Health Meaning

castor oil can have a bad reputation among the people who were force-fed spoonfuls like children, but it is not a myth that tonic has health effects. Today, scientists have elucidated the molecular mechanism of the active ingredient in castor oil, which has been used for thousands of years as a laxative and labor spillway. ricinoleic acid, which fatty acid is about 0% oil, binds to a particular receptor in the gut and uterus, the researchers found. The discovery explains how castor oil and could lead to development of drugs less unpleasant.

While taking a daily spoonful of castor oil diluted as general assistance for health is more fashionable, alternative health stores still sell the liquid foul-tasting as a laxative. The Food and Drug Administration has classified castor oil as "generally recognized as safe and effective," but researchers do not understand its mechanism.

"When you study classic, old drugs, is almost always learn something from them," said first author of the new study Stefan Offermanns, a biologist at the Max Planck Institute for Heart and Lung Research Germany. "The biggest surprise here was how specifically castor oil worked."

Offermanns and his colleagues were screening different fatty acids for their ability to bind to certain cell receptors when they have achieved success with ricinoleic acid. Knowing extensive use of castor oil in traditional and alternative medicine, the team decided to take a closer look at the compound. The use of a large library of molecules that block the cell receptors they studied, they were able to home in two as ricinoleic acid connects to: EP ₃ and EP ₄ . Both are prostaglandin receptors, which have different roles in the body, to change the structure of neurons to control how the blood clots. In experiments on mice, the researchers showed that ricinoleic acid induces its laxative effects and inducing labor by interacting with EP ₃ . When someone swallows castor oil, ricinoleic acid on locks EP ₃ molecules in the smooth muscle cells in the walls of the small intestine and causes contractions, which explains the efficiency of castor oil as a laxative. Similarly, researchers have shown that ricinoleic acid binds to EP ₃ and in the uterus causes contractions. The team published its results today in Proceedings of the National Academy of Sciences .

"There were many theories as to how castor oil worked, including broad toxicity to intestine cells and the effects on water and electrolytes," says Offermanns. But ricinoleic acid is much more accurate than those theories suggest, acting through a single receiver. How the receiver causes contractions, however, is still not known. But the new link between EP ₃ and bowel and muscle cells of the uterus could inspire the work to find out.

"They made these experiences quite elegant and complete," says biologist Phillip Bennett from Imperial College London. "And at one level, this finding is somehow a little quaint curiosity but there is more than that. "

the knowledge that ricinoleic acid binds to EP ₃ could be used to design drugs that target the receptor, said Bennett. These drugs could be used as laxatives or working without inducing side effects such as nausea, castor oil.

a daily dose of castor oil will not keep the doctor and modern medicine n ' has not yet backed claims that he also treats skin conditions, relieves pain and heals infections. So take castor oil with a grain of salt, or a spoonful of sugar.

The researchers understand why a popular therapy for the treatment of colon cancer often eventually stops working: The tumors naturally carry genetic changes that allow certain their cells to evade the drugs and continue to grow. The good news is that doctors may be able to detect these changes in patients' blood, then stop the cancer with another drug before it can grow again to a dangerous size.

Many people with advanced colon cancer are treated with proteins called antibodies that target a weakness of the tumor, a protein that stimulates the growth of cancer cells called EGFR. Antibodies often shrink tumors, but cancer usually comes back within 18 months. To investigate how this developed resistance, a team led by geneticist Alberto Bardelli from the Institute for cancer research and cancer treatment in Candiolo, Italy, increased colon cancer cells in boxes containing a growth medium laced with cetuximab anti-EGFR antibody called. The group now reports in Nature as the cells have become resistant to the drug because of changes in KRAS , a gene encoding a protein that may reactivate the growth path of EGFR when EGFR is itself blocked. The resistant antibody producing cells had mutations in KRAS and sometimes contain additional copies of the gene. The researchers also found these changes in biopsies of six patients with tumors that were resistant to cetuximab or a similar drug called panitumumab.

The blood of a cancer patient typically contains traces of DNA of the tumor. The Italian team and a separate group led by Luis Diaz oncologist at Johns Hopkins University in Baltimore, Maryland, have now found independently that KRAS mutations are detectable in blood samples from patients whose tumors have become resistant to drugs, Bardelli technology called a "liquid biopsy." the warning signs in KRAS appeared up to 10 months before the tumors become large enough to detect various standard imaging techniques such as X-rays. This suggests that clinicians could monitor patients' blood for resistance mutations and when they appear, give patients a second drug that also blocks the path of growth of EGFR, but in a way that KRAS mutation can not replace. the combination of such a drug called a MEK inhibitor with cetuximab killed colon cancer cells in a laboratory dish that were resistant to cetuximab alone group Bardelli reports.

