Health Meaning

The legal battle over patents on breast cancer genes BRCA1 and BRCA2 held by Myriad Genetics of Salt Lake City has taken a new turn today with a decision of a US court of appeal. The decision supports a part of the company's claims and deny others.

This argument of BRCA genetic testing went all the way to the Supreme Court earlier this year, following an appeal by both parties, Myriad and a group of medical organizations coordinated by the American civil Liberties Union and the public Patent Foundation (PUBPAT), both of New York City. The Supreme Court sent down to the Court of Appeals for the Federal Circuit (CAFC) to a new analysis.

In the today CAFC rules that Myriad's gene patents themselves are invalid "because each of the claimed molecules represents a non-naturally occurring composition of matter. " This reasoning presupposes that patents are based on "non-natural" segments of DNA extracted from the cells, and not DNA as occurs in the nucleus. The court also rules that a method for screening potential cancer therapeutics by monitoring their effects on cell growth is patentable, contrary to the opinion of the lower court. But CAFC Judge zero claims company on screening cancer risk by comparing or analyzing DNA sequences because these methods are based on "abstract mental steps" of logic that are not "transformative" .

one of the three judges decide, William Bryson, dissents in part from the majority opinion, arguing that the allegations of the Myriad BRCA fragments of genes and genes are not valid. he writes that he fears that if the opinion of the current majority, he "probably will have broad consequences, such as preempting methods for whole genome sequencing."

the decision unlikely to fully satisfy either party of Battling, although some biotech companies can be relieved that the court did not erase all gene patents.

Myriad has not respond to an email query about what he planned to do. Prosecutor Daniel Ravicher of PUBPAT, who led the legal battle against the BRCA patents, replied that his group has not "taken a final decision on what we will do. ... But we are not satisfied with this result and believe that the dissenting judge in the Court of appeal today's decision is correct that isolated human genes are not patentable. "

August 13, cardiologist Gary Gibbons became director of 3 billion National Heart, Lung, and Blood Institute (NHLBI) $. Gibbons, who turns 56 next week, is the third largest National Institutes of Health (NIH) component of Morehouse School of Medicine in Atlanta, where he founded a research center which studied cardiovascular diseases among minorities. Previously, he was a faculty member at Stanford University and Harvard Medical School.

Gibbons served this year on a working group that advised NIH on how to promote diversity. It was formed after a study found that among scientists that require NIH research grant, blacks had a success rate of 10 percent points less than whites. Part of his reason for coming to NHLBI, said Gibbons was to address this problem. It will maintain a laboratory at the National Clearinghouse on Minority Health and Health Disparities.

Gibbons spoke with Science Insider last week; his remarks were published.

Q: Why were you interested in this position?

g.g. I think this organization has an inspiring and noble mission. It is one that resonates with me as a clinical scientist. I am always motivated me to address scientific issues that have implications for patients and patient care and public health. And what is it.

Similarly, an essential part of the NHLBI mission of this institute about to train the next generation. And I have a passionate commitment especially to expand the diversity of biomedical workforce. This position gives me the opportunity to really pursue that goal.

Q: What motivates you to continue the public service

GG: One of my heroes growing up was my mother, who exemplified this notion of community service, giving back. This comes from his personal experience as an orphan growing up in the Great Depression. Its survival was due to the kindness of strangers. She has always felt compelled to give back. That value system was instilled in us as children. I wear in this kind of family tradition.

Q: What was your reaction to the report in August 2011 to find a low success rate for African American scientists who apply for NIH research grants?

g.g. Having a life experience, it is not surprising that there are differences. I think it is also clear that even if we think we have a review system superb peers, outcomes and results are not always driven only by the assumption that was written and specific objectives. There are other factors that come to bear and race happens to be one of them, apparently. But what institution you are also delivered in the analysis as well.

One of the key points [the diversity working group] report is that it can be assumed that part of the reason why people in some institutions, say the first 25, outperform those of other institutions that have less funding from the NIH perhaps they are not as well supported by people who are successful senior investigators who know the best strategies to receive funding.

I am encouraged that it is something remediable. This mentoring is something we can do more accessible to candidates and I hope it is something that we can expect to tackle.

