began funding a network of 27 centers’ immunotherapy trials in 2011. Every major pharmaceutical company is investing heavily.

Because the target is the immune system rather than the tumor, immune checkpoint drugs are expected to work on all sorts of cancers. Besides melanoma, Allison’s drug and the others in clinical trials already have had success against cancers of the lungs, colon, kidney, breasts, ovaries, pancreas and prostate.

“There’s a sense of paradigms shifting,” Science magazine wrote in an article that declared cancer immunotherapy the Breakthrough of the Year for 2013. “Immunotherapy marks an entirely different way of treating cancer – by targeting the immune system, not the tumor itself. Oncologists, a grounded-in-reality bunch, say a corner has been turned and we won’t be going back.”

For all the excitement, there are still questions about ippy. Researchers have no idea why it benefits some people but not others. Because releasing the brake facilitates an all-out attack by the immune system, it can cause serious side effects – colitis, skin rashes, impaired pituitary function – that must be managed.

And the drug’s price is $130,000, an amount Allison calls obscene.

Still, years of skepticism about immunotherapy have finally faded. Allison notes that even James Watson, Nobel Prize-winning co-discoverer of DNA’s structure and onetime immunotherapy skeptic, recently told him, “This is going to do it.”

Albumin Supplementation in Sepsis Patients.

Fluid administration is one of the most common items managed every day in hospitalized and intensive care unit (ICU) patients. The optimal fluid for sepsis resuscitation remains unknown, with concerns about both crystalloids and colloids.[1]

Caironi and colleagues sought to examine whether albumin supplementation would benefit patients with severe sepsis and septic shock. This study randomly assigned 1818 of these patients within 24 hours of ICU admission to receive either crystalloids or crystalloids plus albumin supplementation, to maintain a serum albumin level of 3 g/dL.

Early in the course, albumin-treated patients had at least intermittently higher central venous pressure, higher mean arterial pressure, and less positive fluid balance. There was no difference in mortality at 28 days or 90 days, although the subset of patients with septic shock treated with albumin did have a lower mortality at 90 days (43.6% vs 49.9%; P = .03).

A growing body of literature suggests that hydroxyethyl starch solutions may cause renal damage, particularly in patients with sepsis.[2-5] Conversely, albumin has been suggested to confer benefit in sepsis resuscitation.[6,7]

In this study, albumin supplementation to maintain normal circulating serum albumin levels was not shown to be superior overall to crystalloid administration alone. This was true for starting the intervention earlier or later (< 6 hours vs 6-24 hours), and for outcomes measured earlier or later. But the subset of patients with septic shock did have statistically greater survival at 90 days, which raises the question of albumin superiority for this subgroup, and perhaps even as a later effect not related to the early resuscitation.[8]

Unfortunately, for general patient care, this study does not provide a definite answer. And the major question of whether different uses of albumin, such as in the earliest phases of fluid resuscitation and targeted to goals other than maintaining circulating level, still needs to be studied.

Mt. Everest Avalanche: Is Climate Change to Blame?

The icy slopes of Mount Everest have seen hundreds of deaths in the years since 1922, when seven people perished during the British Mount Everest Expedition.

An avalanche today (April 18) claimed at least 12 lives, in what may be the single deadliest climbing event in the history of the world’s tallest mountain (29,029 feet, or 8,848 meters). The death toll may rise, because other climbers are still missing, according to the BBC.

mount everest

All of the deceased were guides from the ethnic Sherpa community, who were securing ropes for the start of the spring climbing season. And many Sherpas insist that Mount Everest and other mountains in the area have become more dangerous because of climate change. [Ice World: Gallery of Awe-Inspiring Glaciers]

“In 1989 when I first climbed Everest there was a lot of snow and ice, but now most of it has just become bare rock. That, as a result, is causing more rock falls, which is a danger to the climbers,” said Apa Sherpa, a Nepali climber, as quoted in Discovery News.

“Also, climbing is becoming more difficult, because when you are on a [snowy] mountain you can wear crampons, but it’s very dangerous and very slippery to walk on bare rock with crampons,” he added.

Avalanches and climate change

Avalanches have been around for centuries, of course, and researchers can’t blame any single event on climate change. Some evidence exists, however, that a warming planet and changes in precipitation may increse the likelihood of certain types of avalanches at certain times of the year.

