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A heart attack, or myocardial infarction, is one of the leading causes of mortality worldwide, resulting in 18 million deaths per year. These numbers are expected to increase in coming years because of cardiovascular complications from COVID-19.
In Biophysics Reviews, by AIP Publishing, researchers from the University of Notre Dame explored how human tissue models, outside the body, can be used to improve treatment and diagnosis of heart attacks.
Myocardial infarction occurs when plaque in a major coronary artery slows down and blocks blood flow to the heart, depriving it of oxygen, killing cells, and leading to significant tissue damage. This can cause death or transform regions of the heart into scar tissue, making it more difficult to beat in the future.
Current therapies and drugs for heart attacks, and many other conditions like cancer, are mostly studied in the lab using animal models. However, only one out of 10 therapeutics that work for animals ends up successful in clinical applications. There are also occasional but impactful side effects in humans that are not seen in animals.
“Although animal models give an overall systemic view of how an organism would respond to a pathological condition, it is not the exact response that a human tissue would give,” said author Pinar Zorlutuna. “If you have a human model along with your animal model, chances are that you can catch discrepancies in between the two early on, before taking things to the clinical trial and failing there.”
In vitro human models allow researchers to examine the impact of heart attacks and treatment of the fibrotic tissue outside the body. They use organoids, 3D organlike multicellular models derived from stem cells, to mimic natural development, structural organization, regeneration, and disease progression. Meanwhile, microfluidic devices control cell placement and fluid flow to act like the heart on a chip, while bioprinting allows cardiac tissue to be built up layer by layer.
“These models are very important to push forward what we are doing in preclinical research,” said Zorlutuna. “They can help get therapeutics into more people in a faster, safer, and more efficient manner.”
“Despite advancements in the tissue engineering field, some challenges remain to create in vitro cardiac tissue models because the human heart is a very complex organ,” said author Gozde Basara. “Larger constructs, engineered using mature cardiac cells and quick fabrication methods, would be the next step.”
The team is currently using models to study and identify diagnostic markers for heart attacks. The strategy could be used to catch and prevent cardiovascular diseases in general.
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Researchers at the Nara Institute of Science and Technology have developed a new model of obsessive-compulsive disorder based on principles of reinforcement learning. This model may lead to better treatment for obsessive-compulsive and related disorders.
Scientists from the Nara Institute of Science and Technology (NAIST), Advanced Telecommunications Research Institute international, and Tamagawa University have demonstrated that obsessive-compulsive disorder (OCD) can be understood as a result of imbalanced learning between reinforcement and punishment. On the basis of empirical tests of their theoretical model, they showed that asymmetries in brain calculations that link current results to past actions can lead to disordered behavior. Specifically, this can happen when the memory trace signal for past actions decays differently for good and bad outcomes. In this case, “good” means the result was better than expected, and “bad” means that it was worse than expected. This work helps to explain how OCD develops.
OCD is a mental illness involving anxiety, characterized by intrusive and repetitious thoughts, called obsessions, coupled with certain repeated actions, known as compulsions. Patients with OCD often feel unable to change behavior even when they know that the obsessions or compulsions are not reasonable. In severe cases, these may render the person incapable of leading a normal life. Compulsive behaviors, such as washing hands excessively or repeatedly checking whether doors are locked before leaving the house, are attempts to temporarily relieve anxiety caused by obsessions. However, hitherto, the means by which the cycle of obsessions and compulsions becomes strengthened was not well understood.
Now, a team led by researchers at NAIST has used reinforcement learning theory to model the disordered cycle associated with OCD. In this framework, an outcome that is better than predicted becomes more likely (positive prediction error), while a result that is worse than expected is suppressed (negative prediction error). In implementation of reinforcement learning, it is also important to consider delays, as well as positive/negative prediction errors. In general, the outcome of a certain choice is available after a certain delay. Therefore, reinforcement and punishment should be assigned to recent choices within a certain time frame. This is called credit assignment, which is implemented as a memory trace in reinforcement learning theory. Ideally, memory trace signals for past actions decay at equal speed for both positive and negative prediction errors. However, this cannot be completely realized in discrete neural systems. Using simulations, NAIST scientists found that agents implicitly learn obsessive-compulsive behavior when the trace decay factor for memory traces of past actions related to negative prediction errors (ν-) is much smaller than that related to positive prediction errors (ν+). This means that, from the opposite perspective, the view of past actions is much narrower for negative prediction errors than for positive prediction errors. “Our model, with imbalanced trace decay factors (ν+ > ν-) successfully represents the vicious circle of obsession and compulsion characteristic of OCD,” say co-first authors Yuki Sakai and Yutaka Sakai.
