Publisher Health

Chronic Obstructive Pulmonary Disease (COPD) is a disease caused by cigarette smoking that reduces lung function and causes difficulty breathing. It is the third leading cause of death worldwide. Current treatments for COPD only affect symptoms, not progression. Identifying who is going to get COPD before they get it is key to figuring out how to intercept the disease at an early stage.
Researchers from Boston University School of Medicine (BUSM) have identified a panel of genes that are active in smokers and ex-smokers who experience faster loss of lung function over time. They believe these genes could be useful to predict which people are most at risk for smoking-related decline in lung function.
“Our discovery that airway genes change before a rapid decline in lung function should give patients with COPD a lot of hope. A test like this could help doctors identify people at risk for COPD before they get it, and help scientists find new treatments to stop the disease before it gets worse,” explained corresponding author Katrina Steiling, MD, MSc, assistant professor of medicine at BUSM.
Smoking, and diseases related to smoking, create changes throughout the airways and lungs. These changes can be detected using a procedure called a bronchoscopy, where a small flexible camera inserted through the nose or mouth is used to collect cells with brushes from the sides of the airways. The researchers tested airway brushings from 134 people who were current or former smokers. They found changes in the activity of specific genes in the people that went on to have more rapid worsening of their lung function several years after that initial airway brushing. Some of the genes were more active in the people who rapidly lost lung function while other genes were less active in these people.
According to the researchers, further study of these genes may provide clues as to what causes rapid lung function decline which could be used to develop to new treatments for preventing the development of COPD. “Being able to identify people most at risk for worsening lung function might also make clinical trials of COPD fighting medications easier, by enriching the trials testing new medications for people most likely to benefit from them,” added co-author Beth Becker, PhD, a recent graduate from BU’s bioinformatics program.
This study further shows another use for the ‘airway field of injury’ hypothesis. “Cigarette smoking causes changes to the cells in the lungs and airways. Because the changes in the airways are similar to those that occur deep inside the lung, testing the cells in the airways can be used to detect diseases deep within the lungs,” added Marc Lenburg, PhD, professor of medicine and pathology and laboratory medicine at BUSM.
These findings appear online in the journal Thorax.
Funding for this study was provided by the National Institutes of Health/National Heart, Lung, and Blood Institute (ROI HL095388 and ROI HL 118542-01) and Dutch Longfonds Foundation (4.2.16.132JO).
Story Source:
Materials provided by Boston University School of Medicine. Note: Content may be edited for style and length.

Wastewater testing is an effective way to identify new cases of COVID-19 in nursing homes and other congregate living settings, and it may be particularly useful for preventing outbreaks in college dormitories, a new University of Virginia study finds.
The research, a collaboration of UVA’s School of Medicine and School of Engineering, was led by UVA Health’s Amy Mathers, MD. It offers some of the first clear guidance on the most effective methods to perform testing to detect COVID-19 in wastewater.
The researchers evaluated and compared sampling and analysis techniques by testing them within buildings with known numbers of positive cases. They were then able to determine wastewater testing’s strengths and limitations as a tool for monitoring COVID-19 in a building population. For example, the technique proved better at detecting initial infections than determining the number of occupants infected or how long they had been infected.
One important answer revealed by the research: Wastewater testing can detect even small numbers of asymptomatic cases, something not previously documented.
“This work could be applied to surveillance in buildings where people live in groups, where transmission may be hard to control but the risk of spread could be high,” said Mathers, an infectious disease expert in the School of Medicine’s Department of Pathology. “Since we can identify new infections with high sensitivity, it provides an early warning signal of when to test everyone in the building to find and isolate the newly infected persons before an outbreak becomes large.”
Wastewater Testing for COVID-19
To evaluate the effectiveness of wastewater testing for detecting COVID-19, Mathers collaborated with Lisa Colosi-Peterson, PhD, an associate professor in UVA Engineering’s Department of Engineering Systems and Environment, who connected with Mathers through UVA’s Center for Engineering in Medicine. They and their colleagues monitored wastewater from two student dormitory complexes for eight weeks. The researchers found that the wastewater testing caught more than 96% of cases.

Researchers have mapped out the changes in metabolism that occur after a heart attack, publishing their findings today in the open-access eLife journal.
Their study in mice reveals certain genes and metabolic processes that could aid or hinder recovery, and might be good targets for treatments to prevent damage after a heart attack.