A 2001 study from the Annals of Glaciology found that increases in temperature and precipitation could slightly decrease the risk of avalanches in mid-winter in France, but could significantly increase the risk of spring avalanches.

Those findings were echoed in a 2013 report from the journal Applied Snow and Avalanche Research, which found that in Canada’s Glacier National Park, an increase in rain (instead of snow) during the winter could result in greater instability in the snowpack, leading to more late-winter avalanches.

Glacial lake outburst flooding

Apa Sherpa — who has conquered Everest more than 20 times — was once a farmer in the Himalayan region, but he turned to mountaineering after losing his home and his farm after a glacial lake outburst flood in 1985.

Researchers have warned that glacial lake outburst floods (GLOFs) are a particularly disastrous effect of climate change. As glaciers melt, immense lakes form behind relatively weak ice dams. When the ice dams are breached, the resulting burst of water and debris can cause sudden, catastrophic flooding.

“In the Himalayas, catastrophic risks of GLOFs have increased in recent years because most Himalayan glaciers have experienced remarkable downwasting under a warming climate,” according to the authors of a 2013 study published in the journal PLOS ONE.

The researchers found that between 1990 and 2010, more than 1,000 glacial lakes in the Himalayas expanded rapidly, increasing their surface area by more than 17 percent, presenting an immediate danger to climbers and residents. “An effective monitoring and warning system for critical glacial lakes is urgently needed,” the study authors wrote.

Water supplies under threat

In another alarming finding, researchers from the University of Milan in Italy announced in 2013 that glaciers in the Mount Everest region have shrunk by 13 percent in the last 50 years, and the snowline has shifted upward by 590 feet (180 meters).

The glaciers are also shrinking at a faster rate, as regional precipitation has declined since 1992 by nearly 4 inches (10 cm) during the pre-monsoon and winter months, the Los Angeles Times reports. The loss of these glaciers could be catastrophic, since they provide water and power for about 1.5 billion people living in Asia.

The loss of glaciers in the region isn’t uniform, however. A study published in the April 2012 issue of the journal Nature Geoscience found that glaciers in the Karakoram mountain range are holding steady, and some may even be growing in size due to changes in precipitation patterns.

The future of Everest

There’s some concern in the mountaineering community that mountains like the iconic Everest may be unclimbable in the near future.

“What will happen in the future I cannot say but this much I can say from my own experiences — it has changed a lot,” Apa Sherpa said.

In 2012, he completed a 120-day walk named the Climate Smart Celebrity Trek with the goal of raising awareness of climate change’s impact on high-altitude mountain environments.

“I want to understand the impact of climate change on other people, but also I’d like tourism to play a role in changing their lives as it has changed mine,” Apa Sherpa said.

Pentagon-sponsored study opens door for super lasers, weather control.

Pentagon-sponsored researchers have made the reach of an intensive laser beam longer by an order of magnitude. Researchers say their discovery can be used to seed rain and trigger lightnings, but the potential scope of applications is much larger.

Reuters / Gene Blevins

A short intensive laser pulse produces plasma in its path. This plasma can interact with charged particles in a storm cloud and change weather, starting rain on request and control lightning bolts. But making laser beams travel into the clouds uninterrupted was always a challenge, because beams powerful enough to control weather dissipate very quickly.

A team of optical researchers at the University of Arizona and the University of Central Florida have found a way around this obstacle. They used a second lower-intensity laser beam to ‘dress’ the primary one and act as a power source for it. This extended the range of the high-intensity beam from just several centimeters to several meters in lab conditions.

The potential of the technology goes beyond our interaction with the planet’s atmosphere. It can be applied in areas like remote sensing for spectroscopy, allowing analyzing chemical compounds from long distances, or channeling of microwaves. The US Department of Defense, which green-lit the research with a $7.5 million grant, certainly thought it was worth the investment.

As for weather control, the team needs to find a way to send a laser beam hundreds of meters into the sky and sustain its energy, researchers say. Their report, entitled ‘Externally refueled optical filaments’, was published in the journal Nature Photonics.

The usage of lasers for weather control has been researched for some time. Not any laser is suited for the job however. It must be powerful enough and produce a very short burst.