"The concept of liquid biopsy, both groups used, is really a step forward, and I am sure it will be widely used in the clinic," said Bardelli, named online work today in Nature and the study of the Hopkins group.

another question was how resistance mutations got there. they were present in a few cells before the patient was treated with the drug, or did they occur after treatment? to find out, the team and his Hopkins colleagues at Harvard University have developed a mathematical model of the genetic evolution of the tumor that match their data KRAS mutations in the blood. They concluded that resistance mutations resulting from spontaneous changes in DNA that cells divide are present in some tumor cells even before the treatment. The model shows that the resistance is a "done deal", Diaz and his colleagues write. It is also probably inevitable for other so-called targeted therapies, such as those for melanoma and lung cancer, which also generally work for less than a year, Diaz said.

"The lessons here that resistance mutations occur spontaneously" into a tumor, even before therapy is tried, said Diaz. In rare cases, a patient-targeted therapy lived for years without develop resistance. But these tumors may be very young when the patient is first treated, or abnormally slow growth, Diaz said.

"these results are illuminating and sobering" because they show that resistance drug against the target colon cancer is inevitable, says oncologist Neal Meropol of Case Western Reserve University in Cleveland, Ohio. The treatments will target more than one molecular pathway, he said.

But Dominik Wodarz evolutionary biologist at the University of California, Irvine, also found the Hopkins study "encouraging" because the model seems to describe drug resistance in cancer and diseases such as HIV who are "very different from each other biologically." Although cancer is complex, given that its dynamics are "relatively simple" craft will help researchers better treatments, he said.

A man working for the World health Organization (WHO) on the campaign to eradicate polio was shot dead in Karachi, Pakistan, on the evening of 20 July. Muhammad Ishaq was shot outside his clinic in a slum in Karachi rough known as Gadap. Ishaq, who was the local community, died en route to hospital.

only 3 days earlier, two gunmen killed a Ghanaian doctor working for WHO and his Pakistani driver, participating in a national campaign of vaccination against polio in their car. The doctor was shot in the stomach; the pilot suffered a grazing wound on his shoulder. The two men are recovering.

After the first shot, the WHO has canceled the rest of the vaccination campaign in Gadap and implemented increased security measures instead.

Nobody has claimed responsibility for the shooting and there is no definitive evidence linking the two events, said Bruce Aylward, WHO Deputy Director General and longtime leader of global Initiative to eradicate polio. Similarly, it is unclear whether the shooting was random or polio workers targeted specifically. Until they get more evidence, said Aylward, "Our working hypothesis is that [the shootings] may be linked, and that affects our approach to security."

is Gadap slum densely populated with a large minority and migrant population. most residents of the tribal areas along the border with Afghanistan, where opposition to a government-run or a Western program is intense rumors abound that the vaccine against polio is dangerous and is part of a US campaign to sterilize Muslim children. About a month earlier, a leader of a faction of the Taliban in North Waziristan banned vaccination against polio in its part of the tribal area to stop the US drone strikes.

Expressing deep sadness, the WHO issued a statement saying that the shooting will not distract from the state progress of Pakistan made in its fight to eradicate polio. Pakistan and Afghanistan and Nigeria, is one of three so-called endemic countries where polio transmission has never been interrupted.

The failure of treatment of pancreatic cancer, announced Wednesday by its manufacturer Amgen, is yet another sign that a class once promising treatments against cancer failed to meet expectations. The latest flop treatment called ganitumab, is a monoclonal antibody that targets the factor 1 receptor-like growth to insulin (IGF-1R), type. At Amgen, the drug all the way to a clinical Phase III trial before the company pulled the halfway taken through the trial after finding that the therapy was unlikely to help patients live longer .

IGF-1R has been considered a promising target after researchers have made a number of interesting observations. are linked to a slightly increased risk of cancer circulating levels of IGF-1 hormone in the blood of a person. The receiver is often expressed on epithelial cells, the type of cells that become cancerous, and it promotes cell survival. Finally, in cell cultures and animals overexpressing the hormone might produce something that looks like a cancer, and it would shrink when treated with an inhibitor of IGF-1R.