“Although some studies have looked at how changes in individual body tissues underlie mechanisms of disease, the crosstalk between different tissues and their dysregulation has not been examined in heart attacks or other cardiovascular-related complications,” explains first author Muhammad Arif, a PhD student at KTH Royal Institute of Technology, Stockholm, Sweden. “In this study, we performed an integrated analysis of heart and other metabolically active tissues using a mouse model of heart attack and used systems biology approaches to get a systematic picture of the metabolic changes that occur.”
Systems biology has aided the discovery of new treatment approaches in multiple diseases. Rather than take systems apart and analyse the components, it involves taking measurements from different cells and tissues and using them to reproduce the system being studied. In this research, the team used a systems biology approach called co-expression networks (CNs) to reveal how the functions of genes in different tissues were linked together.
First, they measured the activity of all the genes in four tissue types: heart, fat, skeletal muscle and the liver in mice that had a heart attack. They compared these with the gene activity in mice that did not have a heart attack to generate sets of differentially expressed genes (DEGs) unique to each tissue. Next, in the co-expression network analysis, they looked at the top 5% of genes that were most strongly connected within the four different tissues. They then used the DEG results to see how those top 5% of genes were altered 24 hours after a heart attack.
They found key clusters of genes that were altered in different tissues after a heart attack. In the heart and muscle, the gene changes tended to be linked to energy production and muscle contraction. In the liver, the gene changes were related to fat transport and metabolism, and the metabolism of cell-protecting substances such as glutathione.
The team then used this information to build a multi-tissue model of the metabolic response to a heart attack and compared their results with other studies of heart tissue. They found that four genes were consistently altered across all studies. These genes are known to play roles in energy production, muscle contraction and protein production, and at least one of them is being explored as a drug target for cardiovascular disease.
Taken together, the results reveal a downregulation of heart-specific functions and upregulation of fat metabolism and inflammation in the heart, muscle and fat tissue after a heart attack. By contrast, the team saw a different response in the liver where inflammation was reduced.
“Our integrative analysis highlights both common and tissue-specific biological responses to a heart attack across a range of metabolically active tissues,” concludes senior author Adil Mardinoglu, Professor of Systems Biology at KTH Royal Institute of Technology, Sweden, and King’s College London, UK. “The approach demonstrates a way of using multi-tissue gene activity data to identify changes in biological processes and pathways and systematically explore the effects of a disease. This opens up new opportunities for future research into the pathways identified, and the potential to use a similar approach to understand other complex human diseases.”
Story Source:
Materials provided by eLife. Note: Content may be edited for style and length.

An investigational gene therapy can safely restore the immune systems of infants and children who have a rare, life-threatening inherited immunodeficiency disorder, according to research supported in part by the National Institutes of Health. The researchers found that 48 of 50 children who received the gene therapy retained their replenished immune system function two to three years later and did not require additional treatments for their condition, known as severe combined immunodeficiency due to adenosine deaminase deficiency, or ADA-SCID. The findings were published today in the New England Journal of Medicine.
ADA-SCID, which is estimated to occur in approximately 1 in 200,000 to 1,000,000 newborns worldwide, is caused by mutations in the ADA gene that impair the activity of the adenosine deaminase enzyme needed for healthy immune system function. This impairment leaves children with the condition highly susceptible to severe infections. If untreated, the disease is fatal, usually within the first two years of life.
“These findings suggest that this experimental gene therapy could serve as a potential treatment option for infants and older children with ADA-SCID,” said Anthony S. Fauci, M.D., director of NIH’s National Institute of Allergy and Infectious Diseases (NIAID). “Importantly, gene therapy is a one-time procedure that offers patients the hope of developing a completely functional immune system and the chance to live a full, healthy life.”
People with ADA-SCID can be treated with enzyme replacement therapy, but this treatment does not fully reconstitute immune function and must be taken for life, usually once or twice weekly. Transplants of blood-forming stem cells, ideally from a genetically matched sibling donor, can provide a more lasting solution. However, most people lack such a donor. Additionally, stem cell transplants carry risks such as graft-versus-host disease and side effects from chemotherapy medications given to help the donor stem cells establish themselves in the patient’s bone marrow.