“When a laser beam becomes intense enough, it behaves differently than usual – it collapses inward on itself,” explained study co-author Matthew Mills, a graduate of the Center for Research and Education in Optics and Lasers (CREOL) at University of Central Florida. “The collapse becomes so intense that electrons in the air’s oxygen and nitrogen are ripped off creating plasma – basically a soup of electrons.”

The resulting plasma fights the surrounding air for control, producing a pathway, or ‘light string’. This process of filamentation, as it’s called, creates “excited electrons” everywhere it passes. Those electrons are the building blocks of lightning. They can be used to create and control it.

Unfortunately such filaments are not stable and are not long enough to reach a cloud. Mills and others found a way to create an “extension cable” for the laser: by “dressing” the initial super-intense laser beam with a lower intensity one. This secondary doughnut-shaped “dress” beam gives extra energy to the initial beam mush like a fighter jet gets extra fuel from a refueling aircraft to stay longer in the air.

“Since we have control over the length of a filament with our method, one could seed the conditions needed for a rainstorm from afar. Ultimately, you could artificially control the rain and lightning over a large expanse with such ideas,” Mills believes.

The research is broader than just offering a new way of seeding clouds and protecting buildings from lighting, both of which can be done by more conventional methods. They have managed to extend their high-intensity laser from a few centimeters to a few meters, and it’s only a matter of time until we are also able to “selectively guide microwave signals along very long plasma channels, perhaps for hundreds of meters,” professor Demetrios Christodoulides told the UCF website. This could mean a whole host of science applications and measuring capabilities in areas we could not previously get close enough to work with without getting obliterated by lightning.

But bringing together Pentagon’s interest and weather control gives a somewhat sinister tone to the study, at least for those inclined to see it. For example the United States’ HAARP facility in Alaska, which studies the ionosphere, has a number of conspiracy theories associated with it, claiming that it can control weather and even trigger natural disasters in remote areas on the command from the US generals.

Clinical Trials Paving the Way for Improved Vulvar Cancer Treatment.

Cancers of the vulva – the external portion of the female genitals – are diagnosed in approximately 4,700 women in the United States each year. While many patients can be cured by a combination of surgery, chemotherapy, and radiation therapy, others – particularly those whose cancer has metastasized to other parts of the body – often don’t fare as well.

As one of the rarer forms of gynecologic cancer, vulvar cancer hasn’t attracted as much research funding as other forms. Still, several efforts are under way to make treatment options more effective, according to Neil Horowitz, MD, a vulvar cancer expert at the Susan F. Smith Center for Women’s Cancers at Dana-Farber.
One clinical trial is studying the effectiveness of chemotherapy administered at the same time as radiation therapy for women with extensive tumors confined to the vulva. The size of such tumors and proximity to the urethra (the tube that carries urine from the bladder), clitoris, or anus often means that surgeons would have to remove these important structures to remove the cancer. The new treatment seeks to shrink the tumor prior to surgery, reducing the long-term consequences of surgery or perhaps avoiding surgery altogether. Patients are treated with the chemotherapy agents cisplatin and gemcitabine, along with intensity-modified radiation therapy (IMRT), which uses computer-generated 3-D images to show the size and shape of the tumor. Previous trials have shown the effectiveness of cisplatin and traditional radiation therapy; the new trial is exploring whether the addition of gemcitabine and the use of IMRT offers even better results.

Another trial is confirming the safety and effectiveness of omitting a full lymph node evaluation after using a less-invasive method of determining whether vulvar cancer has metastasized, or spread. The conventional approach is to remove many of the lymph nodes near the diseased vulva and examine them for the presence of vulvar cancer cells – a procedure that can lead to a painful buildup of lymph fluid and swelling of the lower extremities. The trial is analyzing whether removing only the main, or “sentinel,” lymph nodes can be just as effective for detecting metastasis while producing less swelling. Additionally, the trial seeks to determine if radiation therapy rather than a complete lymph node removal can be used if a positive sentinel lymph node is discovered.

Horowtiz and his Dana-Farber colleague Ursula Matulonis, MD, medical director of Gynecologic Oncology at the Susan F. Smith Center, recently completed a clinical trial that found that the drug Tarceva temporarily stalled or reversed the growth of squamous cell vulvar cancers in some women. The trial marked the first time a “targeted” therapy, which aims at a specific abnormal protein in cancer cells, has been tested in patients with vulvar cancer.

