Health Meaning

When a person dying of cancer, the culprit is usually not the original tumor, but the cancer cells that spread throughout the body and replicate in distant organs, a process called metastasis. Researchers have long known that cancer cells metastasize slip their obligations and avoid immune detection by changing the sugars on their surfaces. They even come with a medication would be to avoid such sugar modifications. But this compound interferes with the sugars necessary on normal cells, too, with fatal results in animals. Now Dutch researchers say they have packaged the drug in nanoparticles targeted exclusively to cancer cells, and showed that this combination prevents cancer cell metastasis in mice.

The new therapy nanotechnology still has a long way to go before becoming a drug, including pass safety testing and efficacy in humans. Nevertheless, "it is promising," said Cory Rillahan, a chemical biologist at Memorial Sloan Kettering Cancer Center in New York who was not connected to the study. Rillahan, which it 3 years ago was part of the team the first report of anti-metastatic drug compound, known as P-3F _ax -Neu5Ac said the compound was designed to block a family of 20 enzymes that modify sugars known sialic acids. often sialic acids cap long chains of other sugar molecules that are attached to proteins or lipids that the cell surfaces of the uprights. These channels have been shown to be involved in cell adhesion and recognition, the key processes coopted by metastatic cancer cells.

Several types of cancer cells overexpress enzymes that add sialic acid to sugar chains. But closing off all these enzymes can be dangerous. Last year, a team led by James Paulson, a chemist at the Scripps Research Institute in San Diego, California, who heads the lab where Rillahan did his work on P-3F _ax -Neu5Ac , found that the drug caused fatal kidney damage in mice when injected into the bloodstream. So for P-3F _ax -Neu5Ac to have a shot as antimetastasis drug, it must target cancer cells.

This is the step that researchers led by Gosse Adema, immunologist of the tumor at the University Medical Centre Radboud in Nijmegen, Netherlands, have now taken. In an article published online this month in ACS Nano Adema and colleagues report package P-3F _ax -Neu5Ac nanoscale, biodegradable vesicles made from poly ( lactic- co -glycolic acid) or PLGA, an approved compound for use by the Food and Drug administration of the United States. They then vesicles coated with antibodies that home on a protein overexpressed on the surface of melanoma cells. The melanoma cells often metastasize to the lungs. Thus, in their study, Adema and his colleagues tested whether melanoma cells spread to the lungs in mice.

It is difficult for laboratory researchers to quickly study solid tumor metastasis, because they might have to wait months for rogue cells spinning. So to speed things up, the team of Adema is based on a standard procedure of injecting cancer cells and anti-metastatic drug in the veins of the mouse tail and wait two weeks to see if the cells began to form new tumor nodules. After 14 days, the Dutch team found that the mice that received the drug loaded nanovesicles developed 75% fewer tumor nodules in their lungs than mice not given nanovesicles empty.

Whether this therapy will be successful in humans remains uncertain, because most drugs that work in mice do not in people. The synthesis of sugar chains on cells called glycosylation differs between human and mouse, so that any potential drug should prevent glycosylation in human cancer cells. Still, Paulson said the new finding "opens the door" to the prospect of drugs that inhibit glycosylation as an alternative, or additional, strategy against metastatic cancer. Such a discovery will not make a remedy against day after cancer. But it could help researchers learn how to prevent the spread of cancer, the most lethal weapon of the disease.

Less than 5% of the studies on lung diseases funded by the National Institutes of Health (NIH) over the last 2 decades have included a statistically significant number of participants from racial or ethnic minorities, concludes a new analysis. The discovery highlights the continuing difficulty of adequately represent minorities in biomedical research, the authors say, but they argue that the problem could be solved by a number of steps.

NIH does not dispute the results, but note the focus of the results published survey may underestimate the ongoing efforts of the agency to improve the representation of minorities in research clinical and other studies.

the new survey, published last month in the online American Journal of Respiratory and Critical Care Medicine , examined the respiratory disease studies published between 1993 and 2013. A search of PubMed found 58.0 studies that reported the NIH funding. Among them, in 2534 4.4%-studies reported by police that minorities represented 25% or more of the population studied. Below the 25% participation threshold, it may be difficult for the statistical analyzes to detect racial or ethnic differences in risk factors or the effects of the disease, the authors write, directed by a physician-scientist Esteban Burchard the University of California, San Francisco.

during the period of 20 years, the inclusion of minorities has increased slightly from just over 2% of studies in 1993 to almost 5% 2013, the study found. During the same period, the authors note, the proportion of people in the US who identified as part of a group of racial or ethnic minority rose from 26.5% to 38.9%.

