A batch of new gene discoveries nearly doubles the number of genes known to cause three of the most common cancers – breast cancer, prostate cancer and ovarian cancer. While each gene alone affects only a small number of people, taken together they help explain one-third of cases of these cancers, researchers reported on Wednesday.

It took a giant study to find all the genes – nearly 200,000 people took part at 160 institutions. The findings can not only help doctors decide who needs more frequent screening for cancer, but may eventually help target treatments that will work better for particular patients, the researchers said.

People with several of the genetic changes linked with cancer will have a much higher-than-average risk of the cancers, the researchers said. They published their findings in a series of 13 papers in several medical journals, including Nature Genetics and Nature Communications.

“By looking for people who carry most of these variations we will be able to identify those who are at the greatest risk of getting these cancers and then targeting screening tests to these individuals,” said Douglas Easton of Britain’s University of Cambridge, who led some of the studies.

“We now have 76 common genetic variants which are associated with breast cancer risk,” Easton told a news conference. Combined with other research, including the well-known breast cancer genes BRCA1 and BRCA2, genetic susceptibility explains 40 percent of breast cancer cases, he said.

“Any one of those (variants) is so tiny they don’t affect much,” Dr. Fergus Couch of the Mayo Clinic in Rochester, Minn., who worked on the project, told NBC News. “But when we put them together into a complex model … It’s the power of everything together that can make a difference.”

The researchers found 23 new genes linked with prostate cancer and three more for ovarian cancer. Now researchers know about 78 different genes associated with higher prostate cancer risk, and 16 of them are associated with aggressive disease.

The three cancers affect 2.5 million people globally, killing about a third of them. They all are driven by hormones.

“The most immediate practical application is probably going to be for women already at high risk of (breast cancer),” Easton said. A woman with a BRCA1 or BRCA2 mutation already has a very high chance of breast cancer. If she also has one or more of these other alterations, she’s at even higher risk.

Women who have a BRCA1 mutation along with most of the other, newly discovered mutations have an 80 percent chance of developing breast cancer by age 80, the researchers found.

“The 1 percent of people who have lots of these alterations could see their risk of developing prostate cancer increase by nearly 50 percent and breast cancer by 30 percent,” Easton said.

People may soon be able to take a genetic test to see what their risk is. They could then opt for early screening to watch for the disease. “This will be ready for prime time in a little more than a year,” Couch predicted.

Right now, guidelines vary on when women should get mammograms, for instance. Some guidelines call for annual screening starting at age 50; others say women only need them every two years.

A woman with a high genetic risk might opt to start having mammograms at age 30 or younger. There’s also confusion around testing for prostate cancer. U.S. experts say men shouldn’t be routinely screened using a blood test called a PSA test, because it causes too many “false positives” – when men are initially told they may have cancer but it turns out they don’t.

But men with a high genetic risk might opt to have frequent PSA tests.

“These results are the single biggest leap forward in finding the genetic causes of prostate cancer yet made,” said Rosalind Eeles  of Britain’s Institute of Cancer Research.

“They allow us, for the first time, to identify men who have a very high risk of developing prostate cancer during their lifetime,” she added.

The genes play a variety of roles in cancer. Some are supposed to stop the out-of-control growth that marks a tumor; some help cancer cells spread.

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The biggest study yet into genetics and mental health has come up with a stunning result: The five most common mental illnesses -- autism, attention deficit disorder, bipolar disease, schizophrenia and major depression -- all have a common genetic root.

The finding, published in the journal Lancet on Wednesday, may eventually lead to a complete rewrite of the medical understanding of the causes of mental illness.

“We have been able to discover specific genetic variants that seem to overlap among disorders that we think of as very clinically different,” Dr. Jordan Smoller of Massachusetts General Hospital in Boston, who led the study, said in a telephone interview.

The study does not explain every case of psychiatric disease, the researchers stress.

“We think this is one tiny fraction of the genetic component of these disorders. They involve hundreds and possibly thousands of genes,” Smoller said.

And it didn’t show every case was related. But it demonstrated on a genetic level that the five diseases are more like a continuum of dysfunction than five separate and discrete conditions.

Smoller’s international team included dozens of researchers who looked at the genetics of more than 33,000 psychiatric patients and compared them to nearly 28,000 people without mental illness. They did what is called a genome-wide association study -- a scan of all the DNA.

“We aimed to identify specific variants underlying genetic effects shared between the five disorders in the Psychiatric Genomics Consortium: autism spectrum disorder, attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia,” they wrote in their report.

They linked a considerable number to four places in the genome: a big stretch of chromosome 3; another part of chromsome 10, and two very specific genetic areas known to be involved in controlling cell function called calcium channels.