Six Things to Do When You Learn You Have Cancer.

A cancer diagnosis can put even the most organized person into a state of disarray. That’s not surprising, because it’s normal to feel overwhelmed and out of control in the face of such stress. But there are steps you can take to ensure you’re best prepared for the road ahead. Don’t forget to:

Slow down and give yourself a chance to cope. Set aside time for yourself and your loved ones. It’s easy to feel isolated when you put up a strong front, so keep the lines of communication open with your family, friends, and doctors. Try to gain strength from one another by expressing your emotions honestly and openly.
Learn what services and programs are available. Many patients don’t take full advantage of support and resources simply because they haven’t had a chance to learn what’s out there. The National Cancer Institute offers advice for finding support resources in the general community. At Dana-Farber, patients and their loved ones can leaf through their patient handbook or talk with a concierge in the Shapiro Center for Patients and Families to learn about available programs (they can also call a concierge at 617-632-3750).
Accept help from others. Make a list of ways that friends and family can help, and suggest specific tasks. Friends or family members who assist with the day-to-day challenges of living with cancer can review the helpful advice and tips in Dana-Farber’s downloadable caregiver booklets.
Beth Overmoyer with patientLearn more about your cancer. Gather basic information about your diagnosis, to the extent that you feel comfortable. Take notes when your doctor or nurse explains something, or ask a loved one to do so. If you have questions before an appointment, write them down and ask them when you meet with your cancer care team. At Dana-Farber, you can research more about a cancer diagnosis with help from a trained volunteer or staff member in the Eleanor and Maxwell Blum Patient and Family Resource Center.
Step back and think about how you are coping. Everyone reacts to a cancer diagnosis in his or her own way, so it may help to turn to strategies that have helped you manage and reduce stress in the past. Ideas to consider: Practice relaxation techniques or attend a yoga class (both available through Dana-Farber’s Zakim Center). Rely on your preferred spiritual support. Start (or continue) an exercise routine. At most cancer centers, you can let your doctor or nurse know if you are feeling particularly stressed and they can help you make an appointment with one of our social workers.
Connect with others in your situation. Talking with someone who has previously dealt with cancer can be a great help. Dana-Farber’s One-to-One program links trained volunteer cancer survivors with those who are facing it for the first time. Similarly, CancerConnect offers an online forum where patients and family members can connect with cancer patients, doctors, survivors, family members, and friends for advice, support, and guidance.

ADHD: Scientists discover brain’s anti-distraction system.

Two Simon Fraser University psychologists have made a brain-related discovery that could revolutionize doctors’ perception and treatment of attention-deficit disorders.

Psychologists have made a brain-related discovery that could revolutionize doctors’ perception and treatment of attention-deficit disorders. This discovery opens up the possibility that environmental and/or genetic factors may hinder or suppress a specific brain activity that the researchers have identified as helping us prevent distraction.