Since "The results are worrying that we know many lung diseases disproportionate impact on minorities underrepresented," says Patricia Finn, a pulmonologist at the University of Illinois, Chicago, and outgoing president American Thoracic Society. (Finn was not involved in the study.)

the study is the latest in a long line to focus on minority representation in research clinic. last year, for example, a similar review of cancer studies funded by the National cancer Institute found that less than 2% focused on minorities. in 1993, Congress directed NIH to strengthen its efforts to recruit more minorities in studies funded by the federal government, and the agency has since launched a range of efforts, including programs to recruit Latinos and African Americans in the asthma studies.

the new investigation can not fully grasp these efforts, officials NIH say, because all studies have published results. "The analyzes that focus on selected publications can not ... fully reflect the inclusion of all persons enrolled in studies supported by the NIH," wrote a representative for the Office of NIH research extra- muros Science Insider in an email. The agency said that in 2013, approximately 30% of all clinical research, he financed included a minority interest.

The efforts to fully represent minority populations in biomedical research are becoming increasingly important as new or "precision" "customized" approaches are being developed, researchers say. Approaches aim to use genetic characters and other specific of each person to develop appropriate treatments, and "to harness the power of this science, we must include everyone," says Finn.

better representation also allows researchers to understand the disparities in disease rates among different ethnic groups, said the study authors. studies have shown that African Americans are more likely to develop certain forms of chronic obstructive pulmonary disease after smoking than whites, for example. They are also more likely to die from lung cancer.

health disparities are particularly glaring in asthma, according to Burchard. the asthma is the most common chronic disease among children, affecting about 26 million people in the United States. the prevalence is higher among Puerto Ricans and African Americans than among non-Hispanic whites, other Hispanic groups or Asian. Black children with asthma are four times more likely to die from the disease than white children with asthma, according to studies.

The environmental and socio-economic factors play a role, but so does the descent. In a previous study, Burchard and his colleagues found that a gene mutation linked to the severity of asthma was 40% more common in African Americans.

Even the effectiveness of treatment can vary according to race or ethnicity. For example, albuterol, medication against asthma most commonly prescribed, is less likely to work in African Americans and Puerto Ricans than among whites. "Ethnicity is the only predictor of response to albuterol," said Burchard, who helped start two major asthma gene-environment studies among minority children in the United States. (Studies are known as GALA, or the genetics of asthma among Latino Americans, and SAGE, or the study of African Americans, Asthma, Genes, & environment.)

Burchard and his team say a number of factors contribute to the underrepresentation of minorities in studies funded by NIH. They include a lack of training on how to conduct inclusive education, a lack of incentives to implement inclusive education, the relatively low number of minority scientists, and "a lack of successful partnerships between academic medical centers and underrepresented communities. "Addressing the problems systematically, they suggest, could help change the numbers.

The slowing of the epidemic of Ebola in West Africa news and reasons to be hosted hope but it is also creating a new problem. With fewer new cases occur, it becomes increasingly difficult to test vaccines and medicines. As a result, conflicts loom on which can test drugs and vaccines for Ebola in Guinea and Sierra Leone.

In Guinea, a large consortium including Médecins Sans Frontières (MSF) and the World Health Organization (WHO) vaccinated the first volunteers at risk of Ebola Monday in a large trial of a vaccine produced Merck and NewLink Genetics. But the team feels threatened because researchers from the National Institutes of Health (NIH) looking to spend another vaccine study in Liberia, where the epidemic came to a virtual halt, Guinea.

The US decision could jeopardize the Guinean trial, said John-Arne R ø Göttingen of the Public Health Institute in Oslo, Norway, which chairs the steering committee of the study. "The two tests may be underway in the same place? I think not," said Marie-Paule Kieny, Assistant Director-General of WHO. "There is a risk if it is not done to neatly, neither trial was conclusive in the end. "

But Clifford Lane, director of clinical research at the National Institute of allergy and infectious diseases in Bethesda, Maryland, part of the NIH said that Guinea, which reported 45 new patients last week, can accommodate both studies. "Guinea is essentially as large as Sierra Leone and Liberia together," he said. "it seems reasonable to least explore the possibility. "

Meanwhile, an international team of test an Ebola drug called TKM-Ebola in Sierra Leone is concerned that the NIH is looking for zmapp extend his trial, another Ebola therapy, from Liberia to Sierra Leone. This movement could prevent researchers to expand their trials TKM-Ebola as expected, or even create direct competition to a processing unit Ebola in the city of Sierra Leone Port Loko where it is already underway.