It wasn’t a complete surprise, Smoller says. Doctors have noted some overlap of symptoms and knew that in families prone to one psychiatric disease, another could also occur. “Autism was once known as childhood schizophrenia and the two disorders were not clearly differentiated until the 1970s,” the team wrote.

This finding could suggest that a genetic weakness upstream in the development of the brain could lead to a variety of psychiatric symptoms, perhaps influenced by other genes, or by the environment as well.

“We didn’t know going in that we would be able to find commonality with such a broad array of disorders,” Smoller said. “The fact that a particular pathway emerged as being relevant was also surprising. We didn’t know about that one before.”

Dr. Ken Duckworth, medical director of the National Alliance on Mental Illness, hopes the findings may help dispel some of the stigma that still surrounds psychiatric diseases.

“Ultimately this kind of research will give us a return in terms of social attitudes toward brain-based illness,” Duckworth said in a telephone interview. “If you can understand an illness process, it doesn’t seem so mysterious and terrifying.”

Duckworth said every psychiatrist knows of patients whose symptoms don’t clearly meet the definition of any one disease, and he noted that Sigmund Freud defined schizophrenia as a group of diseases. “This is a corner piece of the jigsaw puzzle,” he said.

And it might lead to better treatments, said Dr. Bruce Cuthbert, who is director of the National Institute of Mental Health’s division of Adult Translational Research. “We are finally starting to make inroads where we have actual physiological mechanisms that we can target,” he said. “We can really start to understand the biology instead of having to guess at it.”

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The Connecticut medical examiner has asked scientists to analyze the DNA of Adam Lanza, the 20-year-old who killed 27 people, including his mother, two classrooms full of small children and teachers, before killing himself on Dec. 14. 

Investigators hope that studying Lanza's DNA for mutations or other abnormalities may shed some light on the tragedy. Connecticut's chief medical examiner, Dr. H. Wayne Carver II, called the University of Connecticut a few days before Christmas asking for help from the UConn Health Center’s Department of Genetics and Developmental Biology, said UConn spokesman Tom Breen.

“They have agreed to offer any assistance they can to help the chief medical examiner in his investigation,” Breen said. Of Carver, Breen said, “He wanted help in conducting tests relating to genetics involving the shooter in the Newtown massacre.”

Breen said did not know what specific tests would be conducted. He said UConn was happy to help.

“This is such a terrible thing,” Breen said. “Everybody in the state has been affected by this.”

Will a DNA analysis help explain Lanza's rampage? 

The study of Lanza's DNA would be for research purposes, not to find a diganosis for his acts, says Arthur Caplan, Ph.D, NBC News contributor and head of Division of Bioethics at New York University Langone Medical Center in New York City. While there has been prior research on genetic mutations and violent behavior, looking at someone’s genes "is like hunting in a DNA haystack," Caplan says.

"We don’t have a database that says there’s a correlation between genes and propenstity to violence or crime or propensity to mental illness," he says.  "A particular DNA message may indicate a propensity to behavior, but at best you might find associations to greater risk. You won’t find a gene that says I’m going to be a mass murderer or a terrorist or an assassin."

James Fallon, a neuroscientist at the University of California, Irvine, who studies serial killers and other violent criminals, argues it will be fruitless to try to pin Lanza’s acts on his genes alone. Genetic data only paints part of the picture, he's found.

"The genes by themselves don’t tell you. If you just have a PET scan or MRI you can’t tell," Fallon said last week. "The psych report alone won't tell you. You put those things together you really get a lot of information." And some of what's been found by Fallon and other researchers provides some surprising insights.

Take for instance the “warrior gene”, the monoamine oxidase-A, or MAOA, gene that, has received widespread media attention, said Fallon.

“People know about the warrior gene and that it is associated with psychopaths and with killing,” Fallon said in a telephone interview.

Only a handful of diseases, such as cystic fibrosis, cause symptoms based on a single mutated gene. Most require thousands of changes and interactions. “So the idea that you have the warrior gene, therefore you are a warrior, it doesn’t hack it,” Fallon says.

It takes something more than just a genetic predisposition to make someone violent.

Fallon says there is no scientifically acceptable body of work on the genetics of violent behavior. "I don’t know of a case where even one killer has been studied genetically to an appropriate level, " Fallon said.

Likewise, brain studies have shed some light but can’t explain or predict the most extreme behaviors, said Dr. Martin Teicher, director of the Developmental Biopsychiatry Research Program at Harvard Medical School and McLean Hospital in Massachusetts.

“I don’t think we have the answer from neuroscience,” Teicher said. “Given the millions of people there are, the tiny handful of people who did these things are quite rare … We are drawing generalities from people who have had bad experiences, and who are maybe more prone to get into a fight, but they never would do anything like this.”

There is something that many violent people do have in common, however. Research done by Teicher, Fallon and others shows that violent criminals are, in fact, excessively anxious and fearful.

