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Human organ transplants offer a crucial lifeline to people with serious illnesses, but there are too few organs to go around: in the U.S. alone, there are more than 112,000 people currently waiting for transplants. The promise of 3D printing organs is one possible solution to address this shortage but has been fraught with complexity and technical barriers, limiting the type of organs that can be printed. Researchers at Stevens Institute of Technology are now pushing through these barriers by leveraging a decades-old technique to reproduce any tissue type.
The work, led by Robert Chang, an associate professor in the mechanical engineering department at Stevens’ Schaefer School of Engineering & Science, could open up pathways for 3D printing any kind of organ at any time, even skin directly on an open wound.
“Creating new organs to order and saving lives without the need for a human donor will be an immense benefit to healthcare,” said Robert Chang, whose work appears in the April issue of Scientific Reports. “However, reaching that goal is tricky because printing organs using “bio-inks” — hydrogels laden with cultured cells — requires a degree of fine control over the geometry and size of printed microfiber that current 3D printers simply can’t achieve.”
Chang and his team, including Ahmadreza Zaei, first author and doctoral candidate in Chang’s lab, hope to change that by fast-tracking a new 3D printing process that uses microfluidics — the precise manipulation of liquids through tiny channels — to operate at a far smaller scale than has been possible. “The recent publication aims to improve the controllability and predictability over the structure of the fabricated microtissues and microfibers enabled by microfluidic bioprinting technology,” said Zaeri.
Most current 3D bio-printers are extrusion-based, squirting bio-ink out of a nozzle to create structures about 200 microns — around a tenth as wide as a strand of spaghetti. A microfluidics-based printer could print biological objects measuring on the order of tens of micrometers on par with the single cellular scale.
“The scale is very important, because it affects the biology of the organ,” said Chang. “We’re operating at the scale of human cells, and that lets us print structures that mimic the biological features we’re trying to replicate.”
Besides operating on a smaller scale, microfluidics also enables multiple bio-inks, each containing different cells and tissue precursors, to be used interchangeably within a single printed structure, in much the same way that a conventional printer combines colored inks into a single vivid image.
That’s important because while researchers have already created simple organs such as bladders by encouraging the tissue to grow on 3D-printed scaffolding, more complex organs such as livers and kidneys require many different cell types to be precisely combined. “Being able to operate at this scale, while precisely mixing bio-inks, makes it possible for us to reproduce any tissue type,” said Chang.
Scaling down 3D bio-printing requires painstaking research to figure out exactly how different process parameters such as channel structures, flow speed, and fluid dynamics affect the geometries and material properties of printed biological structures. To streamline that process, Chang’s team created a computational model of a microfluidic printing head, enabling them to tweak settings and forecast outcomes without the need for laborious real-world experimentation.
“Our computational model advances a formulaic extraction that can be used to predict the various geometrical parameters of the fabricated structures extruded from the microfluidic channels,” said Zaeri.
The team’s computational models accurately predicted the results of real-world microfluidic experiments, and Chang is using his model to guide experiments on the ways that biological structures with varies geometries can be printed. The results of this research work can be used in the printing of combined multiple cell-types bio-ink that can replicate the tissue with gradients geometrical and compositional properties found at the intersection of bone and muscle.
Chang is also exploring using microfluidic-enabled 3D printing for the in-situ creation of skin and other tissues, enabling patients to have replacement tissues printed directly into a wound. “This technology is still so new that we don’t know precisely what it will enable,” he said. “But we know it will open the door to creating new structures and important new types of biology.”

Additional booster doses of vaccine against COVID-19 are particularly important for those who are immunosuppressed, namely those who have had solid organ transplants, a new study shows.
The study, published in the Journal of Infectious Diseases, shows that even after vaccination, patients taking immunosuppressive medications to prevent rejection of an organ transplant have higher risk for severe COVID-19 than those with competent immune systems.
But vaccination with three doses of an mRNA vaccine — the first two COVID-19 vaccines authorized for use in the U.S. are messenger RNA (mRNA) vaccines — led to substantially greater protection than two doses, the study shows.
“The immune response to vaccination is often blunted in people with moderate to severe immunosuppression,” said Wesley Self, MD, MPH, principal investigator of the study and associate professor of Emergency Medicine and Vice President for Clinical Research Networks and Strategy at Vanderbilt University Medical Center. “Hence, throughout the COVID-19 pandemic, there has been a concern that immunocompromised people, such as those with a solid organ transplant, may not benefit from vaccination as much as immunocompetent people,” he said.
