Publisher Health

Researchers from the University of Oxford’s Big Data Institute have taken a major step towards mapping the entirety of genetic relationships among humans: a single genealogy that traces the ancestry of all of us. The study has been published today in Science.
The past two decades have seen extraordinary advancements in human genetic research, generating genomic data for hundreds of thousands of individuals, including from thousands of prehistoric people. This raises the exciting possibility of tracing the origins of human genetic diversity to produce a complete map of how individuals across the world are related to each other.
Until now, the main challenges to this vision were working out a way to combine genome sequences from many different databases and developing algorithms to handle data of this size. However, a new method published today by researchers from the University of Oxford’s Big Data Institute can easily combine data from multiple sources and scale to accommodate millions of genome sequences.
Dr Yan Wong, an evolutionary geneticist at the Big Data Institute, and one of the principal authors, explained: “We have basically built a huge family tree, a genealogy for all of humanity that models as exactly as we can the history that generated all the genetic variation we find in humans today. This genealogy allows us to see how every person’s genetic sequence relates to every other, along all the points of the genome.”
Since individual genomic regions are only inherited from one parent, either the mother or the father, the ancestry of each point on the genome can be thought of as a tree. The set of trees, known as a “tree sequence” or “ancestral recombination graph,” links genetic regions back through time to ancestors where the genetic variation first appeared.
Lead author Dr Anthony Wilder Wohns, who undertook the research as part of his PhD at the Big Data Institute and is now a postdoctoral researcher at the Broad Institute of MIT and Harvard, said: “Essentially, we are reconstructing the genomes of our ancestors and using them to form a vast network of relationships. We can then estimate when and where these ancestors lived. The power of our approach is that it makes very few assumptions about the underlying data and can also include both modern and ancient DNA samples.”
The study integrated data on modern and ancient human genomes from eight different databases and included a total of 3,609 individual genome sequences from 215 populations. The ancient genomes included samples found across the world with ages ranging from 1,000s to over 100,000 years. The algorithms predicted where common ancestors must be present in the evolutionary trees to explain the patterns of genetic variation. The resulting network contained almost 27 million ancestors.
After adding location data on these sample genomes, the authors used the network to estimate where the predicted common ancestors had lived. The results successfully recaptured key events in human evolutionary history, including the migration out of Africa.
Although the genealogical map is already an extremely rich resource, the research team plans to make it even more comprehensive by continuing to incorporate genetic data as it becomes available. Because tree sequences store data in a highly efficient way, the dataset could easily accommodate millions of additional genomes.
Dr Wong said: “This study is laying the groundwork for the next generation of DNA sequencing. As the quality of genome sequences from modern and ancient DNA samples improves, the trees will become even more accurate and we will eventually be able to generate a single, unified map that explains the descent of all the human genetic variation we see today.”
Dr Wohns added: “While humans are the focus of this study, the method is valid for most living things; from orangutans to bacteria. It could be particularly beneficial in medical genetics, in separating out true associations between genetic regions and diseases from spurious connections arising from our shared ancestral history.”
Story Source:
Materials provided by University of Oxford. Note: Content may be edited for style and length.

Divide, differentiate or die? Making decisions at the right time and place is what defines a cell’s behavior and is particularly critical for stem cells of an developing organisms. Decision making relies on how information is processed by networks of signaling proteins. The teams around Christian Schröter from the Max Planck Institute of Molecular Physiology in Dortmund and Luis Morelli from the Instituto de Investigacion en Biomedicina de Buenos Aires (IBioBa) have now revealed for the first time, that ERK, a key player in stem cell signaling processes information through fast activity pulses. The duration of the pulsing interval, might encode information essential for divergent fate decision in stem cell cultures.
During their development into the later embryo, stem cells go through a series of developmental steps. The transition between those steps is controlled by signaling molecules that are exchanged between neighboring cells. One of the most critical signals during early mammalian embryogenesis is the fibroblast growth factor 4 (FGF4). When it is recognized by a cell, this information is processed by a network of signaling proteins, resulting in a cellular response. The key players of the network, their role and interactions are by now well known, however only little is known about the signaling dynamics. But what does dynamics actually mean, and why are dynamics important?
Dynamics determine cell fate
In the posterchild example for the importance of dynamics in signal transduction, two different molecular signals trigger different cellular responses — differentiation and cell growth — even though they use the same signal transduction network. This is possible because the dynamics with which the signal transduction system is activated are specific for each of the two molecular signals: Whereas one activates the system for a short time leading to cell growth, the other activates the same system for a long time resulting in differentiation. Thus, signaling dynamics are clearly important to determine a cell’s fate. However, many studies so far could only look at fairly slow dynamics that unfolded over hours and that were the same in all cells; they were blind to fast dynamics, especially if these were different between stem cells in the same dish.