But in patients, drugs are "a series of failure," says Vuk Stambolic, a cancer researcher at Princess Margaret Hospital and Ontario Cancer Institute in Toronto, Canada. Other trials of this drug target in lung cancer did not work, and the effects of these drugs in colorectal cancer are also doubtful, said Stambolic.

the Achilles heel for many potential cancer drugs is biology. in short, it usually turns out to be more complicated than first thought. it may not be enough to go after only IGF-1R, and patients in these trials have very advanced disease and may be less likely to meet very targeted treatments. the work of animals and cells as real life can not fully emulate. "I think the model is probably only partially representative of what happens in cancer," said Stambolic.

Various companies are also testing a class of drugs that target both IGF-1R and the insulin receptor. The hope is that the double whammy will be more damaging to the tumor.

National Institutes of Health's new Translational Research Center (NIH) has its first head: Christopher Austin, a neurologist and former Merck researcher led drug discovery efforts at NIH for the last 10 years. The NIH Director Francis Collins announced the appointment this morning at the inaugural meeting of the Advisory Board of the 9-month-old National Centre for Advancing Translational Sciences (NCATS).

Congress signed the $ 575 million NCATS last December after months of controversy about whether the NIH tried to become a pharmaceutical company. NIH insists that NCATS will be limited to treating the bottlenecks in the drug development process.

Collins said that after "vigorous international research," NIH chose Austin, 51, who now heads the division NCATS 'preclinical innovation. "Chris has had a remarkable career with a great diversity experiences that put it in a wonderful position to lead this company, "said Collins.

A development neurogeneticist Harvard-trained Austin worked on the discovery of genome-based drugs from Merck for 7 years. In 02 he left to become advisor for translational research at the National Institute for Research on the human genome, where Collins was director. Austin helped launch the Molecular Libraries Program of the NIH, a set of testing centers of small molecules style industry in academic institutions. Until recently, he directed the intramural NIH screening center and other programs, such as the development of drugs for rare diseases. When NCATS was created, they were bent in its preclinical division.

Austin, which begins September 23 (his birthday), described the NCATS appointment today's meeting as the "culmination" of his long career efforts to bridge basic research and clinical. "This is a very difficult mission, ambitious but deeply important that we are all about," he said.

Some observers suggest that the NIH has struggled to recruit a director of NCATS outside because a scientist from the industry who moved to NIH would probably take a steep pay cut and dispose of any company stock medicines he or she belongs. Other deterrents could have been dark NIH budget outlook and the next presidential election, which could cause a change in direction of the NIH.

Steven Paul, a former head of Eli Lilly now looking at Weill Cornell Medical College in New York, who served on the search committee, declined to say if the government rules hindered research. What matters, Paul says, is that "We came with a wonderful person ... Chris is credible with both university researchers and the private sector.".

At the meeting today, leaders of the NIH and its advisers-a mixture of patients, industry experts and university-started this sort NCATS will do. (The meeting also included the board overlapping the Cures network acceleration, CAN, NCATS a component that will give grants for drug development.) US Food and Drug Administration (FDA) Commissioner Margaret Hamburg said NCATS she hopes will not only come up with specific tools to improve regulatory science, such as new trial designs but also get both basic science and clinical thinking about the steps needed to transform a potential drug a product. "We need to think about how we do research a little differently," she said.

Thomas Insel, director of NCATS acting, warned that the center, which consists mostly of existing programs at NIH, will not be much new money to work with. "We really need to be very focused," he said.

But CAN board member Tachi Yamada, Medical and Scientific Director at Takeda Pharmaceutical Co. said NCATS does not necessarily need a big budget to make an impact. "Many solutions can be very cheap if thought strategically," he said. Yamada, who also worked for the Bill & Melinda Gates Foundation, gave the example of an ongoing collaboration, he was involved in to work with the FDA to obtain approval of a cocktail of three drugs for tuberculosis, without passing through "50 years of clinical trials." NCATS, he said, will benefit from "a very serious strategic analysis when true roadblocks may be in selective areas. "

Tuberculosis (TB) continues to cause a "huge" burden of disease, according to an update released today by the World health Organization (wHO) estimates that there were 8.7 million new cases in 2011 and 1.4 million deaths. But there are high hopes that improved diagnosis and medications will, in the coming years to make a significant dent in the search for people who have the disease, the provision of appropriate treatment for their lives, and slow spread Mycobacterium tuberculosis itself.