Before the current outbreak, scientists never had a real chance to test Ebola drugs or vaccines for effectiveness. The products had not moved through Phase I safety studies, and homes were much smaller and still finished in a few months. The current outbreak, which has caused nearly 25,000 cases and over 10,000 deaths, offers a unique opportunity to test candidate vaccines and drugs that could save lives in the future, scientists say.

Ironically, Guinea was first passed over when the vaccine trials were planned. Last October, when some models have suggested more than one million people could get Ebola, scientists, politicians and regulators met in Geneva, Switzerland, to discuss how to move forward with vaccine candidates . At the end of this meeting, plans were agreed to study the vaccine in Sierra Leone and Liberia; Guinea, where the epidemic began, but has had fewer patients, was considered a particularly difficult environment for testing a vaccine. Feeling that was unfair, some participants in the meeting established a working group to design a test for Guinea and make sure that at least some Guineans have quick access to experimental vaccines.

The group came up with an unusual design called a "ring vaccination trial" in which a ring of people around the newly discovered Ebola patient is vaccinated. Whole rings are randomized to be vaccinated immediately or after 21 days. If a lot more people contract Ebola in the last rings, the vaccine is effective.

the NIH study, on the other hand, is designed as a classic randomized controlled trial (RCT) controlled, with one group receiving the genetic -NewLink Merck vaccine candidate, another different group of a vaccine developed by GlaxoSmithKline, and a third group receiving a placebo. the researchers began vaccinating healthy adults in Liberia in early February first to study the degree of vaccine safety are and how much of an immune response they generate. "We think we have a very good safety database and immunogenicity," says Lane.

After several hundred vaccinations, scientists are ready to begin Phase III, where effectiveness is tested. But it will not be possible in Liberia, where one patient was confirmed in the last three weeks, said Lane. "We are committed to trying to complete the study. To do this, we will probably have to work in Guinea and / or Sierra Leone, "he said. The team has reached out to the Guinean Ministry of Health and French researchers working on a drug test in Guinea, "to see if something can be put in place," says Lane. "I hope that a country like Guinea is big enough to make at least two studies. "

no, it's not, said Peter Smith, an epidemiologist at the London School of Hygiene & Tropical Medicine who was asked by wHO to study the issue. (Smith is not directly involved in the ring vaccination trial, but he chairs the board of the Norwegian program of the global health and vaccination research, which is co-funding.) " my conclusion is that it would not be possible to successfully perform both tests in Guinea at the same time (unless a radical change in the epidemiology of the disease in Guinea and the incidence of the disease increases much higher levels than they are today), "he wrote in an e-mail to science Insider.

Allocate a portion of the country to the NIH study and exclusion cases in the field of ring vaccination of the test would not work, Smith said, because the probability of catching Ebola is only big enough in the area around the capital Conakry, where WHO study, MSF has already begun. "It would not only jeopardize the chances of the ring vaccination trial with sufficient power to demonstrate efficacy but also, unless the NIH was prepared to increase significantly the size of their trial the NIH trial would have little or no power to detect effectiveness. "

that Guinea will agree to host the NIH trial and does not know, but there is clearly a need for both groups to speak, R ø Göttingen said. "I hope we can sit down and have a good discussion with them, we have not been able to do it at this stage." A compromise might be to run the two tests one after the other, said Kieny. The ring vaccination trial is expected to enroll 10 rings in late May; the latest vaccinations will take place three weeks later. Add a few months follow, Kieny said, then NIH could begin its own study. "Frankly, they are not ready to start soon now anyway."

Lane said it would probably take 6 to 8 weeks to start the retrial in Guinea. The study should not be delayed further, he argues, in part because the design of the study by WHO-MSF may not be the best to assess the effectiveness of a vaccine. For example, he said, most cases avoided in the trial of ring vaccination would occur shortly after exposure, leaving open how the vaccine protects long term. "If my goal is to get the most effective vaccine as quickly as possible to the greatest possible number of people, I think a RCT is the most direct way," he said.