The new research evaluated an experimental lentiviral gene therapy designed to be safer and more effective than previously tested gene-therapy strategies for ADA-SCID. This gene therapy involves inserting a normal copy of the ADA gene into the patient’s own blood-forming stem cells. First, stem cells are collected from the patient’s bone marrow or peripheral blood. Next, a harmless virus is used as a “vector,” or carrier, to deliver the normal ADA gene to these cells in the laboratory. The genetically corrected stem cells then are infused back into the patient, who has received a low dose of the chemotherapy medication busulfan to help the cells establish themselves in the bone marrow and begin producing new immune cells.
The experimental gene therapy, developed by researchers from the University of California, Los Angeles (UCLA) and Great Ormond Street Hospital (GOSH) in London, uses a modified lentivirus to deliver the ADA gene to cells. Previous gene-therapy approaches for ADA-SCID have relied on a different type of virus called a gamma retrovirus. Some people who have received gamma retroviral gene therapies have later developed leukemia, which scientists suspect is due to the vector causing activation of genes that control cell growth. The lentiviral vector is designed to avoid this outcome and to enhance the effectiveness of gene delivery into cells.
The results come from three separate Phase 1/2 clinical trials, two conducted in the United States and one in the United Kingdom. The U.S. trials, led by principal investigator Donald Kohn, M.D., of UCLA, enrolled 30 participants with ADA-SCID ranging in age from 4 months to 4 years at UCLA Mattel Children’s Hospital and the NIH Clinical Center in Bethesda, Maryland. The U.K. study, conducted at GOSH and led by principal investigator Claire Booth, M.B.B.S., Ph.D., enrolled 20 participants ranging in age from 4 months to 16 years. Most participants acquired and retained robust immune function following gene therapy — 96.7% after two years in the U.S. studies and 95% after three years in the U.K. study — and were able to stop enzyme replacement therapy and other medications. Of the two participants for whom gene therapy did not restore lasting immune function, one restarted enzyme replacement therapy and later received a successful stem cell transplant from a donor, and the other restarted enzyme replacement therapy.
The lentiviral gene therapy appeared safe overall, although all participants experienced some side effects. Most of these were mild or moderate and attributable to the chemotherapy that the participants received.
Researchers observed similar outcomes in all three trials, although there were some differences between the studies. Stem cells were collected from bone marrow in the U.S. trials and from peripheral blood in the U.K. trial. In one of the U.S. trials, 10 children were treated with genetically corrected stem cells that had been frozen and later thawed. The two other trials used fresh stem cell preparations. In the future, the freezing procedure — known as cryopreservation — may allow stem cells to be more easily transported and processed at a manufacturing facility far from the patient’s home and shipped back to a local hospital, reducing the need for patients to travel long distances to specialized medical centers to receive gene therapy. A trial of the cryopreserved treatment is now underway at the Zayed Centre for Research into Rare Diseases in Children in London, in partnership with GOSH.

It is projected that up to 152 million people worldwide will be living with Alzheimer’s disease (AD) by 2050. To date there are no drugs that have a substantial positive impact on either the prevention or reversal of cognitive decline. A growing body of evidence finds that targeting lifestyle and vascular risk factors have a beneficial effect on overall cognitive performance. A new review in the Journal of Alzheimer’s Disease, published by IOS Press, examines research that finds spiritual fitness, a new concept in medicine that centers on psychological and spiritual wellbeing, and Kirtan Kriya, a simple 12-minute meditative practice, may reduce multiple risk factors for AD.
“The key point of this review is that making a commitment to a brain longevity lifestyle, including spiritual fitness, is a critically important way for aging Alzheimer’s disease free,” explain authors Dharma Singh Khalsa, MD, Alzheimer’s Research and Prevention Foundation, Tucson, AZ, USA, and Andrew B. Newberg, MD, Department of Integrative Medicine and Nutritional Sciences, Department of Radiology, Marcus Institute of Integrative Health, Thomas Jefferson University, Philadelphia, PA, USA. “We hope this article will inspire scientists, clinicians, and patients to embrace this new concept of spiritual fitness and make it a part of every multidomain program for the prevention of cognitive disability.”