“Individuals at risk for violence often suffer from tremendous anxiety,” Teicher said. “It’s one of the most striking things I have noticed.” He’s treated high school students expelled or suspended for violence, but when they are in his office, they are anything but threatening.

“These are the frightening children in high school, yet they are essentially sitting in their mother’s laps,” Teicher said. “They were ridden with anxiety.”

And in some cases, this is combined with an inability to “read” other people. Teicher’s found this in some patients.

“We found differences in the (brain) cortex of violence-exposed individuals that play a role in social perception,” Teicher said. “These are regions involved in being able to infer what other people are thinking.” Brain scans show that the blood isn’t flowing normally in those brain regions. “They may be prone to misattribute thoughts and feelings,” Teicher says. 

Such deficiencies can be immensely stressful to a young man or teenager, Fallon says. “He looks at people and doesn’t understand what they are feeling,” he said. 

On top of this, Teicher has seen differences in parts of the brain’s frontal cortex that are involved in impulse control. “Misreading people and having difficulty controlling impulses may foster inappropriate actions,” Teicher says.

And while schizophrenia or bipolar disease do not usually lead to violent behavior, they can contribute to dangerous acts if patients are also racked with anxiety and not getting any sort of treatment.

“The late teens, early 20s, are when people have these psychotic breaks," Fallon said.

Most young people with these developing psychiatric conditions may feel anxious or threatened, but they don’t actually act on their feelings in part because they are unable to, Fallon said. Studies show the adolescent brain lacks the connections to initiate certain actions.

The brain is still growing, making new connections and cutting unneeded circuits, until the early 20s, Fallon said. The prefrontal cortex, involved in “executive function” or decision-making, is the last part of the brain to mature.

In an anxious young man, unable to understand people around him, perhaps ascribing all sorts of mistaken intentions to others, this could come to a climax, said Fallon, who studies how message-carrying chemicals such as dopamine and norepinephrine act in the brain. 

The young man's brain is still growing and changing until, finally, the prefrontal cortex matures. The amygdala, the part of the brain responsible for fear responses on the most basic level, is at the same time being flooded with corticotropin-releasing hormone, which is involved in the brain's stress response. 

“He is finally able to take action,” Fallon says. “Now the moment has come for him to carry out the ultimate act. If you turn it around like that, it makes a lot of logical sense."

Lisa Flam contributed to this story. 

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A gene mutation whose discovery was announced Wednesday triples the risk for Alzheimer’s disease.  It is a headline that might sound frightening but shouldn’t evoke fear.

The mutation in the gene called TREM2 is rare, occurring in about 1 in 150 people.  By comparison one in five people carry a form of a different gene called APO-E that also triples the risk.  One in 50 carries a form of APO-E that raises risk 13 times. APO-E’s relation to Alzheimer’s was discovered in 1993.   So in terms of public health implications, TREM2 is a small player, and is one of an ever growing list of genes implicated in Alzheimer’s

Still, the research from two teams, one headed by  Dr. Kari Stefansson at DeCode Genetics in Iceland and the other by Dr. John Hardy of University College London and both published in the New England Journal of Medicine, is critically important science that may yield clues about the causes of Alzheimer’s disease and the search for better treatments. 

TREM2 in its normal form plays a role in inflammation, the body’s response that sends white blood cells to destroy invading germs and diseased tissue.  The mutation cuts the ability to mount an inflammatory response, so it ispossible the ability to fight other diseases is tied up with the risk for Alzheimer’s.  For more than a century pathologists have noted a buildup of white blood cells in the brains of people who died from Alzheimer’s.

No one is sure what causes Alzheimer’s, which already affects more than 5 million Americans and costs the U.S, economy more than $148 billion a year, according to the Alzheimer’s Association. The numbers are projected to worsen as the baby boomer generation ages. There is no treatment and no cure.

The leading contender as the main cause of Alzheimer’s is the accumulation of plaques of protein called amyloid-beta.  It is likely that the inflammatory response is attempting to keep that buildup at bay. Last July, Stefansson’s team discovered a different gene mutation, even more rare, that actually protects against Alzheimer’s. That, too, was important science because that gene is responsible for production of amyloid-beta.  So it both supports the hypothesis about the cause and leads to ideas about how to make drugs to stop it.

Stefansson established DeCode in 1996 to find disease-causing genes in Iceland, a country with a homogenous population and national health service with excellent records.  At first it was a profit making venture, but despite an impressive record of locating genes associated with several diseases, the company was forced to declare bankruptcy in 2009.  It continues as a non-profit enterprise.  The two Alzheimer’s genes discovered in the past few months illustrate why the genetic research is so important even though it does not lead to immediate public health benefits or profits.