In Sierra Leone, researchers from Oxford University recently began a trial of TKM-Ebola, a therapeutic experimental Ebola synthetic siRNAs. Now the effort to test the antibody cocktail of zmapp is expanding from Liberia to Sierra Leone and NIH-led. "We hear rumors that the NIH has concluded an agreement with the government of Sierra Leone to conduct the trial in any zmapp Ebola treatment unit, even those who have already tests running," said Peter Horby, the principal investigator of the study TKM-Ebola. "If true, it undermines the ongoing trials and lead to conflict."

Lane said the government of Sierra Leone decide what treatment units will participate, and Port Loko, where TKM-Ebola study is running, are not currently included in the list. "We forgive our local partners," says Lane.

However, Lane says that patients should have access to the most promising experimental drugs available, and data on animal zmapp look better than those for TKM-Ebola. Horby agrees with this assessment, but said he does not know how this translates into humans. (He says his team proposed to test zmapp in Sierra Leone, but has not had access to the product because the Food and Drug Administration of the United States has not approved the study design, in which the patients receiving TKM-Ebola patients are compared to Ebola to another processing units that do not receive the drug.) "It would not be reasonable or ethical to stop a trial well in running a promising product for a promising alternative product, "said Horby.

early study of ring vaccination in Guinea on Monday came exactly one year after the first case of the deadly disease had been diagnosed in the country, alerting the world on what has become the worst Ebola outbreak ever seen. the implementation of the trial was a huge challenge, given the poor infrastructure in Guinea and the general distrust of the health system among the population, said Kieny. "This is a great success," she said. "There was a large participation of the community and no problems with violence."

* Ebola files: Science and Science Translational Medicine made a collection of research and articles on the Ebola virus and the current epidemic available for researchers and the general public.

At 44, the man seemed to recover well after a double lung transplant at Northwestern Memorial Hospital in Chicago, Illinois. One week after surgery, however, the patient, whose own lungs had been ruined by the inflammatory lung disease sarcoidosis, was confused and became delirious. Although a brain scan found nothing wrong, the tests showed that the amount of ammonia in his blood had enriched and continued to rise even after dialysis to remove the toxin. Forty days after his surgery, he died.

Now, a new study involves bacteria that normally live in the urinary tract as the cause of the deadly disease of man and the death of other lung transplant patients. The work suggests a way to treat a rare but fatal complication of organ transplantation and cancer treatment.

Although our body normally produce small amounts of ammonia when it breaks down protein, liver enzymes convert it into a safer compound, urea, which is excreted in urine. In some recipients of organ transplants and cancer patients, however, the amount of ammonia in the explosion of blood. Although this condition, known as hyperammonemia name is unusual, "when it took place, it was disastrous," said Mark Wylam pulmonologist at the Mayo Clinic in Rochester, Minnesota. The brain swells, and the patients fall into a coma. "The end of the test is that they die," he said.

Not only is resistant to treatment and usually fatal hyperammonemia, but the cause was also difficult to achieve. In 2013, Wylam and colleagues discovered the likely culprit in one case, a woman of 64 years who died of hyperammonemia after a double lung transplant. They found that his blood and tissues were positive for a type of bacteria, Mycoplasma hominis , which often causes benign genital infections in women.

But the man who died at Northwestern Memorial hospital showed no signs of M. hominis Bharat Ankit thoracic surgeon at Northwestern University Feinberg School of Medicine in Chicago and colleagues found. instead, they detected a different bacterium, Ureaplasma urealyticum in the blood of man and in samples of bladder, spleen, liver and lungs. The team then tested the tissue of three other lung transplant patients who were dead hyperammonemia, including the patient studied by Wylam and colleagues. All three showed signs of infection U. urealyticum , or a close microbe U. parvum . In contrast, 20 lung transplant recipients who develop hyperammonemia were negative for three microbes, the researchers report online today in Science Translational Medicine .

The researchers also checked for bacteria in two lung transplant recipients who had hyperammonemia, but were still alive. Both patients transported U. urealyticum or U. parvum bacteria, and both recovered after antibiotic treatment.