ERK activity pulses every six to seven minutes
The teams around Christian Schröter and Luis Morelli were now able to gain a better understanding of the fast signaling dynamics in stem cells. By introducing a fluorescent sensor in living stem cells, the scientists could measure the activity of the major signaling protein ERK in real-time. ERK activity is important for translating molecular signals into a genetic response and thus for regulating stem cell differentiation. “Measuring ERK activity in single stem cells at short timescale is experimentally very demanding and was never done in such a way before. For the first time, we could observe, that ERK activity pulses every six to seven minutes, faster than similar signals previously shown in other cell systems. In single cells, the pulses occurred often very regularly one after the other, but pulsing patterns were strikingly different between individual cells,” Christian Schröter says. The researchers could also observe, that with increasing FGF4 signal, the number of pulses increases when summing up over many cells, even though the durations of single pulses did not change with FGF4.
Interdisciplinary approach — Intercontinental collaboration
“This kind of data and its role on cell signaling is very hard to interpret. And that is the point, where our expertise kicked in,” Luis Morelli says, longstanding collaboration partner and group leader at the IbioBa, a partner Institute of the Max Planck Society. “We had to develop a new theoretical approach to describe the dynamics in time series. By doing this, we saw that the duration of the pulsing interval might encode information, since we could find pulses and silence. We call this new dynamic feature intermittent oscillations .”
“Oscillations are a more and more recognized feature of signaling processes. We hypothesize that the intermittent oscillations we found in stem cells work like a kind of morse code that encodes differentiation information. Presumably, it is the switch from pulsing to silence that plays a decisive role. The question is now, what do the dynamics tell us about the organization of signaling in stem cells? How are cells able to read the oscillations, and how do they affect the cell’s behavior? I am convinced that close collaboration between experimentalists and theorists is required to unravel the origins and functions of this new dimension in stem cell biology one day,” Christian Schröter says.
Story Source:
Materials provided by Max Planck Institute of Molecular Physiology. Note: Content may be edited for style and length.

Researchers at the University of North Carolina at Chapel Hill and the UNC Lineberger Comprehensive Cancer Center have uncovered a new role of a chromatin-modulatory enzyme, termed EZH2, during cancer development. They then developed a new therapeutic approach with a potent small-molecule inhibitor of this enzyme.
Certain subtypes of blood cancers such as acute leukemias rely on multiple mechanisms for sustaining growth of aggressive cancer cells. Notably, these mechanisms include those driven by EZH2, a chromatin-modulatory enzyme, and cMyc, a prominent cancer-causing factor. UNC researchers now show that these two factors can directly associate with one another, modulating cancer-cell-specific programs of gene expression.
To develop pharmacological means of targeting both EZH2 and cMyc, they teamed with the chemical biologists at Icahn School of Medicine at Mount Sinai and designed a new small-molecule, MS177, based on the proteolysis-targeting chimera (PROTAC) technology. MS177 targets both EZH2 and cMyc and thus inhibit cancer growth.
Their findings are published online in Nature Cell Biology.
“EZH2 plays a very important role during cancer progression and is a known target suitable for drug development,” said UNC Lineberger’s Greg Wang, PhD, associate professor of Biochemistry and Biophysics and Pharmacology at the UNC School of Medicine and co-lead author of this research article. “We are amazed by the efficiency of small-molecule PROTAC in simultaneously targeting EZH2 and cMyc in cancer cells.”
They found that EZH2 possesses two different binding patterns on chromatin in acute leukemia cells, eliciting two distinct gene-regulatory programs. On the one hand, EZH2 forms a canonical protein complex termed PRC2, leading to gene repression at a set of genomic regions; on the other hand, EZH2 interacts with cMyc to activate gene expression at genomic sites distinctive from the above ones. “This explains why the current small-molecule inhibitors of EZH2 cannot block EZH2 completely. PROTAC addresses this gap,” said Jun Wang, PhD, postdoctoral researcher at UNC Lineberger and co-first author of the work.