Although the data in the study confirms that after vaccination patients taking immunosuppressive medications to prevent rejection of an organ transplant have higher risk for severe COVID- 19 than those with competent immune systems, there’s also good news.
“Additional vaccine doses appear to substantially increase the effectiveness of vaccination for transplant patients,” Self said.
For example, among transplant patients, a regimen of two doses of mRNA COVID-19 vaccine was only 29% effective at preventing hospitalization due to COVID-19, while a regimen of three doses was 77% effective.
“The results of this real world, multicenter collaborative study indicate that solid organ transplant recipients benefit from three doses of mRNA COVID-19 vaccine, and support CDC recommended vaccine policies for a three-dose primary series in this vulnerable population,” said Jennie Kwon, DO, MSCI, the first author of the study and assistant professor of Medicine at Washington University in St. Louis and associate healthcare epidemiologist at Barnes-Jewish Hospital.
“We believe these results demonstrate that solid organ transplant recipients remain at risk for COVID-19 despite vaccination and support the need for continued efforts to mitigate the risk of COVID in this population. It illustrates that booster vaccine doses are particularly important for immunosuppressed people,” Self said, adding that fourth doses of the mRNA vaccines are now recommended for people with moderate-to-severe immunocompromising conditions, including solid organ transplant.
The study looked at 10,425 hospitalized patients across 21 hospitals — 440 who had had solid organ transplants, 1,684 with other immunocompromising conditions and 8,301 whose immune systems were competent. Future analysis will be important to understand the effectiveness of fourth doses, the residual risk of severe COVID-19 among solid organ transplant recipients after four vaccine doses and the durability of protection. In addition, other measures to reduce the risk of COVID-19 among solid organ transplant recipients should be considered, including vaccination of close contacts, individual immune monitoring and infection prevention strategies such as face masking in public spaces and physical distancing.
The study is part of the IVY (The Influenza and Other Viruses in the Acutely Ill) Research Network, originally created in 2019 to investigate the epidemiology of severe illnesses caused by viral respiratory infections and the effectiveness of vaccines in preventing these illnesses. The network, funded by the Centers for Disease Control and Prevention and led by Vanderbilt University Medical Center, consists of 21 large adult hospitals geographically dispersed across the U.S. Self is principal investigator for the network.
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Materials provided by Vanderbilt University Medical Center. Original written by Nancy Humphrey. Note: Content may be edited for style and length.

MIT engineers have developed a telerobotic system to help surgeons quickly and remotely treat patients experiencing a stroke or aneurysm. With a modified joystick, surgeons in one hospital may control a robotic arm at another location to safely operate on a patient during a critical window of time that could save the patient’s life and preserve their brain function.
The robotic system, whose movement is controlled through magnets, is designed to remotely assist in endovascular intervention — a procedure performed in emergency situations to treat strokes caused by a blood clot. Such interventions normally require a surgeon to manually guide a thin wire to the clot, where it can physically clear the blockage or deliver drugs to break it up.
One limitation of such procedures is accessibility: Neurovascular surgeons are often based at major medical institutions that are difficult to reach for patients in remote areas, particularly during the “golden hour” — the critical period after a stroke’s onset, during which treatment should be administered to minimize any damage to the brain.
The MIT team envisions that its robotic system could be installed at smaller hospitals and remotely guided by trained surgeons at larger medical centers. The system includes a medical-grade robotic arm with a magnet attached to its wrist. With a joystick and live imaging, an operator can adjust the magnet’s orientation and manipulate the arm to guide a soft and thin magnetic wire through arteries and vessels.
The researchers demonstrated the system in a “phantom,” a transparent model with vessels replicating complex arteries of the brain. With just an hour of training, neurosurgeons were able to remotely control the robot’s arm to guide a wire through a maze of vessels to reach target locations in the model.
“We imagine, instead of transporting a patient from a rural area to a large city, they could go to a local hospital where nurses could set up this system. A neurosurgeon at a major medical center could watch live imaging of the patient and use the robot to operate in that golden hour. That’s our future dream,” says Xuanhe Zhao, a professor of mechanical engineering and of civil and environmental engineering at MIT.