Q: How will you balance priorities in a flat budget NHLBI

GG: The success of NHLBI is based on sustainable principles including being a priority investment in the fundamental basic science discovery. This will be a main part of our portfolio. Another key element is a balanced portfolio that appreciates the basis of additional value, translational, clinical and scientific population. I think it is essential that we maintain this balance because they all mutually reinforcing.

Q: Do you have to think more if you can finance large clinical trials

GG: It will be important to take careful consideration in ensuring that each of our budget lines that we are more strategic, thinking about the profitability of our approaches. ...

I can understand that the clinical trial costs can attract attention within our overall budget, but I think it is also important to step back and recognize the impact of these tests. Many of them are truly transformative to change the way we treat patients.

Q: What are the major challenges ahead

gg. One is: We are in the midst of an obesity epidemic . And we have children who start to get the risk factors for cardiovascular disease at an age earlier and earlier. This has an incredible impact on our nation and our public health. And so it will be very important to work on preventive measures that can be a mediator obesity-related cardiovascular disease. ...

This will take a multidimensional approach. There is certainly the basis of scientific discovery to be done that can help narrow the effect of obesity on cardiovascular disease. In terms of clinical investigation, there may be opportunities to intervene in ways such as inflammation in a prevention strategy.

To be more provocative, we tend to think of [heart, lung, and blood diseases] that chronic diseases. Hypertension is something that you just forever. You take a pill forever. And yet, what we learn in the fields of biology remedial in terms of epigenomics, these advances suggest ways to intervene so that can delete or restart the body's memory and modify these processes such as atherosclerosis that span decades and change the natural history [of these conditions].

We often get jealous of our colleagues in oncology [who] about the remission of the disease. We are not quite there, but these are the boundaries that we would be happy to continue.

The fight against HIV with antibodies is like fighting against a forest fire with hoses watering. They can slow down the virus, but copies itself vigorously, making mutant versions that dodge this critical immune response. Now, experience suggests that infusing the mice with rare antibodies, exceptionally powerful products in laboratories and then combined into a cocktail might work as a treatment to supplement or even replace antiretrovirals (ARVs). It is a long way from mouse to man, and the cost of production of therapeutic antibodies can be prohibitive. But the concept intrigues many researchers.

The most potent antibodies against HIV are isolated from untreated individuals who failed to control their HIV infection for many years. These so-called neutralizing antibodies (bNAbs) do little to help the people who produce them, but their existence shows that mutations have created a population increasingly diverse virus, prompting the immune system to evolve a response which is both more potent and works against more variants. Unfortunately, the virus mutates easily around bNAbs of each individual, too. But a team led by immunologist Michel Nussenzweig of Rockefeller University in New York showed that it may be possible to thwart the virus by combining several bNAbs that target different parts of it.

As Nussenzweig and colleagues explain in a paper published online today in Nature , they tested bNAbs in a "humanized" mouse model. HIV can not copy itself to mouse cells, so they bought mice that had deliberately crippled immune system, then rebuilt with human stem cells. After infecting mice with HIV, the group tested five different bNAbs recently isolated from humans and artificially produced in laboratory monoclonal cultures.

ARV cocktails are extremely effective in treating people infected with HIV, but the drugs have serious long-term toxicities and should be taken daily. In addition, several clinical studies have shown that even when ARVs completely suppress HIV for years, viral levels rise almost always sharply in the weeks following discontinuation of therapy. If bNAb therapy worked, it would have distinct advantages, says Nussenzweig. "These antibodies are a natural product of man and should not have many side effects, and they can be very long," he said. "Potentially, they could be used twice or three times a year."