MS177 achieves on-target effect in cancer cells and exhibits profound tumor killing effects, the researchers report. “Compared to the existing enzymatic inhibitors, MS177 is more likely to behave much better for the treatment of patients with acute leukemias. To our knowledge, an agent for dual targeting of EZH2 and cMyc has not been developed before. cMyc is hard to ‘drug,'” Greg Wang said. “MS177 thus represents a promising candidate for treating other cancers depending on the above tumorigenic pathways.”
Authors
In addition to Greg Wang, Jin and Jun Wang, the paper’s other authors are Weida Gong, PhD, Xijuan Liu, PhD, Yi-Hsuan Tsai, PhD, David F. Allison, PhD, Ling Cai, PhD, UNC; Xufen Yu, PhD, Kwang-Su Park, PhD, Anqi Ma, PhD, Yudao Shen, PhD, and Jing Liu, PhD, Icahn School of Medicine at Mount Sinai, New York; Takashi Onikubo, PhD, and Robert G. Roeder, PhD, Rockefeller University, New York; Wen-Chieh Pi, PhD, and Wei-Yi Chen, PhD, National Yang Ming Chiao Tung University, Taipei, Taiwan.
This work was supported in part by grants from the National Institutes of Health, R01CA218600, R01CA268519, R01CA211336, R01CA215284, R01CA230854, and R01GM122749; Kimmel Scholar Award; Gabrielle’s Angel Foundation for Cancer Research; When Everyone Survives Leukemia Research Foundation; and the University Cancer Research Fund. Wang is an American Cancer Society Research Scholar, a Leukemia and Lymphoma Society Scholar, and an American Society of Hematology Scholar in Basic Science.
Yu, Ma, Shen, Lui, and Jin are inventors of patent applications filed by the Icahn School of Medicine at Mount Sinai. The Jin Laboratory received research funds from Celgene Corporation, Levo Therapeutics, Cullgen, Inc., and Cullinan Oncology. Jin is a co-founder, scientific advisory board member and equity shareholder in Cullgen Inc., and is a consultant for Cullgen Inc., EpiCypher Inc. and Accent Therapeutics Inc. The remaining authors declare no competing interests.

Infections linked to medical devices such as catheters, dental implants, orthopaedics and wound dressings could be dramatically reduced using a simple technique, according to new research.
Scientists at Aston University have found a way to significantly increase the antimicrobial properties of a material used in many medical devices and clinical surfaces: bioactive glass.
The Aston University team had already developed bacteria-killing bioactive glass laced with a single metal oxide of either zinc, cobalt or copper. Their latest research combined pairs of metal oxides in the material — and found that some combinations were more than 100 times better at killing bacteria than using single oxides alone.
Bioactive glass is made from high-purity chemicals designed to induce specific biological activity, but the type currently in clinical use — often as a bone filler — does not contain antimicrobial substances. The Aston University research showed that combinations of metal oxides can improve the antimicrobial properties of bioactive glass and the researchers believe this approach could be applied to other materials for clinical use.
Many bacteria that cause infections — such as Escherichia coli and Staphylococcus aureus — are becoming increasingly resistant to antibiotics, so new ways to prevent infections are urgently needed.
Professor Richard Martin, who led the research at Aston University’s Engineering for Health Research Group, said: “Antibiotic drugs have been used in combination since the 1950s, as two antimicrobials can broaden the spectrum of coverage by aiming for different bacterial targets at the same time. Our research is the first to show that this combination approach can work with materials as well.”
Professor Martin and his colleagues Drs Tony Worthington and Farah Raja created bioactive glass laced with small amounts of cobalt, copper or zinc, and combinations of two of the three oxides. They then ground these into a powder which they sterilised, before adding it to colonies of E. coli, S. aureus and a fungus, Candida abicans. They compared the effects of the standard glass and glass with either solo metal oxides or the combinations, measuring bacterial and fungal kill rates over 24 hours.
All of the metal oxide-laced glass — both single and combined — performed better than the glass alone. Copper, combined with either cobalt or zinc, had the strongest effect on the bacteria, followed by a combination of cobalt and zinc. Both copper combinations were over one hundred times better than single oxides at killing E. coli, while copper and zinc was similarly effective against S. aureus. The cobalt and zinc combination had the strongest effect on the fungus.
Professor Martin said: “It was exciting to run our experiments and find something that is significantly better at stopping infection in its tracks and could potentially reduce the number of antibiotic treatments that are prescribed. We believe combining antimicrobial metal oxides has significant potential for numerous applications including implant materials, hospital surfaces and wound healing dressings.”