As the COVID-19 pandemic unfolded, a team at the U.S. Department of Energy’s (DOE) Brookhaven National Laboratory set out to better understand how well face masks, ventilation, and physical distancing can cut down transmission of airborne pathogens like SARS-CoV-2, the virus that causes COVID-19.
Using a new computational model that simulates the life cycle of pathogen-laden particles, the researchers found that a combination of distancing of six feet, universal mask-wearing, and increased room ventilation could reduce the risk of infection by more than 98 percent in more than 95 percent of scenarios studied.
“Wide adoption of layered controls dramatically reduces exposure to existing airborne viruses, such as SARS-CoV-2, and will be critical to control outbreaks of novel airborne viruses in the future,” said Laura Fierce, an atmospheric scientist formerly with Brookhaven Lab, now at DOE’s Pacific Northwest National Laboratory. “These nonpharmaceutical interventions can be applied in combination with vaccinations.”
The study is published in the journal Indoor Air. It focuses on how face masks and ventilation work alone and in combination with distancing to reduce the likelihood of someone inhaling virus-laden aerosol particles in particular scenarios — namely, where an infectious person is speaking continuously in an indoor space for three-hours — while also accounting for uncertainty in factors governing airborne transmission.
Fierce collaborated with Alison Robey and Catherine Hamilton — who were participants in the DOE’s Science Undergraduate Laboratory Internships (SULI) program at Brookhaven — to develop the model of respiratory aerosols and droplets used in the study. The model simulates how virus-laden particles move through the jet of air expelled by an infectious person and within the larger indoor space. It considers how expelled particles change in size as water evaporates, how pathogens within those particles become inactive, and how particles are removed through ventilation, deposition on surfaces, and gravitational settling.
The researchers’ simulations showed that exposure to airborne pathogens is significantly lowered by individual controls, such as face masks. But layering controls — that is, using them in combination — can be even more effective. According to the study, the combination of universal mask-wearing and distancing of even just three feet reduced a susceptible person’s risk of infection by 99 percent. On the other hand, without the use of face masks, distancing of at least six feet was needed to avoid increased exposure to respiratory pathogens near an infectious person. The team also showed that increasing ventilation rates by completely replacing the air in a room with fresh or filtered air four times per hour reduces the risk of transmission by more than 70 percent, so long as the infectious person and susceptible person are distanced by at least six feet. On the other hand, ventilation does little to reduce the risk of infection when the infectious person is close by.
“Our detailed modeling of respiratory particles shows how different controls on airborne transmission work in combination, which is important for prioritizing mitigation strategies for different indoor spaces,” Fierce said.
This research was supported by the DOE Office of Science through the National Virtual Biotechnology Laboratory, a consortium of DOE national laboratories focused on response to COVID-19, with funding provided by the Coronavirus CARES Act. This project was supported in part by the U.S. Department of Energy through the Office of Science, Office of Workforce Development for Teachers and Scientists (WDTS) under the Science Undergraduate Laboratory Internships Program (SULI). The quadrature-based model was originally developed with support from the DOE Atmospheric System Research program.
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Materials provided by DOE/Brookhaven National Laboratory. Original written by Kelly Zegers. Note: Content may be edited for style and length.

A 19th century rural Dutch village had unusually low rates of breastfeeding, likely because mothers were busy working, according to a study published April 13, 2022 in the open-access journal PLOS ONE by Andrea L. Waters-Rist of the University of Western Ontario and colleagues.
Artificial feeding of infants, as opposed to breastfeeding, is considered a fairly modern practice, much rarer before the advent of commercially available alternatives to breast milk. However, studies of past populations in Europe have found that breastfeeding practices can vary significantly with regional cultural variation. In this study, researchers examine a 19th century dairy farming rural village in the Netherlands to explore factors linked to lower rates of breastfeeding.
Breastfeeding leaves its mark in the bones of infants in the form of altered ratios of stable carbon and nitrogen isotopes. In this study, researchers tested isotopic signatures in the remains of 277 individuals, including nearly 90 infants and children, from Beemster, North Holland. They found little to no evidence of breastfeeding, surprising given that this community exhibits features commonly associated with breastfeeding communities of the time, such as a Protestant population of moderate socioeconomic status, and mothers commonly working in or near the home.