When the researchers tested the bNAbs as monotherapies, the levels of HIV generally decreased but rebounded in 2 weeks after stopping treatment, the virus mutated to escape the given antibody. A cocktail three bNAbs that GLOM the surface protein of HIV at different Fared places only slightly better. But when combined investigators five different bNAbs (see graph), the virus remained suppressed in seven of eight mice for 60 days.

the idea lost steam bNAb therapy many years after two small-scale human studies have failed. in the June 05 issue of Nature Medicine , a group led by Alexandra of Trkola the University of Zurich in Switzerland described how he had little success with a cocktail of three bNAbs given in 14 humans infected with HIV. Trkola but noted that the existing bNAbs had so much less punch than those available today. "The powerful new monoclonal antibodies and new humanized mouse models undoubtedly open up fantastic opportunities," she said.

immunologist Dennis Burton, who specializes in bNAbs against HIV at the Scripps Research Institute in San Diego, California, said the concept "exciting" "still has a long way to go" before therapy bNAb proves its value by the HIV. firstly infected humans, HIV does not copy itself to particularly high levels in the humanized mouse, meaning that those infected for many years have much more diverse swarms virus which would be more difficult for bNAbs to thwart These mice also do not have an intact immune system.. humans can develop antibodies against monoclonal antibodies, rendering them ineffective in strictly practical terms, the monoclonal antibodies are expensive and difficult to produce in large quantities.

Nussenzweig realizes the challenges. "this does not mean it will work in people," he said. "I think what it means is that it has to be tested in people."

BETHESDA, Maryland- The end of one, 13 months long historical global debate on the safety and wisdom of H5N1 bird flu research may finally be in sight.

After a 2-day meeting here, the US government officials said today they are moving quickly to adopt a new policy for reviewing some studies on H5N1 in order to identify high-risk research before it begins. The scientists said the move long discussed will allow them to quickly lift a historic moratorium on certain types of H5N1 research they have voluntarily imposed in January. The controversy was sparked by two studies that showed how to make the virus transmissible in mammals, which could spark a deadly human pandemic. Some researchers flu working outside of the United States said they may even declare the moratorium dead before the US National Institutes of Health (NIH) adopts its new policy review, scheduled no earlier than the month next.

"I think we'll see a lifting of the moratorium on the part of people who are not funded by the NIH," Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases (NIAID) said today at the end of a special meeting to discuss, fine tune, and test drives of the proposed policy H5N1. Many of the 39 flu researchers who organized the moratorium, he said, were "waiting patiently for this particular event ... I would not be surprised if they [now say] :. 'OK, we've heard all this." ... Some will move forward with their experiences if their country and donor permit. "

" We will discuss lifting the moratorium soon. ... I'm sure I'll be seeing a lot of emails about it tomorrow morning, "said virologist Ron Fouchier of Erasmus MC in Rotterdam, the Netherlands, who led one of the teams research that helped create controversy and also helped organize the moratorium. "it would be nice if all 39 of us agree to lift, or at least 37 or 38. But I think that some researchers outside the US will decide to resume "their studies in break even without unanimity, he said.

the last debate was held in front of some 0 people, including many top researchers H5N1 the world who gathered in an auditorium on the NIH campus to discuss the draft guidelines for consideration. the rules are supposed to help NIH reviewers decide what types of research H5N1 agency should, and should not, funds . participants also implemented the project, which the US Department of Health and Human Services (HHS) published on 27 November, four hypothetical studies.

The moratorium and the new rules apply only to a small range of experiences, called the studies "gain of function" in which researchers use genetic engineering or other techniques to naturally more deadly H5N1 virus or able to jump to new hosts, such as mammals. many researchers say that such studies are essential to understanding how the virus could mutate into a form that is capable of triggering a deadly human pandemic but others argue that the risks of this type of research outweigh its benefits. the issue came into focus hard at the end of 2011, when two research teams created the H5N1 virus capable of infecting ferrets . This work has aroused worldwide controversy as to whether the results should be published and whether funding agencies should do more to identify issues before they start school.

The review framework is designed to do. It sets out seven criteria that a study had to meet to be eligible for NIH funding. A researcher should show a gain of function experiment "great importance to public health," for example, and that there was "no possible alternative methods" to do. Scientists should also provide "evidence" that the H5N1 virus, they want to create "could be produced by a natural process of evolution in the foreseeable future." A study that fails to meet one of the criteria would get further review by HHS and other agencies and possibly a recommendation that he be transferred to a body that classified research, such as security services defense or homeland if their authors thought the results would be too dangerous to share.