The WHO figures Global Tuberculosis Report 2012 are similar to those published the previous year. "TB control and care is at a crossroads," said Mario Raviglione, who heads the STOP TB program of WHO, during a press conference in Washington, DC "Firstly we have existing as well as new tools on the horizon which could make a significant difference and even support dreams of elimination in some settings. But then, we are at risk of stagnation if additional resources are not mobilized urgently by governments of endemic countries first and if the international community is not ready to fill the gaps. "

the new report of 272 pages underlines that much progress has done against tuberculosis between 1995 and 2011, during which 51 million people have received a full course of treatment, which lasts a minimum of 6 month and lives 20 million were saved. But multidrug-resistant (MDR-TB) remains a huge problem, with 630,000 cases worldwide; only one in five of these people receives a proper diagnosis necessary for effective treatment.

The estimated new cases fell by 100,000, which, even taking into account the population growth is a modest decline of 2.2% between 2010 and 2011. The proportion of people with TB are co-infected with HIV remains broadly unchanged at 13%, but it is more than 50% in several countries in sub-Saharan Africa. What is clearly new to the report this year, Raviglione said, is the first estimate ever made of the burden of TB in children: half a million TB developed in 2011 and 64,000 died of the disease.

The report highlights some improvements. Many countries have begun using a new diagnosis, a machine called GeneXpert, which has a much higher accuracy than the centennial microscopy test, which is widely used and requires a lot less work. The GeneXpert test two hours can also determine if a person has MDR TB; before, it took several weeks for the culture Mr. TB , and then test the bacilli drug sensitivity. But the Xpert test is considerably more expensive: In South Africa in 2011, the government paid at least $ 15 for each test of the machine, compared to $ 3 for a microscopic test of sputum.

As noted in the report, the company that makes GeneXpert, Cepheid of Sunnyvale, California, in August agreed to sell the cartridge from the machine uses, making the chain reaction of the polymerase on sputum samples -to a discount of 41% to hit hard and countries with limited resources. June 2012, 67 countries had purchased the reduced system.

The report also highlights that for the first time in decades, two new TB drugs are about to hit the market. The drugs, which should receive regulatory approval in the coming months, will be first used to treat MDR and promise to have less toxicity and work faster than treatments currently in use. A short-term plan to cure the regular TB and a vaccine that can reliably prevent most cases of the disease are still far - although attempts to make these dreams become reality longheld intensified.

A particularly disappointing part of the report focuses on the funding of prevention, care and control, which is expected to total $ 4.8 billion in 2013 for 104 countries with 94% of cases. But these low- and middle-income and need as much as $ 3 billion more each year to effectively meet their TB epidemics. "We are facing actually the main financial risks in a scenario where efficient technologies are now available," Raviglione said. Although he acknowledged that large increases in funding from governments and multinational organizations such as the Global Fund against AIDS, Tuberculosis and Malaria, the financial deficit "means millions of unnecessary gaps in the coming years. "" history teaches us that in the fight against tuberculosis, collect achievements we have had so far as "done" is an absolutely fatal error. "

future boom in space tourism will increasingly expose members of the public or at least those lucky few able to pay the ticket price a range of ills that so far, most of the time, only the astronauts healthy superbly met. In a new analysis, the researchers surveyed previous studies of space medicine and compiled the list to alert physicians to the myriad ways that spaceflight could worsen pre-existing conditions in their patients, whether during short suborbital flights from commercial space operators (launch of Sierra Nevada Corp. 's Dream Chaser represented by an artist) to a getaway week of the international space station, or relay monthlong construction or working in hotels or orbiting laboratory commercial research. Almost no body function is spared, but most ailments could be managed with medication or with the quantities and types of exercise in proper orbit, the researchers suggest. in addition to motion sickness, headaches and sinus congestion possibly triggered by short flights, long flights could aggravate osteoporosis, back pain, acid reflux, and certain types of cancer, as well as increase the risk of infections and calculations kidney, the researchers report online today in BMJ . The new compilation is not just an abstract exercise, the researchers say: Previous studies suggest that, once the fleets of vehicles capable of space available, commercial launch companies together could expect up to 13 000 tourists space during their first decade of operation.

See Science Shots

nearly a year after they announced it, leading researchers flu ending a voluntary moratorium on certain types of controversial experiments involving the H5N1 avian influenza.