Since other evidence indicates that mothers in 19th century Beemster were commonly working as dairy farmers, the researchers suspect that a high workload and a ready supply of cow’s milk as an alternative infant food source were important factors contributing to these low rates of breastfeeding. At a few urban archaeological sites, mothers who worked long factory shifts have been found to have low rates of breastfeeding, but a similar phenomenon has not been found in a rural population until now. Future study on more sites will help elucidate how regional cultural practices impacted rates of breastfeeding over time, and in turn, how these factors have impacted infant health over recent centuries.
The authors add: “Artificial feeding of infants is not just a recent phenomenon. Female dairy farmers from 19th century Netherlands chose to not breastfeed, or to wean their infants at a young age, because of the availability of fresh cow’s milk and high demands on female labor.”
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Cardiovascular risk factors are associated with an increased risk of depression in older adults, according to a new study published April 13 in the open-access journal PLOS ONE by Sandra Martín-Peláez of University of Granada, Spain, and colleagues.
Cardiovascular disease and depression are thought to be closely related due to similar risk factors, including inflammation and oxidative stress. Although it has been shown that depression could be a risk factor for developing cardiovascular disease, studies analyzing the potential impact of cardiovascular health on developing depression are scarce.
In the new study, the researchers used data from an ongoing 6-year multi-center randomized trial in Spain which analyzes the effect of a Mediterranean Diet on men aged 55-75 and women aged 60-75 with overweight or obesity. 6,545 individuals with no cardiovascular or endocrine disease at baseline were included in the current analysis. A cardiovascular risk score according to the Framingham-based REGICOR function was calculated for each person, dividing participants into low (LR), medium (MR), or high/very high (HR) cardiovascular risk groups. Depressive status was gauged using a questionnaire at baseline and after 2 years of follow-up.
At baseline, women in the HR group showed higher odds of depressive status than LR women (OR 1.78 95% CI 1.26-2.50). In addition, among all participants with baseline total cholesterol below 160 mg/mL, MR and HR individuals showed higher odds of depression than LR (MR: OR 1.77 95% CI 1.13-2.77; HR: OR 2.83 95% CI 1.25-6.42). On the contrary, among participants with total cholesterol of 280 mg/mL or higher, MR and HR individuals had a lower risk of depression than LR (MR: OR 0.26 95% CI 0.07-0.98; HR: OR 0.23 95% CI 0.05-0.95). After two years, during which time all individuals were instructed to follow a Mediterranean Diet as part of the trial, participants, on average, decreased their depressive status score, with the greatest decreases seen for MR and HR participants with high baseline cholesterol levels.
The authors conclude that high and very high cardiovascular risk are associated with depressive symptoms, especially in women, and that the role of other factors, such as adherence to the Mediterranean Diet, deserves further research.
The authors add: “High cardiovascular risk, especially in women, is associated with symptoms of depression in the elderly.”
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Researchers at The Ottawa Hospital and the University of Ottawa have discovered that a kind of kiss between cells, called trogocytosis, plays a key role in the battle between the immune system and blood cancer cells.
Trogocytosis is a phenomenon by which immune cells, such as Natural Killer (NK) cells, make close contact with another cell and steal a chunk of its membrane. Dr. Michele Ardolino and his team discovered that when NK cells steal membranes from blood cancer cells, a protein called PD-1 comes along for the ride and puts the NK cell to sleep, shutting down their anti-cancer activity.
“NK cells are exceptional cancer killers, and we previously discovered that PD-1 prevents them from working properly,” said Dr. Ardolino, senior scientist at The Ottawa Hospital and assistant professor at the University of Ottawa. “A missing piece of the puzzle is how NK cells produce PD-1, which was surprisingly hard to address. Now we understand why: NK cells do not make their own PD-1, but they steal it from cancer cells! We don’t know exactly why NK cells steal membranes from cancer cells, but it seems clear that tumors hijack the process to put NK cells to sleep and evade the immune system.”
Fortunately, drugs that block PD-1, also called PD-1 inhibitors or immune checkpoint inhibitors, are now routinely used to “wake up” the immune system and help it fight cancer cells. These drugs have significantly improved survival for people with certain kinds of skin cancer, blood cancer and lung cancer, among others.
PD-1 inhibitors were originally developed to wake up the immune system’s T cells. Dr. Ardolino’s research, published in Science Advances, solves a mystery about how PD-1 inhibitors work on NK cells. A better understanding of how these drugs work on different kinds of immune cells could lead to new kinds of immunotherapy for cancer.