Research reveals that religious and spiritual involvement can preserve cognitive function as we age. The authors observe that today, spirituality is often experienced outside the context of an organized religion and may be part of every religion or separate to it. Spiritual fitness is a new dimension in AD prevention, interweaving basic, psychological and spiritual wellbeing. The authors discuss the research on how these factors affect brain function and cognition. For example, psychological wellbeing may reduce inflammation, cardiovascular disease, and disability. Significantly, individuals who have a high score on a “purpose in life” (PIL) measure, a component of psychological wellbeing, were 2.4 times more likely to remain free of AD than individuals with low PIL. In another study, participants who reported higher levels of PIL exhibited better cognitive function, and further, PIL protected those with already existing pathological conditions, thus slowing their decline.
Stress and stress management are under-discussed topics in AD prevention, yet the authors point out that there is ample evidence that physical, psychological, and emotional effects of stress may elevate AD risk. Kirtan Kriya (KK) is a 12-minute singing meditation that involves four sounds, breathing, and repetitive finger movements. It has multiple documented effects on stress, such as improving sleep, decreasing depression, and increasing wellbeing. It has also been found to increase blood flow to areas of the brain involved in cognition and emotional regulation and increases grey matter volume and decreases ventricular size in long-term practitioners, which may slow brain aging. Research in healthy individuals, caregivers, and those with cognitive decline found that the practice improves cognition, slows memory loss, and improves mood.
The overall relationship between spiritual fitness and a person’s complete physical and mental health is a topic of investigation in the emerging field of study called neurotheology. Early work has focused on the development of models regarding which brain areas are affected through spiritual practices such as meditation or prayer. Over the last 20 years, there has been an extensive growth in neuroimaging and other physiological studies evaluating the effect of meditation, spiritual practices, and mystical experiences. A neuroimaging study of KK found long term brain effects, during meditation and afterwards. Neurotheological studies can help understanding of how a practice such as KK can lead to more permanent effects in brain function that support spiritual fitness, according to Dr. Khalsa and Dr. Newberg.
“Mitigating the extensive negative biochemical effects of stress with meditation practices, in tandem with the creation of heightened levels of spiritual fitness, may help lower the risk of AD. Small shifts in one’s daily routine can make all the difference in AD prevention,” Dr. Khalsa and Dr. Newberg conclude. “We are optimistic this article will inspire future research on the topic of spiritual fitness and AD.”
Story Source:
Materials provided by IOS Press. Note: Content may be edited for style and length.

Low doses of a four-drug combination helps prevent the spread of cancer in mice without triggering drug resistance or recurrence, shows a study published today in eLife.
The findings suggest a new approach to preventing cancer metastasis in patients by simultaneously targeting multiple pathways within a metastasis-promoting network. They may also help identify people who would most likely benefit from such treatment.
Metastasis, the spread of cancerous cells through the body, is a common cause of cancer-related deaths. Current approaches to treating metastatic cancer have focused on high doses of individual drugs or drug combinations to hinder pathways that promote the spread of cancer cells. But these approaches can be toxic to the patient, and may inadvertently activate other pathways that cause the drugs to stop working and the tumours to return.
“There is an urgent need for new strategies to suppress cancer metastasis, especially for cancers such as triple-negative breast cancer that currently lack effective therapies,” says first author Ali Yesilkanal, a postdoctoral scholar at the Ben May Department for Cancer Research at the University of Chicago, US.
In the study, Yesilkanal and colleagues analysed gene expression data from patients participating in the Cancer Genome Atlas study to understand how a metastasis-suppressing protein called Raf Kinase Inhibitory Protein (RKIP) works. They found that RKIP reduces the expression of a network of genes that promote the spread of cancer cells.
They then created a four-drug combination that mimics how RKIP suppresses the ability of cancer cells to spread. They administered low doses of this treatment to mice with metastatic cancer that mimics metastatic breast cancer, and found that it blocked the spread of cancer and increased the animals’ survival. Importantly, the treatment did not trigger the compensatory mechanisms that often cause high-dose, anti-metastasis drugs to stop working and tumours to return.
Finally, the team used computer modelling to explain why reducing, but not completely stopping, the expression of this network of genes helped prevent metastasis without triggering drug resistance or relapse. They also identified patients with breast cancer in the Cancer Genome Atlas who might be most likely to benefit from such treatment based on their cancer’s gene expression patterns.
“Our findings could lead to a new cancer treatment strategy where patients first receive low-dose combination drugs that block metastasis and then receive traditional cancer treatments such as radiation, chemotherapy or immunotherapy,” says co-senior author Marsha Rosner, the Charles B. Huggins Professor at the Ben May Department of Cancer Research at UChicago.