This discovery opens up the possibility that environmental and/or genetic factors may hinder or suppress a specific brain activity that the researchers have identified as helping us prevent distraction.
The Journal of Neuroscience has just published a paper about the discovery by John McDonald, an associate professor of psychology and his doctoral student John Gaspar, who made the discovery during his master’s thesis research.
This is the first study to reveal our brains rely on an active suppression mechanism to avoid being distracted by salient irrelevant information when we want to focus on a particular item or task.
McDonald, a Canada Research Chair in Cognitive Neuroscience, and other scientists first discovered the existence of the specific neural index of suppression in his lab in 2009. But, until now, little was known about how it helps us ignore visual distractions.
“This is an important discovery for neuroscientists and psychologists because most contemporary ideas of attention highlight brain processes that are involved in picking out relevant objects from the visual field. It’s like finding Waldo in a Where’s Waldo illustration,” says Gaspar, the study’s lead author.
“Our results show clearly that this is only one part of the equation and that active suppression of the irrelevant objects is another important part.”
Given the proliferation of distracting consumer devices in our technology-driven, fast-paced society, the psychologists say their discovery could help scientists and health care professionals better treat individuals with distraction-related attentional deficits.
“Distraction is a leading cause of injury and death in driving and other high-stakes environments,” notes McDonald, the study’s senior author. “There are individual differences in the ability to deal with distraction. New electronic products are designed to grab attention. Suppressing such signals takes effort, and sometimes people can’t seem to do it.
“Moreover, disorders associated with attention deficits, such as ADHD and schizophrenia, may turn out to be due to difficulties in suppressing irrelevant objects rather than difficulty selecting relevant ones.”
The researchers are now turning their attention to understanding how we deal with distraction. They’re looking at when and why we can’t suppress potentially distracting objects, whether some of us are better at doing so and why that is the case.
“There’s evidence that attentional abilities decline with age and that women are better than men at certain visual attentional tasks,” says Gaspar, the study’s first author.
The study was based on three experiments in which 47 students performed an attention-demanding visual search task. Their mean age was 21. The researchers studied their neural processes related to attention, distraction and suppression by recording electrical brain signals from sensors embedded in a cap they wore.
Story Source:
The above story is based on materials provided by Simon Fraser University. Note: Materials may be edited for content and length.
Journal Reference:
J. M. Gaspar, J. J. McDonald. Suppression of Salient Objects Prevents Distraction in Visual Search. Journal of Neuroscience, 2014; 34 (16): 5658 DOI: 10.1523/JNEUROSCI.4161-13.2014

5 Vitamins You Might Be Overdoing.

Americans aren’t eating as many fruits and vegetables as we should be. In fact, Americans nationwide are significantly below the fruit and vegetable consumption guidelines set forth by the Centers for Disease Control and Prevention and the USDA.

Enter supplements. As people seek alternative sources of crucial vitamins and minerals, supplement intake has skyrocketed. Supplements can be helpful, but getting nutrients in a pill rather than food is not always the best way to improve your health. In some cases, it can even hurt.

vitamins you may be overdoing

Here are five vitamins and minerals you may be overdoing if you pop them as pills.

Iron and Copper

Iron plays a key role in younger women’s diets for menstrual cycles and pregnancy, but the recommendations for iron after menopause decrease significantly. Despite the lower guidelines (8 mg per day after age 50) many postmenopausal women still take supplements that contain iron. The risks of getting too much iron include a condition called hemochromatosis, which can damage your organs. Further, a 2010 study linked excess iron and copper to increased incidence of alzheimers disease and heart disease.

“Getting nutrients in a supplement rather than food is not always the best way to improve your health. Here are five vitamins and minerals you may be overdoing if you pop them as pills.”
Kristin Kirkpatrick, MS, RD, LD

Wellness Institute

Best bet: If you’re over 50, ditch the multivitamins with iron and copper unless a doctor instructs you to take them.


Beta-carotene and vitamin A — which is formed by beta-carotene — is easy to consume. If you have a bowl of cereal for breakfast, anything orange (carrots, sweet potatoes) for lunch and then a multivitamin or supplement for eye health, you’ve probably consumed too much. Too much beta-carotene has been associated with increased risk for lung cancer and overall increased risk of death.

Best bet: Skip the supplement and stick to food sources such as sweet potatoes, watermelon, cantaloupe, red bell peppers, carrots and spinach.

Vitamin C

When most people think of vitamin C, they think of oranges. But if your first thought is a vitamin C pill, you may be overdoing it. A recent study found that men who took vitamin C pills had higher risk for developing kidney stones.

Best bet: Enjoy the culinary delights of vitamin-C rich foods such as papaya, strawberries, brussels sprouts and kale. But don’t take extra unless a doctor advises you to.


While calcium is important for strong bones, data suggests getting too much of it can strain your heart. Studies have suggested that women who take high amounts of calcium increase their risk of cardiac death and moderately increase their risk for heart attack.

Best bet: To avoid overdoing it, get your calcium through food sources such as dairy, tofu, sardines, broccoli and almonds. If you think you need supplemental calcium, talk to a doctor before buying a bottle.

The recommended daily allowance for any vitamin or mineral will depend on your age, medical conditions and other factors, and a doctor or registered dietitian can help you fine-tune your intake.