The plan has drawn mixed reviews scientific, with critics saying that some of the criteria, especially one that requires researchers to show that their designed virus could appear one day in nature are formulated too vaguely and set too high a bar for funding. Others fear that politics could undermine international collaboration, particularly if other countries do not follow the example of the United States.

Participants here had many suggestions to avoid such problems. A major recommendation seems to be gaining traction is to limit additional notice HHS level for a subset of studies that propose to create particularly dangerous H5N1 specifically, viruses that may infect mammals and spread through the air, eg by saliva droplets. A "growing chorus" of researchers seems to approve the idea, according to Amy Patterson of the NIH, which helps write the new policy. These limits, supporters argue, could allow reviewers to sift less risky experiences that are easier to hold and more difficult to exploit for evil purposes. Researchers could, for example, propose experiments aimed at making a more infectious or deadly virus among birds, but not the air in mammals, regardless roadblocks. And the narrower scope would reduce the number of proposals that could be lost in the bureaucracy, they say.

"As written, many of H5N1 studies that are not intended to come to the examination will be considered," said Nancy Cox, a virologist at the Centers for Disease Control and Prevention in Atlanta. "If you read this conservatively [HHS is] will have to review 75% of H5N1 in the NIH studies portfolio," said Richard Webby, a researcher H5N1 at St. Jude Children's Hospital. Bureaucratic delays, he said, could lead researchers to leave the field or discourage students to work on the virus.

Patterson and other officials of the NIH could not promise they would do this and other proposed changes; the meeting was to gather information and not make decisions, they said. And the government plans to release a second version of rules based on public comments received to January 10. But Fauci was clear that he wants to move quickly. "I am sensitive to the fact that it can be drawn over a long period," he said. "We want to accelerate it."

The new policy will affect many studies. H5N1 gain of function studies represent less than 10 million or $ less than 1% -of overall influenza research spending NIAID, Fauci said, and less than 10% of the subsidies it gives to research on H5N1 (there many other flu viruses).

It is unclear whether other countries will follow the example of the United States. At the meeting, researchers from Indonesia, Malaysia and other countries where the H5N1 virus is a simmering problem generally expressed support for studies and concerns about policies that might hinder the function of gain field. But many said they are more interested in making studies characterizing the natural virus found in their country, or to help more directly with drug and vaccine development. Europe's researchers noted that some of their nations develop their own systems for the examination of potentially risky research. Many researchers of influenza, however, say that the requirements of safety and laboratory safety in many countries are already strong enough to allow the gain of function studies of H5N1 proceed.

The voluntary moratorium on these studies, Fouchier said, "has now achieved its goal." He gave governments, scientists and the public time to discuss and implement new policies and ensure that the H5N1 researchers do their work safely. It is time, he says, "to get back to work."

Not everyone at the meeting agreed. "I think we should continue the moratorium," said Thomas Inglesby, head of the Center for Biosecurity at the University of Pittsburgh Medical Center. Scientists have not yet demonstrated that the benefits of gain of function studies outweigh the risks, he said. And "if we decide to proceed, all should recognize the extraordinary risk."

fish animals face a tough race when shipping their territorial waters to aquariums around the world. To avoid infection, antibiotic use is widespread in the ornamental fish industry. But the practice is proving increasingly inefficient and contributes to antibiotic resistance in these ornamental fish, according to a study published this month in the Journal of Fish Diseases . The scientists studied bacteria in 32 species of freshwater fish, which were imported from Singapore, Colombia and Florida, the main export centers of ornamental fish. They found new bacterial species are not susceptible to any of the antibiotics tested. The most effective antibiotic has 16% resistance. The least effective drug face resistance at 77%. Although the risks to human health remains low, the biggest problem is that the ornamental fish industry of $ 15 billion will face a growing challenge treat sick fish that antibiotics are not regulated. Researchers plan to use this information to educate fish farmers on the need to curb the widespread use of antibiotics in fish feed.

See Science Shots .

for decades, doctors have been admonishing us to reduce salt to reduce the chances of a heart attack or stroke. Now there may be another reason to avoid seasoning: studies in rodents and cultured cells, reported today, show that dietary salt could promote autoimmune diseases such as multiple sclerosis and inflammatory bowel diseases.