To test this prediction, the researchers had 45 patients with OCD and 168 healthy control subjects play a computer-based game with monetary rewards and penalties. Patients with OCD showed much smaller ν- compared with ν+, as predicted by computational characteristics of OCD. In addition, this imbalanced setting of trace decay factors (ν+ > ν-) was normalized by serotonin enhancers, which are first-line medications for treatment of OCD. “Although we think that we always make rational decisions, our computational model proves that we sometimes implicitly reinforce maladaptive behaviors,” says corresponding author, Saori C. Tanaka.
Although it is currently difficult to identify treatment-resistant patients based upon their clinical symptoms, this computational model suggests that patients with highly imbalanced trace decay factors may not respond to behavioral therapy alone. These findings may one day be used to determine which patients are likely to be resistant to behavioral therapy before commencement of treatment.
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Huntington’s disease — a hereditary and fatal genetic disorder — has long been considered a neuronal disease due to the permanent loss of medium spiny motor neurons, the death of which over time is responsible for the clinical hallmarks of the disease: involuntary movements, problems with coordination, cognitive decline, depression, and psychosis.
However, a growing body of research, including a new study appearing in the journal Cell Reports, suggests that the disease may also flow from defects in glia, important support cells found in the brain. The new study expands our understanding of the underlying mechanisms of the disease, and reinforces the potential of therapies that target glia cells.
Years of research in the lab of University of Rochester Medical Center (URMC) neurologist Steve Goldman, M.D., Ph.D., have shown that the two populations of glia found in the brain — astrocytes and oligodendrocytes — are dysfunctional in Huntington’s disease, and may trigger much of the neuronal pathology seen in the disease. Goldman is co-director of the URMC Center for Translational Neuromedicine and senior author of the new study. Glia cells play a critical role in maintaining the health of neurons and facilitating the chemical signaling between nerve cells. In Huntington’s, glia are unable to perform these functions, leading to a breakdown in communication between neurons and, over time, cell death.
“Huntington’s is a complex disease that impacts both neurons and support cells. To use an analogy, not only is the patient sick, but so are the doctor and the nurse,” said Abdellatif Benraiss, Ph.D., a research associate professor in the URCM Department of Neurology and first author of the study. “While the loss of neurons gives rise to the symptoms and the ultimate fatal nature of the disease, reversing glial dysfunction may give us an opportunity to intervene early in the course of the disease, keeping neurons healthy for longer and slowing disease progression.”
The new study focuses on oligodendrocytes and identifies how the suppression of a specific transcription gene called Tcf7l2 triggers a series of changes that impair the function of oligodendrocyte progenitor cells (OPCs). These cells constantly resupply the brain with oligodendrocytes, which, in turn, refresh the myelin insulation that helps signals travel in the brain more crisply. In Huntington’s, OPCs are not able to meet demand, leading to deficient myelination in the brain, which can be observed in Huntington’s patients in the form of white matter atrophy. When the researchers overexpressed Tcf7l2 in mice with the Huntington’s disease mutation, their OPCs recovered and restored the myelin that had been lost to the disease.
A sister paper from the Goldman lab, which appeared in Cell Reports last year, examined how the genetic defect that lies at the heart of the disease impacts the development and function of astrocytes, which support neurons and their synaptic connections. That paper highlighted genetic pathways aligned with Tcf7l2, found in both mouse and human Huntington’s astrocytes, that is a major contributor to synaptic dysfunction in Huntington’s, which in turn leads to the behavioral and psychiatric symptoms of the disease. Taken together, these papers provide a clearer picture of the genetic mechanisms by which Huntington’s disease impairs glial cell function and ultimately leads to neurological disability, while providing new cellular and molecular targets for potential treatment.
The researchers believe that these findings put new therapies within reach. Replacing or “fixing” defective glia cells may prove a far easier proposition than replenishing neurons lost in the disease. A study from Goldman’s lab in 2018 showed the complexity of the genetic defects in Huntington’s glia, and pointed to the utility of swapping out sick cells with healthy ones, an approach that the lab had shown effective in mouse models of the disease in an earlier study in 2016. Taken together, this series of studies has laid the foundation for targeting glial cells for treatment, and potentially outright replacement, in Huntington disease.