Wylam, who was not connected to the new study, says the results are conclusive. "They showed that U. urealyticum can also cause these unexplained cases of hyperammonemia." The paper recommends testing the lung transplant recipients who have to hyperammonemia Ureaplasma infection. The study also provides guidance on the treatment of the condition. Although man Bharat and his colleagues studied had received azithromycin antibiotic, bacteria may have become resistant to it. Microbes are vulnerable to three families of antibiotics, so a combination of drugs would be a better choice to avoid resistance, said Bharat.

About two-thirds of us Ureaplasma bacteria living in our urinary system, where they feast urea decomposing to produce energy and release ammonia as a byproduct. Why bacteria may trigger sepsis and death are not clear. Cancer patients and transplant recipients suppressed immune system and microbes could benefit from their weakened defenses. However, another possibility is appeared when Bharat and colleagues found that the lungs from a donor already contained bacteria before organs were transplanted in the recipient. Thus, the donor organs could deliver germs to patients who develop hyperammonemia.

Ureaplasma microbes are difficult to diagnose because they do not like to grow in cultures that hospitals often use to identify the culprits in bacterial infections. unrecognized infections may be responsible for additional hyperammonemia cases and even other diseases, says Bharat. For example, he notes, the microbes could be the cause of the disease in patients with malnutrition. "These organisms could be a bigger problem," he said.

Despite their growth out of control in cancer patients, most tumors do not survive in dishes lab long enough for doctors or researchers to study their effectiveness. Now a team took the intestinal cancerous tissue of people and grown miniature human gut which retain the properties of the original tumor, an advance that may help identify better, or more personalized, treatments for colon cancer. There

several years, Hans Clevers of Hubrecht Institute in Utrecht, the Netherlands, and colleagues have developed a way to grow stem cells in intestinal miniature organelles in the intestinal tissue laboratory. With a combination of growth factors and gellike environments, researchers can coax the cells to form cell aggregates approximately 0.1 mm in diameter with a hollow center and the folded signatures crypts that form the wall of the intestine. Organelles can be kept alive in the laboratory for years, and they can also survive freezing and thawing.

Now, with colleagues from the Wellcome Trust Sanger Institute in Hinxton, UK, and the Broad Institute in Cambridge, Massachusetts, the Dutch team has adapted the technique to cancer. Researchers have increased tissue mini tripe taken from tumor samples from 27 patients with colorectal cancer. The technique is surprisingly effective, more organelles of up to 0% of patient samples, reports the team today cell .

To see how the mini-guts looked like tumors, the researchers sequenced the genomes of organelles. Although the match was not perfect, the mini-guts had many of the same cancer-causing mutations found in the sample of the original tumor. The tumors are often composed of several types of cells bearing different pools of mutations. And in that part of the tumor of a sample came, an organoid may not include all types present in patient cells. Nevertheless, "they capture most, if not all of the most important changes," says Eduard Batlle at the Biomedical Research Institute in Barcelona, ​​Spain.

The technique has advantages over the two techniques leading to the study of tumors of patients: the creation of immortal cell lines and transplantation of human cancer cells into mice, explains Alberto Bardelli from the Institute for research and treatment of cancer in Candiolo, Italy lines. of immortal cells frequently acquire new mutations in their adaptation to growth in culture, and so they are less accurate model of cancer, said Bardelli. tumors transplanted into immunodeficient mice, called xenografts, are more accurate, but they are expensive and difficult to maintain. "Xenos are wonderful, but you can not do large-scale [drug] screening on xenos," he said.

with cancer organelles, by contrast, researchers were able to test more than 80 drugs and could measure the sensitivity of mini-guts were each compound. The mini-guts "fill a critical gap," Bardelli said. "It's very exciting."

Clevers said two clinical trials are already evaluating the usefulness of mini-cancerous guts. The first tests how an organoid created from a person newly diagnosed with colorectal cancer can predict tumor response to treatment. a second will verify if the organelles can help identify combinations of drugs effective in people whose cancer has spread in several tissues.

For years, scientists have noticed an interesting trend of childhood cancer. Those who went to daycare early in life were less likely to develop later a most common childhood cancers: acute lymphoblastic leukemia (ALL). Now, a 7-year study seems to have deciphered the molecular mechanism of ALL training. The work may explain why early exposure to infections in places like day care appears to protect against the disease and why vaccines unrelated help protect against this cancer.