The studies "have done a wonderful job of pushing knowledge forward and explore something that is potentially clinically important," says immunologist David Fox from the University of Michigan Medical School in Ann Arbor, who was not involved in the research. Daniel Cua, an immunologist at Merck Research Laboratories in Palo Alto, California, agrees. The work "is really well done with a lot of mechanistic understanding."

The results suggest that the salt stimulates the specialization of T _H 17 cells. Although these immune cells protect us against bacteria and fungi, they have also been implicated in diseases such as inflammatory bowel disease, multiple sclerosis and psoriasis. T _H 17 mature cells from non-specialized T cells, and, according to their influences, they can be beneficial or destructive.

The researchers have converged on the results of different directions. Immunobiologist David Hafler of the Yale School of Medicine and colleagues found that people who admitted to eating lots of fast food harbored more T _H 17 cells. An ingredient that fast food contains prodigious amounts is salt. To determine whether the salt represented excess T _H 17 cells, Hafler and colleagues doped T cell cultures with unskilled sodium chloride. "The results were perhaps the most dramatic of my career as a researcher," he said. Modestly raise salt concentrations, mimicking the levels in the tissues of an animal a diet high in salt, increased the number of T _H 17 cells that matured in crops almost 10 times . And these T _H 17 cells began to molecules causing inflammation, indicating that they had become the harmful variety.

The scientists then tested whether this effect sinister occurred in animals. They made mice develop encephalomyelitis experimental autoimmune (EAE), a neurological disease similar to multiple sclerosis which is favored by "bad" T _H 17 cells. They fed some meals rodents that contained about as much salt as a typical Western diet. Compared to animals that lived on the poor food salt, mice that nibbled chow rich in salt developed EAE earlier and had more severe symptoms, the team reports in Nature .

Working independently of the group Hafler, calculating biologist Aviv Regev of the Broad Institute in Cambridge, Massachusetts; Vijay Kuchroo immunologist at Harvard Medical School in Boston; and colleagues also hit a link between salt and autoimmunity. They tracked gene activity during the period T _H 17 cell maturation three days and revealed the molecular circuitry that controls the process. One of the most influential genes of this network was SGK1 , and it has a salt connection, helping cells to manage the levels of sodium. Using T cell cultures, the team found that salt promotes specialization of T _H 17 cells SGK1 .

The sodium content is higher in the fluids of the body tissues, where T _H 17 cells fight against pathogens in the blood stream. T _H The sensitivity of 17 cells salt can be adaptive in normal conditions, ensuring that they rotate in the right place. "You do not want the activated T cells in peripheral blood," said Hafler. "You want them to be activated when they go into the tissues."

But rising salt levels by eating a lot of salty foods could mean trouble. The medical implications of the results could be profound, human genetics notes Judy Cho of the Yale School of Medicine, who was not involved in the research. For example, autoimmune diseases such as multiple sclerosis and type 1 diabetes have become more common in recent decades, "a massive increase in salt intake could easily explain."

Researchers must now confirm that the salt is a factor in human autoimmune diseases, says immunologist John O'Shea from the National Institute of Arthritis and Musculoskeletal and Skin Diseases Bethesda, Maryland. People should not assume that the link is "a done deal" in humans. Scientists are ready to discover Kuchroo said. "The scene is ready to make accurate experiments to test the hypothesis."

Our guts are awash in bacteria, and now a new study fingers as culprits in heart disease. A complex dance between microbes and a component of red meat could help explain how food can lead to atherosclerosis. The work also has implications for some energy drinks and energy supplements, which contain the same nutrients as these bacteria like chasing.

Red meat is considered bad news regarding heart health, although studies are not compatible how can hurt and if it always does. In addition, it is unclear which components of meat are bad. Various studies have examined the fat or saturated sodium, but the results are inconsistent and sometimes depend on whether the meat has been processed or not. Stanley Hazen, section chief of preventive cardiology and biochemist at the Cleveland Clinic in Ohio, questions whether another ingredient could be harmful: L-carnitine, a nutrient that helps transport fatty acids into energy plants the cell mitochondria. L-carnitine is a popular additive to energy drinks and supplements that claim to boost energy levels. In food, the highest levels of L-carnitine in red meat.