Additional authors of the study include John Mariani, Ashley Tate, Pernille Madsen, Kathleen Clark, Kevin Welle, Renee Solly, Laetitian Capellano, Karen Bentley, and Devin Chandler-Militello with URMC. The research was funded with support from National Institute of Neurological Disorders and Stroke, the Hereditary Disease Foundation, CHDI, and Sana Biotechnology.

Preeclampsia is a condition that affects the placenta during pregnancy and is dangerous for both the fetus and the mother. Scientists from the Institut Pasteur, Inserm and the CNRS have proposed a new therapy, tested in two rodent models, that corrects the defects identified in placental cells, and restores placental and fetal weight. The treatment successfully lowers blood pressure in the mother and resolves the characteristic preeclampsia symptoms of excess protein in urine and cardiovascular abnormalities. The research was published on July 30 in the journal Redox Biology.
Preeclampsia is a placental dysfunction that affects approximately 2 to 8% of pregnant women worldwide. It can have fatal complications, with more than 50,000 maternal deaths each year and indirectly more than a million fetal or perinatal deaths worldwide. The primary symptoms of preeclampsia are arterial hypertension, proteinuria (increased levels of protein in the urine), abnormal coagulation in the placenta, cardiovascular abnormalities in the mother and fetal growth restriction. Preeclampsia can also have long-term effects on the cardiovascular system, brain, liver and kidneys of the mother several years after pregnancy. The current first-line treatment for preeclampsia is limited and involves the preventive use of aspirin for at-risk patients. This treatment reduces the procoagulant state in the placenta and partly relieves pressure on the vascular network.
Preeclampsia is characterized by a defective placenta caused by trophoblast dysfunction. Trophoblasts are specific cells in the placenta that help organize and manage the vascular network, allowing the provision of oxygen, nutrients and other elements that are essential for fetal growth. At the molecular level, preeclampsia is characterized by an uncontrolled increase in oxidative stress, with excessive production of various reactive species including reactive oxygen and nitrogen species. There is a genetic component: the first gene to be identified as being implicated in the genetic forms of preeclampsia was the STOX1 transcription factor, which controls the expression of thousands of genes, especially those involved in the production of nitric oxide (NO). In a transgenic mouse model, high accumulation of STOX1 in the placenta induced a preeclampsia-like syndrome. In preeclampsia, nitric oxide, a powerful vasodilator that dilates blood vessels to promote blood flow to the placenta, is mobilized to produce potentially toxic molecules (nitrosative stress) and its levels become insufficient in the placental vascular network, affecting trophoblast function and the vascular network and destabilizing other reactive species. This creates a vicious circle and causes uncontrollable oxidative/nitrosative stress with multiple complications, also affecting maternal blood vessel cells, with potentially fatal consequences.
NO is produced by a family of enzymes known as nitric oxide synthases (NOSs). Finding a way of restoring NO production in the placenta via NOSs could represent an effective new therapy to treat preeclampsia. A years-long collaboration between the team led by Dr. Daniel Vaiman (Institut Cochin, Inserm/CNRS/Université Paris Cité) and the team led by Dr. Miria Ricchetti (Department of Developmental & Stem Cell Biology, Institut Pasteur/CNRS) with Dr. Laurent Chatre*, and more recently an American team from Mississippi, gave rise to a potential solution. The scientists’ research was based on trophoblasts overexpressing STOX1 and on two rodent models of preeclampsia, one mimicking early-onset forms via placental overexpression of STOX1 and the other mimicking late-onset forms by partial occlusion of the lower abdominal aorta. The research revealed a cascade of events that ultimately led the scientists to propose a new therapy. Treating trophoblasts with BH4 (or tetrahydrobiopterin, a cofactor that stabilizes the NOS enzyme producing NO) corrected the defects identified in these cells, restoring production of NO rather than potentially toxic molecules. More importantly, administering BH4 to the two preclinical rodent models restored placental and fetal weight. Finally, in the early-onset STOX1 preclinical model with significant arterial hypertension and proteinuria, the BH4 treatment corrected blood pressure, excess protein in urine, and cardiovascular abnormalities in the mother. The results even suggest that the treatment may be effective in addressing the long-term effects of preeclampsia on mothers (vascular abnormalities in the brain, kidneys, heart and liver).