In a letter published online today Science and Nature , 40 researchers say the studies should restart now that scientists, government officials and public have had time to discuss the need for research and to impose new security measures. "[T] it is the voluntary moratorium have been achieved in some countries and are close to being met in others," they write, and researchers "have a public health responsibility to take this important work."

The movement essentially ended the H5N1 controversy, which began in late 2011, when two research teams showed how to redesign the virus that normally infects birds, so that it can move between the mammals. The discoveries have triggered intense global debate about whether newspapers should publish the results, some critics fear could be used by terrorists to trigger a deadly human pandemic. It also led to a discussion of whether scientists should make such studies "gain of function" at all. The results were finally published in Science and Nature , but the controversy has prompted governments in the US and elsewhere to impose increased surveillance on H5N1 research.

Today's letter comes as little surprise to those who have followed the controversy. The moratorium, which was announced January 20, 2012 in a letter signed by 39 prominent researchers H5N1, was originally intended to last only 60 days. But researchers extended it indefinitely in March 2012, when the debate intensified. Last year, however, many of those who agreed to the break began to lobby for lifting the moratorium that the United States and other nations finalized new systems of review proposals H5N1 gain function research and implemented safety guidelines for laboratories working with particularly dangerous forms of the virus. Last month, after an international meeting of two days on the issue organized by the US National Institutes of Health, which funded the two controversial studies, leading researchers and government officials said they were waiting for the moratorium to end soon .

The H5N1 research should resume in two stages, the researchers write in today's letter. scientists Influenza working in countries that have completed the safety rules and laboratory funding should now be free to resume experiments involving the re-engineering of the virus, they wrote. But "[s] Scientists are not expected to return to work in countries where, yet, no decision has been reached on the terms of the search for the transmission of H5N1. At that time, including research to United States and the United States financed conducted in other countries. "funded US researchers might not have to wait much longer to lift the moratorium, however, because officials are in the final stages of approval laboratory safety and consideration of the proposal guidelines.The Japanese government has also not yet finalized its rules for the H5N1 research, researchers say.

"There probably is not a scientific question in these time that was not so widely thrown to the public consultation that one, "one of the signatories of the letter, virologist Wendy Barclay of Imperial College London, said in a statement released by the science Media Centre in London. The moratorium was necessary, she said, because of a "reflex response from some quarters ... express the horror that scientists were preparing fatal diseases. It became clear that the public needed comfort and justification for these experiments. "

Now she and others from influenza want to return to try to understand how the H5N1 virus could become more dangerous to humans and how health officials would be able to stop a pandemic emerging. "[B] s the risk that exists in nature H5N1 virus capable of transmission in mammals may emerge," the researchers say, "the benefits of the job outweigh the risks."

in a conference call today, the main author of the letter said he does not expect researchers to be able to start the study immediately. "it takes time to stop the search, and it takes time to begin to save it, "said virologist Ron Fouchier of Erasmus MRC in Rotterdam, the Netherlands, who led a controversial studies. But Fouchier already has an idea of ​​what kind of studies he would like to do. Emphasis will determine exactly which mutations allow the H5N1 virus to move between mammals in the air or respiratory droplets. Researchers have found so far "five to nine" mutations that enable the transmission in mammals, he noted. Fouchier is also interested in whether the same mutations may make other H5N1 strains "in the air."

* Correction, 17 hours: The moratorium on H5N1 research was extended indefinitely in March 2012, not March 2011.

The World Health Organization (WHO) today released a report saying that the Fukushima nuclear disaster will cause no increase observable in cancer rates among residents of other countries and very small increased risk of cancer among residents near the plant. Workers struggled problems at the plant do not face higher risks of certain cancers.

The environmental group Greenpeace immediately condemned the report as "a political declaration to protect the nuclear industry." But at least one radiation health expert believes the report overestimate some risks.

wHO assessment of potential health effects is based on a report of May 2012, which estimated that the radiation exposure in different places around the Fukushima Daiichi nuclear plant, which released large quantities of radioactive material after having suffered several explosions and collapses in the earthquake and tsunami of 11 March 2011.

the team of 13 experts from the WHO estimated the increased risk of life of leukemia, cancer thyroid, and breast cancer in women for people living in geographical locations ranging from the most affected areas adjacent to the power plant to distant parts of the world. Beyond the areas near the plant, radiation doses were below levels known to have effects on health, the report says. "Apart from geographical areas most affected by radiation, even in areas of Fukushima Prefecture, the anticipated risks remain low and no observable increase in cancer above the natural variation of the reference rates are to be expected" reads the summary. the report notes that in the two most affected areas of Fukushima, estimated doses in the first year ranged from 12 to 25 millisieverts (mSv).