You may also notice a common theme here: Most vitamins and minerals are best obtained and absorbed through real food. To ensure you’re getting enough — but not too much — of any vitamin or mineral, avoid supplements that contain “mega doses” unless your doctor recommends them for medical reasons.


Renal denervation—implications for chronic kidney disease.

Catheter-based renal denervation to treat patients with resistant hypertension and chronic kidney disease (CKD) has generated considerable interest. Data from the majority of, but not all, observational studies and randomized controlled trials suggest that the procedure does not impair renal function and can effectively reduce office and ambulatory blood pressure in patients with primary hypertension. The putative beneficial effects of renal denervation seem to result from the interruption of renal efferent and afferent nerves. In patients with resistant hypertension and CKD, interruption of afferent reflexes might lead to a reduction in global sympathetic tone. The subsequent sustained reduction in blood pressure is expected to slow the progression of renal disease. However, renal denervation might also improve glucose metabolism, increase insulin sensitivity and reduce renal inflammation, with renoprotective effects in patients with CKD. Additional large randomized controlled trials of renal denervation in hypertensive and normotensive patients with CKD are required to precisely define the clinical value of the procedure in this population.

Renal sympathetic denervation.

Sympathomodulation of the efferent sympathetic nervous system.


Scientists Make First Embryo Clones From Adults.

Advancement Could Lead to Treatment for Alzheimer’s, Heart Disease

Scientists for the first time have cloned cells from two adults to create early-stage embryos, and then derived tissue from those embryos that perfectly matched the DNA of the donors.

The experiment represents another advance in the quest to make tissue in the laboratory that could treat a range of maladies, from heart attacks to Alzheimer’s. The study, involving a 35-year-old man and one age 75, was published Thursday in the journal Cell Stem Cell.
The creation of the first early-stage human clones, using infant and fetal cells rather than those from adults, was reported last year. The new experiment, with a few tweaks, confirms that striking and controversial breakthrough and also shows the technique works on mature cells.

“The proportion of diseases you can treat with [lab-made tissue] increases with age. So if you can’t do this with adult cells, it is of limited value,” said Robert Lanza, co-author of the study and chief scientific officer at Advanced Cell Technology Inc. ACTC +1.43% of Marlborough, Mass. The study was funded in part by the government of Korea and done at a lab in California.

Such experiments are controversial because when cells are extracted from an early-stage human embryo, it destroys the embryo, which some people believe is equivalent to taking a life.



And while the embryos created in these recent experiments may have certain limitations that would prevent them from giving rise to a human clone even if implanted in a womb, that prospect is now scientifically closer.

As with the 2013 experiment, done by researchers at the Oregon Health and Science University, Dr. Lanza and his colleagues first extracted the DNA from an unfertilized human egg and replaced it with the DNA from one of the older donors. The egg automatically “reprogrammed” its DNA until it reached a stage of the embryo known as a blastocyst—a hollow ball of 50 to 100 cells.

Cells from the blastocyst then were cultured in a lab dish and yielded stem cells that were an exact match to the donor’s DNA. Those stem cells subsequently were turned into other tissue types, such as heart cells, which potentially could be transplanted into the patient without triggering an immune rejection.

“I’m happy to hear that our experiment was verified and shown to be genuine,” said Shoukhrat Mitalipov, a development biologist at Oregon Health and Science University, in Portland, Ore., who led the 2013 study that Dr. Lanza and his colleagues have now replicated.

DNA is extracted from an unfertilized human egg, the first step in the cloning process that led to the creation of an embryo from adult cells.
Despite this advance, experts say it wouldn’t be easy to create a full-fledged human clone. Scientists have been trying for years to clone monkeys and have yet to succeed. Even the cloning of less-complicated creatures—from sheep to rabbits and dogs—required years of tweaking, and lots of wasted eggs and deformed fetuses, before it worked.

The recent experiments, nonetheless, have some observers worried. Dozens of countries have laws explicitly banning human reproductive cloning, though there is no equivalent federal law in the U.S. Most U.S. states don’t have such laws either, though a few, such as California, do.

“If we’re closer to some rogue scientist or fertility doctor using published techniques to create cloned humans, it certainly ups the stakes and means we should be moving to put a federal law in place,” said Marcy Darnovsky, executive director of the Center for Genetics and Society, a nonprofit public interest group in Berkeley, Calif.