“Our results challenge current approaches to cancer treatment and suggest an alternative strategy for controlling metastasis in breast cancer and potentially other types of cancer,” concludes co-senior author Alexandre Ramos, Group Leader at the School of Arts, Sciences and Humanities, University of São Paulo, Brazil.
Story Source:
Materials provided by eLife. Note: Content may be edited for style and length.

A new approach to road safety that relies on design and engineering principles — the “Safe System” approach — could lead to dramatic reductions in vehicle-related deaths and injuries if implemented in the U.S., according to a report from a consortium of experts convened by researchers at Johns Hopkins Bloomberg School of Public Health and the Institute of Transportation Engineers.
The Safe System approach engineers road systems so that they are safe when used intuitively, the way people tend to use them. A Safe System minimizes the chances for mistakes by drivers, pedestrians, and bicyclists, and reduces the intensity of crashes when they do occur. This approach — which may include the use of roundabouts, separated bike lanes, rumble strips, and other measures — has already been applied successfully in several other countries. In Sweden, where the approach was first implemented, road deaths fell by about 67 percent from 1990 to 2017.
The report’s authors advocate that the Safe System approach can improve road safety equity if it is implemented in ways that close the safety gap between well-served and historically underserved communities.
According to the National Safety Council, highway deaths increased 8% last year over the previous year even though people were driving considerably less, with an estimated 42,000 deaths in motor vehicle crashes and 4.8 million injuries. Since 2009, the traffic death rate has remained relatively steady at about 11 deaths per 100,000 population, and crashes have persisted as the leading cause of death among young people. The rate of traffic deaths in the U.S. declined sharply between the 1960s and 1990, largely as a result of the car safety revolution.
The report, “Recommendations of the Safe System Consortium,” was released on May 11. The Safe System Consortium, a group of more than two dozen leading highway engineers, scientists, and public health professionals, convened earlier this year to reimagine road safety and equity in this country, as a new presidential administration got underway.
“With this report, we’re encouraging policymakers to adopt what would be a paradigm shift in the approach to road safety in the U.S., with the potential to dramatically reduce the vehicle-related injuries and deaths that we’ve been seeing on a daily basis,” says co-author Shannon Frattaroli, PhD, associate professor in the Department of Health Policy and Management at the Bloomberg School and director of the Johns Hopkins Center for Injury Research and Policy.

Two groups of researchers at Sandia National Laboratories have published papers on the droplets of liquid sprayed by coughs or sneezes and how far they can travel under different conditions.
Both teams used Sandia’s decades of experience with advanced computer simulations studying how liquids and gases move for its nuclear stockpile stewardship mission.
Their findings reinforce the importance of wearing masks, maintaining social distancing, avoiding poorly ventilated indoor spaces and washing your hands frequently, especially with the emergence of new, more transmissible variants of SARS-CoV-2, the virus that causes COVID-19.
One study used Sandia-developed high-performance computer simulation tools to model coughing with and without a breeze and with and without protective barriers. This work was recently published in the scientific journal Atomization and Sprays.
Stefan Domino, the lead computer scientist on the paper, said his team found that while protective barriers, such as plexiglass partitions in grocery stores, offer protection from larger droplets, very tiny particles can persist in the air for an extended time and travel some distance depending on the environmental conditions.
Separate computer modeling research at Sandia looked at what happens to the smaller aerosol droplets under different conditions, including when a person is wearing a face covering. That study showed that face masks and shields keep even the small droplets from a cough from dispersing great distances, said researcher Cliff Ho, who is leading that effort. This work was published in the journal Applied Mathematical Modelling on Feb. 24.

DNA is composed of nucleobases represented by the letters A, T, G and C. They form the basis of the genetic code and are present in all living beings. But in a bacteriophage, another base, represented by the letter Z, exists. This exception, the only one observed to date, has long remained a mystery. Scientists from the Institut Pasteur and the CNRS, in collaboration with the CEA, have now elucidated the biosynthesis pathway of this base. This work has been published in the April 30th, 2021 issue of Science.