For Mel Greaves, a cell biologist cancer at the University of London Cancer Research Institute, the discovery provides an explanation for the hypothesis that it promotes a long time: that when infants in modern societies are immune to common infections, their immune systems are more likely to overreact in subsequent infections, paving the way for ALL. "I see it as the missing link," he said of the new research.

Most childhood involves all malfunction of B cells, scouts immune patrolling in the bloodstream in search intruders such as viruses and bacteria; they make antibodies that help fight infections, but with leukemia, the immune system goes haywire, imperfect churning B cells, immature at a prodigious rate and crowding out healthy blood cells [

normal B cells are a marvel of adaptation. As they age, they reprogram their own DNA, allowing the immune system to produce millions of different B cells programmed to recognize the wide range of potential infections. the DNA shuffling based on a sequence of enzymes. first, the proteins known under the name RAGs cutting and pasting whole chunks of DNA. After that, another enzyme, AID, will work 'fine tuning' DNA nucleotides by changing simple.

But Greaves and his colleagues suspected that process could go wrong, introducing mutations that create faulty B cells that might cause leukemia. In a series of experiments, they found evidence that much of the problem lies in a break in the ordered sequence of editing genes during infection. Rather than RAGs do their business, then step aside for IDA, IDA began at the same time, potentially increasing the risk of gene-editing errors.

These mouthwatering results came to a head in an experiment on mice with a genetic defect linked to childhood ALL. The condition in which two genes associated with blood formation are fused together, is found in the umbilical cord blood of 1% of all newborns. But most children with her are never going to develop ALL in itself. The researchers wondered if unregulated mutations triggered by repeated infection later in childhood could make the difference, the trigger leukemia.

The scientists made mouse B cells with this genetic defect. Some products both RAG and using enzymes and other cells made only one of two. They then simulated repeated illnesses by subjecting the rodents to five cycles of exposure to a molecule that acts as an antigen of a substance eliciting an immune response. In this case, it mimics a bacterial infection. At the same time, they removed the protein which normally acts as a traffic cop, coordination when enzymes are involved.

When the cells were injected into mice, 14 mice that B cells obtained with both enzymes quickly got leukemia and died, reports the online team today Nature Immunology . The mice with B cells producing a single enzyme were even five months later without disease.

"This is a smoking gun," says Markus Müschen, lead author of the paper and a cancer researcher at the University of California, San Francisco (UCSF). "Now we know that this is AID and RAG. And now we know it can be triggered by bacterial antigens. "

The results, Müschen said, referring to why several studies have found a link between a decrease in all cases and the vaccine Haemophilus influenzae type B (Hib) , a bacterial infection that most often affects young children. the vaccine could trigger a mild immune response in infants that mimics normal sniffling children learn in child care, while preventing more intense infections that could lead to dysfunction immune system, he said.

the document could become ammunition political struggle on the vaccination of children, if vaccines proponents argue that highlights the benefits of vaccines. the California State Senate last week adopted a bill which eliminates the exemption that allows parents to opt out of vaccination for their children according to personal convictions. It is now before the State Assembly. The move comes on the heels of a measles epidemic centered in Disneyland, that those responsible for public health were linked to lower immunization rates.

Joseph Wiemels, a researcher of childhood leukemia at UCSF who was not involved in the research, praised the work as important evidence of how infections may play a role in such leukemia. It could also help explain the apparently contradictory results that even so early day care reduces all risks, this same risk is higher in children with more doctor visits. There may be mild infections early in life, such as those that often circulate in child care, help build the immune system. More serious infections that are worth a visit to the doctor, however, could trigger a damaging immune "storm," he said.

But Wiemels warns against hasty conclusions. The study offers a plausible explanation why a Hib vaccine as might help. But he notes that scientists are not actually test the impact of the vaccine or a previous illness. "They do not take these mice and vaccinate them or having their immune system, and then hit them."

Greaves said the most striking reduction in ALL is for children who spend time at the beginning of day care. Although the Hib vaccine appears to have an advantage, it is not perfect. And there is less evidence that other vaccines help, he said. "If it really worked as well as this, we would not have leukemia."

A big unanswered question is whether some infections are more likely to trigger the mutations leading to ALL. Greaves said although there is little evidence that a single virus is still the case, he is working on a document that highlights a virus in a cluster of leukemia cases. Meanwhile, Wiemels prepares the results of a study that points to a link between a specific viral infection in pregnancy and childhood leukemia.