"in leukemia [sic], the lifetime risks are expected to increase by around 7% compared to the basic rate of cancer in exposed male infants, for breast cancer, the risk to estimated life increases up to about 6 % compared to the reference rate in females exposed infants, "the report concluded." [F] or all solid cancers, the risks to the estimated life increases up to about 4% from the rate reference in females exposed as infants, and for thyroid cancer, said the risk increases for life by up to 70% on the basic rate line in women exposed in infancy. "

The report explains that these are relative increases compared to the reference rate and not absolute risks. Thus, because the risk of thyroid cancer the basic life among women is just 0.75%, the additional risk due to exposure to the most affected area is 0.5%. The risks in the second most affected location are half of those in the most affected region.

Kazuo Sakai, a radiation biologist at the National Institute of Radiological Sciences in Japan, believes that the risks "are overstated." He explained that the estimates of doses used were based on preliminary data; Actual measurements showed real dose levels to be lower. He also said that the risk is based on a calculation that takes 4 months of exposure to radiation in different areas. But because of the timely evacuation, there is probably no infant females, for example, who actually received the doses estimated for the most affected area, he said.

Greenpeace, however, believes the doses are widely underestimated. "The WHO report minimizes shameless the impact of radioactive discharges beginning of the Fukushima disaster on people inside the evacuation zone of 20 km that are not able to leave quickly, "a statement quoted Rianne Teule, Greenpeace International nuclear radiation expert, as saying. The statement says the modeling by the German nuclear expert Oda Becker concluded that the people inside the 20-kilometer evacuation zone were possibly exposed to hundreds of mSv.

The WHO report said that the emergency of the central workers face a higher lifetime risks for leukemia, cancer of the thyroid, and all solid cancers.

For cancer patients, things go from bad to worse when tumor cells escape into the blood stream. Cells sometimes marauding just one among a billion blood cells can lodge anywhere in the body, the spread of cancer in a process called metastasis. Now researchers have developed a device that can detect even a single cell of any type of cancer in the blood, allowing early treatment of metastasis and new knowledge of cancer genetics.

The cancer cells that migrate into the bloodstream are called circulating tumor cells (CTC). In 07, a team led by Mehmet Toner biomedical engineer at Massachusetts General Hospital in Boston has developed a method to trap and detect CTCs on a silicon chip the size of a microscope slide etched with microchannels each no wider that 'a strand of hair. Toner pumped from whole blood samples through the channels, which have been coated with an antibody designed to trap any cancerous cell that carries a common surface protein, as far as flypaper snags annoying insects. But cancer cells without the protein, such as melanoma (a type of skin cancer), slipped unnoticed.

The new system gets around this limitation. CTC-called iChip system (the "i" is for "inertial focusing"), it targets the blood cells instead of cancer cells. Sorting by size of the cell, the first chip creams out of small cells and red blood platelets, leaving only CTCs and white blood cells flow past. Then, a second chip winds cells through curving channels, channeling the remaining cells in a single file line. Magnetic beads of the size of bacteria attach to specific surface proteins on white blood cells, and a magnetic field nudges these cells out of the flow of CTC. That leaves just the CTCs, which can be collected in a vial and analyzed individually by conventional laboratory methods.

The clinical application of this technology is clear, said lead author Emre Ozkumur, a biomedical engineer also at Massachusetts General Hospital who developed the system with toner. Early detection of CTC allows doctors to begin anti-metastatic therapies, he said, which could slow or stop final fatal attack cancer.

all CTCs not develop into metastatic tumors, however, and cancer researchers are still discovering why. Because the CTC show such large amounts of genetic variation, bulk analysis of cells will not reveal the reason, said Ozkumur. "You have to analyze one by one."

The team reports its findings online today in Science Translational Medicine is already pondering its next improvements to reduce manufacturing costs down and prepare CTC-iChip for clinical use. The researchers' task list includes the integration of the system with two current chips into one, said Ozkumur.

The group's work is "a solid lead," said the engineer Robert Langer of the Massachusetts Institute of Technology in Cambridge. Langer, who owns more than 800 biomedical patents, welcomes the improvements in this device relative previous models. other diseases, like rare LAM lung disease, also involve circulating abnormal cells, says Langer. This technology can advance research in these diseases.