DNA, or deoxyribonucleic acid, is a molecule that serves as the medium for storing genetic information in all living organisms. It is a double helix characterized by alternating purine nucleobases (adenine and guanine) and pyrimidine nucleobases (cytidine and deoxycytidine). The bases of each DNA strand are located at the center of the helix and are bonded together, thereby linking the two DNA strands: adenine forms two hydrogen bonds with thymine (A-T), and guanine forms three hydrogen bonds with cytosine (G-C). This applies to all living beings, with one exception.
Cyanophage S-2L, an exception to conventional genetics
Cyanophage S-2L is a bacteriophage, in other words a virus that infects bacteria. In this phage, adenine is completely replaced by another base, 2-aminoadenine (represented by the letter Z). The latter forms three hydrogen bonds with thymine (Z-T), instead of the usual two bonds between adenine and thymine. This higher number of bonds increases the stability of the DNA at high temperatures and changes its conformation, meaning that the DNA is less well recognized by proteins and small molecules.
2-aminoadenine biosynthesis pathway elucidated
Since it was discovered in 1977, cyanophage S-2L has been the only known exception, and the biosynthesis pathway of 2-aminoadenine has remained unknown. Scientists from the Institut Pasteur and the CNRS, in collaboration with the CEA, recently elucidated this biosynthesis pathway and demonstrated its enzymatic origins. They achieved this by identifying a homolog of the known enzyme succinoadenylate synthase (PurA) in the genome of cyanophage S-2L. A phylogenetic analysis of this enzyme family revealed a link between the homolog, known as PurZ, and the PurA enzyme in archaea. This indicates that the homolog is an ancient enzyme that probably conferred an evolutionary advantage. The research was carried out using the Institut Pasteur’s Crystallography Platform.
The new Z-T base pair and the discovery of the biosynthesis pathway show that new bases can be enzymatically incorporated into genetic material. This increases the number of coding bases in DNA, paving the way for the development of synthetic genetic biopolymers.
Story Source:
Materials provided by Institut Pasteur. Note: Content may be edited for style and length.

A hallmark of cancer is its ability to evade the immune system. It is why researchers are focused on finding new strategies and targets to jumpstart the immune system so it can mount a response against tumors. One such target is the inhibitory receptor T-cell immunoglobulin and mucin domain 3 (TIM-3), a protein that is overexpressed in many different types of cancer and is associated with poor patient outcomes. It is known to block the activity of immune cells, such as dendritic cells, but how remains unclear. In a new article published in the journal Immunity, Moffitt Cancer Center researchers show that TIM-3 inhibits the STING signaling pathway in dendritic cells, thereby blocking their ability to elicit an immune response.
Dysregulation of the immune system is an important contributor to cancer development. Many new therapies target T cells to restimulate them to attack cancer cells. However, dysregulation of dendritic cells and other cells of the immune system can also contribute to the development of cancer. Dendritic cells are specialized cells that capture, process and display antigens, which are then recognized by T cells that become activated. Cancer patients often have dysregulated or lower dendritic cells levels, suggesting that approaches to augment their activity may be effective against cancer.
Previously, Moffitt researchers demonstrated that antibodies that block TIM-3 enhanced the activity of chemotherapy in mouse models of breast cancer, even though T cells in this model had very low levels of TIM-3. They also found that the effect of TIM-3 blocking antibodies was dependent on the presence of dendritic cells.
To further understand the role of TIM-3 in dendritic cells, the Moffitt team performed preclinical laboratory experiments in cell lines and mouse models. They discovered that TIM-3 inhibits activation of the cGAS-STING pathway and downstream immune cell activation. The cGAS-STING pathway is an important mediator of immune cell function and activators of STING can stimulate anti-tumor activity of immune cells. They found that TIM-3 was able to block activation of the STING pathway in dendritic cells by inhibiting the internalization of double-stranded DNA derived from tumor cell debris in the extracellular space. The researchers also confirmed that chemotherapy plus TIM-3 blockade effectively prevented tumor growth in mice, which was dependent on STING activity.
“Our results suggest that we can enhance T cell activity by targeting TIM-3 to activate the STING pathway in dendritic cells,” said Brian Ruffell, Ph.D., associate member of the Department of Immunology at Moffitt. “While more research is needed, we believe understanding this process will help us develop combinations with anti-TIM-3 antibodies as a possible therapy for certain types of cancer.”
Story Source:
Materials provided by H. Lee Moffitt Cancer Center & Research Institute. Note: Content may be edited for style and length.