Dr. Ardolino notes that this research was possible because of a large team of trainees, postdoctoral fellows and staff.
“There is a great sense of collaboration in research at The Ottawa Hospital and this was instrumental for the success of this project,” said Dr. Ardolino. “We are very lucky to collaborate with physicians invested in performing research to advance patients treatment, such as Dr. Arleigh McCurdy, as well as basic scientists in the Cancer Therapeutic Program, such as Dr. Doug Gray who is a microscopy wiz!”
Authors: Mohamed S. Hasim*, Marie Marotel*, Jonathan J. Hodgins, Elisabetta Vulpis, Olivia J. Makinson, Sara Asif, Han-Yun Shih, Amit K. Scheer, Olivia MacMillan, Felipe G. Alonso, Kelly P. Burke, David P. Cook, Rui Li, Maria Teresa Petrucci, Angela Santoni, Padraic G. Fallon, Arlene H. Sharpe, Giuseppe Sciumè, Andre Veillette, Alessandra Zingoni, Douglas A. Gray, Arleigh McCurdy, Michele Ardolino. * contributed equally
Funding: This research was supported by the Canadian Institutes of Health Research, the Prostate Cancer Fight Foundation, Myeloma Canada, the National Institutes of Health, Sapienza University, Science Foundation Ireland, AIRC, CAAIF and the Government of Ontario. All research at The Ottawa Hospital is also enabled by generous donors to The Ottawa Hospital Foundation.

Researchers at Mayo Clinic’s Center for Individualized Medicine have devised an immunotherapy technique that combines chimeric antigen receptor-T cell therapy, or CAR-T cell therapy, with a cancer-killing virus to more effectively target and treat solid cancer tumors.
The combination approach, published in Science Translational Medicine, involves loading CAR-T cells, which are engineered to look for antigens on cancer cells, with an oncolytic virus. Oncolytic viruses are naturally occurring viruses that can infect and break down cancer cells. They either naturally replicate well in cancer cells or can be engineered to selectively target cancer cells.
The study suggests CAR-T cells can deliver the oncolytic virus to the tumor. Then the virus can infiltrate tumor cells, replicate to bust the cells open, and stimulate a potent immune response.
“This approach allows the tumor to be killed by the virus as well as by the CAR-T cells,” explains Richard Vile, Ph.D., co-leader of the Gene and Virus Therapy Program within Mayo Clinic Cancer Center. “In addition, when the virus is delivered, it turns the tumor into a very inflammatory environment, which the patient’s own immune system then sees and starts to attack.”
The therapeutic strategy addresses two major challenges that make solid tumors difficult to treat with CAR-T cell therapy alone. First, the oncolytic virus can break down the molecular shield that some solid tumors use to avoid an immune system attack. Second, the virus can invade into the core of the cancer cells — a near-impossible feat for immune cells alone, which often lose their power in the attempt.
The researchers also found that the combination approach provided an immune memory phenotype against the tumor.

Alternative splicing is a fundamental biological process that allows cells to make many different types of mRNAs and proteins from a limited number of genes. For many animals, including humans, it is a feature that is essential for the development of complex cells such as muscles or neurons.
Its fundamental importance means that alternative splicing is a very tightly regulated process. But a new study published today in the journal Science Advances has found evidence that the regulation of alternative splicing, which rarely goes wrong in healthy cells, goes haywire in an unexpected place — the cells of a newly formed embryo.
Researchers at the Centre for Genomic Regulation (CRG) in Barcelona made the discovery after creating an atlas of splicing events during the early development of cows, humans and mice.
They found that when human embryos are balls of just 8 cells, they express a huge variety of alternative mRNAs, so much so that the splicing diversity was the highest ever recorded across any cell or tissue studied to date. When the embryos transitioned to the next stage of development, their splicing activity returned to normal.
According to the authors of the study, this is evidence that the regulation of alternative splicing collapses temporarily at a crucial stage of development known as zygotic genome activation. This is when an early embryo transitions from using maternal resources such as proteins and RNA and making its own.