Hazen focus on L-carnitine was something of a wild guess based on the earlier work he had done. There are two years, he and his colleagues published a paper in Nature identifying a compound in the blood called trimethylamine N -oxide (TMAO). It seemed to correlate with future heart disease risk and cause heart disease when fed to mice. TMAO is created when intestinal bacteria decompose certain compounds in food. Hazen wondered if bugs can also convert L-carnitine OTMA, which, in turn, could put the heart at risk.

To find out, Hazen, his PhD student Robert Koeth, and colleagues bought a George Foreman grill and started cooking steaks. "People lined up for the study," says Hazen, and participants "tend to be young, hungry students." Blood tests administered after revealed level rise OTMA. This showed that something was the conversion of L-carnitine to TMAO, but researchers could not say yet that the culprits were bacteria. To pin it down, they gave five of antibiotics broad spectrum volunteers for a week to remove microbes from the gut, and then repeated the experiment. This time, there was virtually no TMAO in the blood or urine after the volunteers ate a steak, suggesting the conversion could not be done without the bacteria.

"When you measure things in people's blood, you do not think of [them] as from bacteria," says Hazen, but in this case appears to be what is happening. The situation is the latest in a series of studies that have shown that the population of bacteria in our intestines, collectively known as the microbiome of the gut-can influence everything from weight loss to brain chemistry.

as the researchers now describe in Nature Medicine , mice fed a diet supplemented with L-carnitine for 15 weeks had significantly higher levels of TMAO than control animals. animals obtain additional L carnitine had roughly twice the burden of atherosclerosis in arteries compared to mice a normal diet.

And the intestines of mice get additional L-carnitine also adapted, becoming enriched for various classes of bacteria that could more easily convert L-carnitine OTMA. This suggested that people who eat lots of red meat may be particularly effective for converting L-carnitine to TMAO and that the consumption of food in moderation might be less damaging because the conversion could be slower. Twenty-three vegans and vegetarians given L-carnitine supplements were, Hazen's group found, less able to synthesize TMAO than those who regularly eat red meat.

It is still unclear why TMAO seems to promote atherosclerosis. Hazen group work by suggesting that TMAO seems to make it easier for the immune cells in the arteries to accumulate cholesterol. Another mystery is how other foods containing L-carnitine could have an impact TMAO levels. For example, the fish, which is thought to reduce cardiovascular risk, also contains much lower levels of L-carnitine, as chicken and milk, says Dariush Mozaffarian, an epidemiologist at the Harvard School of Public Health in Boston, who has studied meat and heart disease, in an email. Inconsistencies also remain about how red meat is really dangerous. That said, although more work needs to be done to unravel the connection L-carnitine-microbe in people, "these results may prove seminal in the field," writes Mozaffarian.

"It tells a very compelling story, "says Daniel Rader, a preventive cardiologist at the University of Pennsylvania. The best way to determine exactly how L-carnitine affects cardiovascular disease, he said, is a clinical trial that manipulates the amount of L-carnitine people take in. Whether a trial such as this is feasible, however, this study "at least would suggest well, even if you have checked your LDL [cholesterol]" with drugs, "eating red meat could still be bad for you. "

Neuroscientists from across the country are wrapping a meeting today in drizzly Arlington, Virginia, where they discussed guidelines potential for brain research through the advancement Innovative neurotechnologies (bRAIN) Initiative a federal investment of $ 100 million in research of the brain that has not yet been clearly defined. This meeting focuses on how the project should focus on the physical and mathematical principles underlying brain function. An open call for white papers on the "main obstacles impeding progress in brain science" inspired responses from more than 70 major Neuroscientists. Scientists cite the problems that must be addressed, such as "to increase the density and longevity neural recordings untethered, free to include animals "and find" beautiful patterns "of brain function that can be analyzed mathematically.