This research is the first step towards the development of a therapy for preeclampsia. The scientists also performed genetic (transcriptomic) analyses of placentas treated with BH4 and showed that it corrects the expression of several genes disrupted by excess STOX1 in a different way from the deregulation induced by aspirin in the placenta. In conclusion, the scientists propose that a treatment combining BH4 and aspirin could be the ultimate therapeutic solution for many cases of preeclampsia. This hypothesis needs to be validated in clinical trials.
*Dr. Laurent Chatre was previously a CNRS scientist at the Institut Pasteur. Since September 2018 he has been a CNRS scientist in the Imaging and Therapeutic Strategies for Cancers and Cerebral Tissues (ISTCT) laboratory (CNRS/University of Caen Normandy).
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Aortic valve stenosis occurs when the aortic valve narrows, constricting blood flow from the heart through the artery and to the entire body. In severe cases, it can lead to heart failure. Identifying the condition can be difficult in remote areas because it requires sophisticated technology, and diagnoses at early stages are challenging to obtain.
In the Journal of Applied Physics, by AIP Publishing, researchers from the University of Kerala, India, and the University of Nova Gorica, Slovenia, developed a method to identify valve dysfunction using complex network analysis that is accurate, simple to use, and low-cost.
“Many rural health centers don’t have the necessary technology for analyzing diseases like this,” said author M.S. Swapna, of the University of Nova Gorica and the University of Kerala. “For our technique, we just need a stethoscope and a computer.”
The diagnostic tool works based on the sounds produced by the heart. The organ creates a “lub” noise as it closes the mitral and tricuspid valves, pauses as ventricular relaxation occurs and the blood fills in, then makes a second noise, “dub,” as the aortic and pulmonary valves close.
Swapna and her team used heart sound data, collected over 10 minutes, to create a graph, or a complex network of connected points. The data was split into sections, and each part was represented with a node, or single point on the graph. If the sound in that portion of the data was similar to another section, a line, or edge, was drawn between the two nodes.
In a healthy heart, the graph showed two distinct clusters of points, with many nodes unconnected. In contrast, a heart with aortic stenosis contained many more correlations and edges.
“In the case of aortic stenosis, there is no separation between the lub and dub sound signals,” said Swapna.
The researchers used machine learning to examine the graphs and identify those with and without disease, achieving a classification accuracy of 100%. Their method takes the correlation of each point under consideration, making it more accurate than others that only consider the strength of the signal, and it does so in less than 10 minutes. As such, it could be useful for early-stage diagnoses.
So far, the method has only been tested with data, not in a clinical setting. The authors are developing a mobile application that could be accessed worldwide. Their technique could also be used to diagnose other conditions.
“The proposed method can be extended to any type of heart sound signals, lung sound signals, or cough sound signals,” said Swapna.
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Published2 hours agoSharecloseShare pageCopy linkAbout sharingImage source, ReutersThe EU is giving more than five million anti-radiation tablets to Ukraine, as fears grow of an accident at Europe’s largest nuclear power plant. The Zaporizhzhia plant is under Russian occupation and has recently come under fire, with both sides blaming each other for the attacks. In some areas, officials are already handing out the pills, which can stop the body absorbing radioactive iodine.Residents have been told only to take it if a radiation leak is confirmed. So far, only people living within 50km (30 miles) of the power plant are being offered the potassium iodide tablets, but the European Union is providing Ukraine with more than five million doses which would allow for much wider distribution. How risky is the stand-off over Ukraine’s nuclear plant?Preparing for the worst at Ukraine nuclear plantZaporizhzhia in southern Ukraine was occupied by Russia soon after it invaded Ukraine in February. Ukrainian staff who continue to operate the plant have told the BBC that Russian troops have used it as a military base and that workers are in effect held at gunpoint.While recent fighting in the area has caused some damage to the plant, so far there has not been any recorded increase in radiation levels in the area.Nevertheless, officials are concerned further damage could cause a radiation leak, which could spread over a large area. The UN’s nuclear agency has been demanding access to the facility for several months, and a team has arrived in Ukraine in the hope of finally being allowed to inspect the site in the coming days.The EU said on Tuesday it was providing the tablets as a “preventative safety measure” to increase protection in the area around the nuclear plant. Five million pills will come from its emergency reserves and another 500,000 