Importantly, the researchers believe the newly-discovered phenomenon occurs because it is developmentally programmed — a purposeful act of sabotage. “We think this happens because there are instructions in our genome that tell a few genes to not do their job at that developmental stage. The embryo cells mess up their splicing on purpose and they do so for a functional reason,” says ICREA Research Professor Manuel Irimia, senior author of the study.
An important clue for why the regulation of splicing fails at this crucial moment lies in the function of the proteins affected. The researchers found that splicing failure destroyed proteins responsible for responding to DNA damage.
“We saw that the DNA damage response at this stage of development was low. While splicing failure isn’t the only factor affecting this defense mechanism, it’s partly responsible for destroying the proteins involved. We don’t know why this happens, but it’s possibly because transcription itself carries a risk of DNA damage. As embryos activate their genome for the first time and start to transcribe, there may be trade-offs involved in order to avoid developmental failure.” says Dr. Barbara Pernaute, postdoctoral researcher at the CRG and co-first author of the study.
According to Dr. Pernaute, these results improve our understanding of how embryos develop during these early stages and could open doors for improvements in assisted reproductive technologies.
The findings could also be useful for advancing research efforts in the creation of totipotent cells from stem cells, a long-term aspiration for regenerative medicine. As these early embryonic cells are truly totipotent cells, knowledge of the mechanism could lead to advances that reverse engineer stem cells to induce totipotency.
“Recent studies carried out by other research groups around the world have shown that artificially inducing the mechanism we find in our study transforms stem cells into totipotent cells. We believe these programmed splicing failures also occur in other physiological contexts. We are only just scratching the surface for the importance this mechanism has for biological processes,” concludes Dr. Irimia.
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Cancer cells can disrupt a metabolic pathway that breaks down fats and proteins to boost the levels of a byproduct called methylmalonic acid, thereby driving metastasis, according to research led by scientists at Weill Cornell Medicine. The findings open a new lead for understanding how tumors metastasize, or spread to other tissues, and hints at novel ways to block the spread of cancer by targeting the process.
The new results, published March 31 in Nature Metabolism, show that metastatic tumors suppress the activity of a key enzyme in propionate metabolism, the process by which cells digest certain fatty acids and protein components. Suppressing the enzyme increases production of methylmalonic acid (MMA). That, in turn, causes the cells to become more aggressive and invasive.
Cancer is the second leading cause of death worldwide, and metastasis drives much of that mortality. Once a tumor begins to metastasize to different tissues and organs around the body, it can quickly become difficult or impossible to treat. However, researchers have made few inroads in understanding how a tumor cell acquires the ability to metastasize.
“A lot of work has been focused on primary tumor initiation and growth, or examining the metastatic tumor, but to go from the primary tumor to the metastatic tumor, that transition has not been studied very extensively,” said co-senior author Dr. John Blenis, the Anna-Maria and Stephen Kellen Professor in Cancer Research, professor of pharmacology and associate director of basic science of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine.
To address that gap, Dr. Blenis and his colleagues have worked for several years to characterize the metabolic changes that cells undergo during the metastatic transition. That effort previously revealed that as people age, their bodies produce more serum MMA (although the source remains unknown), and that higher MMA levels drive worse cancer outcomes. Healthy cells also produce MMA, though, so in the new study Dr. Blenis’s team probed the metabolite’s cancer-related activities more deeply.
“Cancer cells themselves can hijack the pathway that makes methylmalonic acid and this forms a feed-forward cycle that drives cancer progression towards more aggressive and more metastatic forms,” said co-first author Dr. Vivien Low, a postdoctoral fellow in Dr. Blenis’s lab. The other co-first authors Dr. Ana Gomes and Dr. Didem Ilter, were also postdoctoral fellows in the lab at the time of the study. Dr. Gomes is now a faculty member and Dr. Ilter is a research scientist at H. Lee Moffitt Cancer Center & Research Institute.
The discovery adds to a growing body of work showing that specific products of metabolism, called oncometabolites, can drive many aspects of cancer progression and metastasis.
While the new paper focused on various models of breast cancer, Dr. Low said the team is now analyzing other types of cancer cells as well, where they expect to find similar mechanisms operating. The scientists are also searching for ways to attack the process.
“Metastasis is responsible for about 80 to 90 percent of cancer-related mortality, so if we can predict when someone has the potential to develop metastatic tumors, or treat those metastatic tumors that might have this pathway up-regulated, then we might have a very effective, novel therapy,” Dr. Blenis said.
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