To avoid being destroyed by our immune system, cancer cells engage in a little cunning. As they divide to form tumors, they fly under the radar of macrophages, immune cells whose job is to ingest dead cells and harmful invaders. Nowadays, many cancer patients are treated with antibody drugs that work in part by the marking of tumor cells to killing by macrophages. Although these drugs have extended the lives they do not always work very well partly because cancer cells to fight by sending a signal "do not eat me" to immune cells. Now, researchers have created a small protein that cuts the signal and increases the potency of antibody drugs to shrink tumors in mice dramatically.

stem cell biologist Irving Weissman of Stanford University in Palo Alto, California, studied a protein responsible for broadcasting the signal "do not eat me." Known as CD47, it protects the leukemia cells and other cancer cells unchained macrophages. Last year, the group reported that a Weissman antibody that blocks CD47 on cancer cells can stimulate macrophages to destroy tumors in mice. The anti-CD47 antibody will soon be tested for safety in humans with $ 20 million in funding from the California Institute for Regenerative Medicine.

As promising as this approach is, antibodies have drawbacks-their relatively large size limits how they can easily penetrate the tumors, for example, and can have toxic side effects so-effects group Weissman has also partnered with the structural biologist Christopher Garcia's lab at Stanford to test another way to block CD47. The team and Weissman Garcia describe the new work online today Science .

The collaborators began the study of a protein called SIRPα that grows out of the surface of macrophages and connects with CD47 to receive "do not eat me" signal of the tumor cell. Their idea was to block CD47 with a floating form, synthetic SIRPα which was designed so that the real SIRPα macrophage could not lock to the cancer cell and be deceived leaving alone. Garcia laboratory synthesized many versions of the SIRPα protein, determined their structures, and found that two forms related 50,000 times more closely to CD47 that natural SIRPα receiver.

Added to a Petri dish of tumor cells and macrophages, synthetic SIRPα proteins do not have as yet the macrophages ignored the cancerous cells. However, when the researchers threw in a drug-specific antibody of the tumor, that they realized that it was necessary to draw attention macrophages to cancer cells , first, the combination packed a powerful punch in cell cultures and in mice implanted with cancer cells. For example, while lymphoma tumors simply grew more slowly in the mice that received either rituximab drugs or SIRPα protein, the tumors disappeared for at least 7 months in most of the mice treated with both drugs. And adding SIRPα drug against breast cancer Herceptin decreased faster tumors in mice with the disease. "SIRPα weakens the ability of the cancer cell to protect itself from destruction," says Garcia.

Because SIRPα synthetic proteins are relatively nontoxic, Garcia and Weissman hope they can find funds to develop quickly in an experimental drug. "I want to see this test in humans as soon as possible," said Garcia.

Drew Pardoll cancer immunologist at Johns Hopkins University in Baltimore, Maryland, said the idea of ​​blocking CD47 with a small protein instead of a large antibody is "pretty cool. I'm not aware that this kind of approach has been taken before. "However, he warned that, as with other new treatments that work by raising the brakes on the immune system, there could be side effects. "These negative regulatory pathways were not there for no reason at all" but may have an important role in normal cells, he said. For example, the CD47 'do not eat me "signal also protects red blood cells from destruction by the immune system.

Amsterdam University cell biologist Timo van den Berg adds that although" the data is quite convincing and exciting, "because CD47 is expressed on most cells in the body, these cells will suck SIRPα protein, potentially it is difficult to obtain sufficient tumor cells. His own group works an antibody that blocks the receptor SIRPα, which appears primarily on macrophages, as a way to prevent these immune cells receive a misleading message to the cancer cell. Garcia said that although he thinks the approach of his team will work well for patients, "certainly blocking the other direction is a viable strategy and interesting to watch."

The youngest patient to receive an artificial trachea seeded with stem cells died, The New York Times reported today. Hannah Warren, who was born with a rare congenital defect that left her without a trachea, underwent surgery in April to have a synthetic trachea implanted which was seeded with stem cells from his bone marrow. She would have had 3 August.

His doctors told The New York Times that his death was due to complications from a second surgery was needed to repair her esophagus, which had not properly healed after initial surgery. They said that the trachea had been a good performance. The experimental technique used its surgeons received criticism from some experts, who say that 5 years after the first recipient of a similar transplant, the evidence is still lacking that the implanted trachea function as they should.