from Austria.Potassium iodide tablets were already being handed out to residents in one part of Zaporizhzhia city on Monday, and 25,000 tablets have been sent to Enerhodar – the city closest to the nuclear plant.”In the event of an emergency, both adults and children will already be provided with iodide and will be able to protect themselves in time,” said Anatoliy Kurtyev from Zaporizhzhia city council.He stressed that residents should only take the drug if an accident happens – not as a precautionary measure. Potassium iodide is taken to prevent radioactive iodine – the main cancer-causing isotope also known as iodine-131 – from being absorbed by the thyroid gland. High levels of radioactive iodine can increase the risk of thyroid cancer in infants, children and young people, even years after exposure. If taken at the right time at the right dose, potassium iodide will be absorbed by the thyroid gland instead of the more dangerous iodine-131, reducing the associated health risks. The European Commission says it is to distribute 5.5 million potassium iodide tablets for residents living in vicinity of Zaporizhzhia nuclear plant. Many countries, including the UK, have a stockpile of these tablets in case of a major nuclear accident or leak. They should only be used if recommended by medical experts, though, for good reason.There are health risks associated with taking them, so they are not something people should try and buy or acquire themselves to take.They are a useful countermeasure because radioactive iodine that is breathed in or consumed in food and drink can be stored in the thyroid gland for some time.The tablets only help protect the thyroid, not other parts of the body.War in Ukraine: More coverageANALYSIS: The war is static, but ousting Russia is a seismic taskON THE GROUND: What weapons are being supplied to Ukraine?READ MORE: Full coverage of the crisisMore on this storySecure Ukraine nuclear sites, Western allies urge21 August

Our cells are constantly communicating, and scientists have developed an efficient way to find out what messages they are sending in protein-packed biological suitcases called exosomes.
These spherical exosomes, which reside in the internal membrane of a cell but will eventually head out to get inside another cell, transport large molecules like proteins, a basic building block in the body and drivers of biological activity, and RNA, which produces protein.
“This is an ongoing process,” says Dr. Sang-Ho Kwon, cell biologist in the Department of Cellular Biology and Anatomy at the Medical College of Georgia at Augusta University, and there is increasing evidence that it occurs both in states of health and disease.
“We are trying to figure out this puzzle of what exosomes are doing in different scenarios,” says Kwon. He is corresponding author of a study in the Journal of Extracellular Vesicles detailing a labeling technique he and his research team have developed to analyze the contents of exosomes from any specific cell type to better understand their role in wellbeing and illness.
“Their contents can help tell us what our cells are telling each other,” Kwon says, and likely provide early clues that we are getting sick and help us better understand how we get sick.
It’s thought that cargo gets loaded early in the formation of exosomes by their precursor endosomes, near the cell membrane, which work much like filling the mail truck at the post office before it heads out on its route. Exosomes will stay there until released by the cell to travel to other cells.

Pregnant women in the U.S. are being exposed to chemicals like melamine, cyanuric acid, and aromatic amines that can increase the risk of cancer and harm child development, according to researchers at UC San Francisco and Johns Hopkins Bloomberg School of Public Health.
Melamine and cyanuric acid were found in nearly all study participants’ samples, but the highest levels were found in women of color and those with greater exposure to tobacco. Four aromatic amines that are commonly used in products containing dyes and pigments were also found in nearly all pregnant participants.
People can be exposed to melamine and aromatic amines in a variety of ways: through the air they breathe, by eating contaminated food or ingesting household dust, as well as from drinking water or by using products that contain plastic, dyes, and pigments.
“These chemicals are of serious concern due to their links to cancer and developmental toxicity, yet they are not routinely monitored in the United States,” said Tracey J. Woodruff, PhD, a professor of obstetrics, gynecology and reproductive medicine who directs the UCSF Program on Reproductive Health and the Environment, and is the co-senior author of the study published August 30, 2022, in Chemosphere.
Melamine and its major byproduct, cyanuric acid, are each high production chemicals that exceed 100 million pounds per year in this country alone. When exposure to these chemicals happens together, they can be more toxic than either one alone. Melamine is found in dishware, plastics, flooring, kitchen counters, and pesticides; cyanuric acid is used as a disinfectant, plastic stabilizer, and cleaning solvent in swimming pools; aromatic amines are found in hair dye, mascara, tattoo ink, paint, tobacco smoke, and diesel exhaust.