Follow Robert Bazell on Facebook and on Twitter @RobertBazellNBC

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University of Washington

Dr. John A. Stamatoyannopolous, associate professor of genome sciences, in his lab. Stamatoyannopolous worked on the giant ENCODE project that is re-defining human biology.

In what many scientists say is a revolution in biology, a giant new project is rewriting our understanding not only of what causes diseases or what makes our eyes a certain color, but what makes us human. And it turns out scientists have been looking in the wrong place for a very long time.

The bounty of new discoveries, released in a batch of 40 research papers on Wednesday, shows the stretches of DNA that we call genes are only a very small piece of what makes the body work. Much more important is the stuff in between the genes – stuff once dismissed as “junk DNA”. It turns out that junk DNA is what is in control, they report in the series of papers in the journals Nature, Science and elsewhere.

“This has opened up whole new galaxies. It’s like having a bigger telescope,” says Dr. Bruce Stillman, president of Cold Spring Harbor Laboratory, which played a major role in the work. 

Scientists already knew in 2003, as they finished the giant Human Genome Project, that they did not have the understanding they had hoped for.  It turned out that humans had just a measly 22,000 genes – fewer than some animals and far fewer even than a plant such as rice. How could something as complex and advanced as a human be boiled down into something so simple?

“We understood precious little about the processes that turns genes on and off. In short we had more questions than answers about how the human genome works,” said Dr. Eric Green, director of the National Human Genome Research Institute, which conducted the study.

The next phase of work, called ENCODE for Encyclopedia of DNA Elements, shows there’s nothing simple about it. As many as 40 million different switches are controlling these genes, turning them on and off in complex and subtle ways.

“The genome is loaded with gene controlling switches. There are literally millions of these,” Dr. John Stamatoyannopoulos of the University of Washington, who worked on the studies, told reporters in a telephone briefing.

Dr. Francis Collins, director of the National Institutes of Health, calls the findings “awesome and elegant.”

“This is the first truly comprehensive view, of how the three billion letter instruction book for human biology actually carries out its work, across many tissues and over the course of development,” he told NBC News in an interview.

Stanford University genomic expert Michael Snyder says it looks like gene mutations -- the changes in DNA sequences that we associate with causing diseases -- may only affect rare diseases. Common diseases, like heart disease, cancer, and allergy, are probably controlled elsewhere. “We think that most of the changes that affect disease don’t lie in the genes themselves, but the switches,” Snyder says.

So treating these common diseases may lie in trying to affect the switches. “The pharmaceutical industry has largely given up on genomics and the genome in favor of older approaches,” said Stamatoyannopoulos. These new findings may reinvigorate new drug research, he said. “Now we have a huge amount of genetic data about human disease that we can actually put to work to find the right kind of genes and proteins to target,” he said.

This new data will also help doctors diagnose disease in the first place, predict which treatments will work best for patients, and monitor their progress. It  points the way to studies to determine the causes of hundreds of diseases including  all kinds of cancer, Alzheimer’s disease, schizophrenia, heart disease, type 1 and type 2 diabetes, lupus, rheumatoid arthritis and asthma.  It also may lead to a better understanding of how our genetics determine such non-disease factors as height, weight and expected life span.

Not only that, it also can help explain why humans and chimpanzees share 98 percent or more of our genes, yet are so different.

"Genes occupy only a tiny fraction of the genome, and most efforts to map the genetic causes of disease were frustrated by signals that pointed away from genes. Now we know that these efforts were not in vain, and that the signals were in fact pointing to the genome's 'operating system' -- the instructions for which are hidden in millions of locations around the genome," said Stamatoyannopoulos. "The findings provide a new lens through which to view the role of genetics and genome function in disease."

Another surprising finding was that the regulatory circuitry blueprints could be used to pinpoint cell types that play a role in specific diseases -- without requiring any prior knowledge about how the disease worked. For example, DNA changes associated with Crohn's disease (a common type of inflammatory bowel disease) are concentrated in the switches controlling two types of immune cells.

Researchers can use this same method to identify cell types not previously known to play a role in a particular disease, expanding our understanding of the disease process and potentially leading to new therapies.

"We now have a parts list of what makes us human," says Mark Gerstein of Yale university, who worked on the project. "What we are doing is figuring out the wiring diagram of how it all works."

The findings rewrite biology 101 for most of us.  Each gene, we were taught, provided the code for a single protein. The proteins were the building blocks of cells, and the products made by the cells, from compounds called growth factors to signal-carrying chemicals. An intermediary genetic structure called RNA carried this information. ENCODE shows this is not quite so straightforward, that RNA generates the 40 million switches that can affect how and when many things happen within the cells.

“This is another grand chapter in the ongoing and historic research story that is unraveling the details about how life works, and how disease occurs,” Collins said.

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