Melamine was recognized as a kidney toxicant after baby formula and pet food poisoning incidents in 2004, 2007, and 2008 that caused several deaths as well as kidney stones and urinary tract obstruction in some people. Additional animal experiments suggest melamine reduces brain function.

Studying the role of mitochondria — the specialized structures within cells responsible for energy production — in metabolic diseases has been difficult because of a lack of animal models with the necessary mitochondrial mutations to observe these tiny organelles. However, a team from the University of Tsukuba have now generated the first mouse model carrying a disease-associated mitochondrial mutation and have shown that the resulting disease is caused by faulty RNA processing.
Mitochondria are surrounded by a membrane and contain a small amount of their own DNA. This mitochondrial DNA codes for some components of the energy-generating machinery, as well as genes for both ribosomal RNAs (components of the machinery that makes proteins) and transfer RNAs that play a key role in protein synthesis. Mutations in the mitochondrial genome are known to be linked to some human disorders such as diabetes, neurodegenerative diseases, infertility, and cancer.
Researchers at the University of Tsukuba fused cells that contained mitochondria carrying mutant DNA, but no nucleus, with embryonic stem cells that had had all their mitochondria removed by a drug called rhodamine 6G, thus creating a mouse model containing the A2748G mutation. This mutation is found in human patients, where it is known as the A3302G mutation, and is one of the common mitochondrial mutations associated with some human diseases, such as certain neuromuscular diseases, encephalopathy (brain damage), and metabolic disorders.
The mice carrying this mutant mitochondrial DNA developed metabolic disorders that mimicked the symptoms shown by human patients carrying the equivalent human mutation. This enabled further study to uncover the underlying molecular mechanism of the associated disease, which showed that this mutation affected the processing of RNAs by interfering with protein synthesis in the affected mice.
“The faulty processing of the RNA containing the A2748G mutation led to a decrease in the translation of a protein known as ND1,” explains main author Professor Kazuto Nakada. “ND1 is a component of a protein complex known as Complex 1, the first of five key protein complexes in the process of energy generation known as oxidative phosphorylation.” The resulting Complex I deficiency affected the function of the cellular energy-generating pathway, which then went on to cause mitochondrial dysfunction and metabolic disorders.
The development of this model will open new avenues for scientific discovery in the study of mitochondria and multiple diseases.
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Researchers at the University of Gothenburg have identified a previously unknown mechanism controlling tumor growth in cultured cells and mice. This discovery may potentially enable future development of new drugs against a range of cancer diseases.
In a research article published in the journal Nature Communications, the Gothenburg scientists have described their discovery. It concerns a protein that binds genetic material and, as the researchers now show, also controls properties that regulate tumor development.
The protein — known as HnRNPK — binds to messenger-RNA (mRNA), which the two genes IER3 and IER3-AS1 code for. These genes are highly active in several forms of cancer. By binding to the mRNA of these genes, the HnRNPK prevents double-strand RNA forming between them and keeps them separate.
Changes in tumor growth
“Keeping these two genes’ RNA separate promotes growth of tumors that depend on growth factors. Without the HnRNPK protein, the properties that promote tumor growth are neutralized, paving the way for development of drugs that block the HnRNPK,” says Chandrasekhar Kanduri, Professor of Medical Genetics at Sahlgrenska Academy, University of Gothenburg, who is one of the research leaders behind the study.
The study also shows that, similarly, the HnRNPK protein binds to the mRNA of several other genes, preventing the formation of double-strand RNA.
The discovery affords scope for indirectly influencing the FGF-2 growth factor, which is well known to be key both to the process whereby stem cells mature into various cell types and to early embryonic development.
Fewer side effects
Meena Kanduri, Associate Professor (Docent) of Molecular Medicine at Sahlgrenska Academy, is the corresponding author of the article.
“Given the crucial role of FGF-2 in normal human development, using drugs that target the growth factor directly would have too many side effects. The mechanism we’ve now identified is part of the same signaling chain, but further downstream. So, the mechanism has the potential to become a more attractive cancer treatment option, with fewer side effects,” she says.
More research is needed to verify the transferability of the finding from cell culture and mouse studies to humans. In the next stage, the group plans to conduct extended studies to examine in more detail how the pair of genes regulated by FGF-2 govern the growth environment of tumors.
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