Dr Worthington added: “We have shown that co-doping surfaces with these combined antimicrobial metals, including copper, zinc and cobalt, could reduce bacterial adhesion and colonisation to surfaces or devices used in clinical practice. The use of antimicrobial metals is potentially the way forward, given discovery of new antibiotics is currently limited. We would urge manufacturers to investigate whether our new approach could be used for their biomedical materials.”
Story Source:
Materials provided by Aston University. Note: Content may be edited for style and length.

The data, released in a report Thursday, is a sign that medication abortion has become the most accessible and preferred method for terminating pregnancy.More than half of recent abortions in the United States were carried out with abortion pills, according to preliminary data released on Thursday, a sign that medication abortion has increasingly become the most accessible and preferred method for terminating pregnancy.The report, issued by the Guttmacher Institute, a research organization that supports abortion rights, found that in 2020, medication abortion — a two-pill method authorized in the United States for pregnancies up to 10 weeks’ gestation — accounted for 54 percent of all abortions. The figure represents a substantial increase from the institute’s previous report, which found that the method accounted for 39 percent of abortions in 2017.The increase in medication abortion is most likely the result of several factors. The method — which is less expensive and less invasive than surgical abortions — had already become increasingly common before the coronavirus pandemic, driven partly by restrictions from conservative states that imposed hurdles to surgical methods, especially later in pregnancy.As of 2017, according to the Guttmacher Institute, which collects data by contacting every known abortion provider in the country, nearly a third of clinics offered only medication abortion. In 2019, according to data from the Centers for Disease Control and Prevention, which did not include California, Maryland and New Hampshire, pills accounted for 42 percent of all abortions — and 54 percent of abortions that were early enough to qualify for medication because they occurred before 10 weeks’ gestation.The pandemic fueled that trend, as medical groups filed a lawsuit asking the federal government to lift the Food and Drug Administration’s requirement that the first of the two abortion pills, mifepristone, be dispensed to patients in person at a clinic or doctor’s office. Citing years of data showing that medication abortion is safe, the medical groups said that patients faced a greater risk of being infected with the coronavirus if they had to visit clinics to obtain mifepristone and pointed out that mifepristone was the only drug that the F.D.A. required patients to get in person from a medical provider but that patients were also allowed to take at home on their own without having the provider present.A judge granted the request that summer, allowing patients to see a physician by telemedicine and receive pills by mail, but, after a challenge by the Trump administration, the Supreme Court reinstated the restriction early last year.Under the Biden administration, however, the F.D.A. permanently lifted the in-person requirement in December and also said that pharmacies could begin dispensing mifepristone if they met certain qualifications. The F.D.A.’s action means that medication abortion will become more available to women who find it difficult to travel to an abortion provider or prefer the privacy of being able to terminate a pregnancy in their homes.As a result, while the new report from the Guttmacher Institute is preliminary — only reflecting information from 75 percent of the clinics and including only percentages, not raw data — the proportion of abortions carried out with pills is expected to increase further.Nearly 80 percent of all abortions in the C.D.C.’s 2019 data occurred before 10 weeks’ gestation, suggesting that there were many more women who might choose abortion pills over an in-clinic procedure if they could.At the same time, the growing interest in medication abortion has made it a focus of the highly polarized abortion debate.In 19 states, mostly in the South and the Midwest, telemedicine visits for medication abortion are banned, and so far in 2022, according to the Guttmacher Institute report, 16 state legislatures have introduced bills to ban or limit medication abortion.With the Supreme Court now considering whether to roll back abortion rights or even overturn the 1973 Roe v. Wade decision, which legalized abortion, experts and advocates on all sides expect medication abortion to play an even more pivotal role in the divisive abortion debate.

It’s one of the most polarizing questions among clinicians: Is treating obesity while also reducing weight stigma and eating disorder risk mutually exclusive?
In a recent commentary published online ahead of print in the Journal of the Academy of Nutrition and Dietetics, a team of researchers takes aim at what they say is an outdated approach many health care providers still have when it comes to treating patients with overweight or obesity.
In short, health professionals on both sides of the debate should strive to improve access to compassionate, evidence-based and patient-centered care in order to fight weight stigma and end diet culture, the researchers argue, adding that the emphasis should be on health, not weight.
“It is absolutely critical to unlink weight from diet culture,” said co-author Katherine N. Balantekin, PhD, RD, an assistant professor in the Department of Exercise and Nutrition Sciences in the University at Buffalo School of Public Health and Health Professions.
“In my opinion, this is the biggest disconnect we are currently seeing in society,” added Balantekin, who studies eating behavior in children with obesity and disordered eating. “Working together to eliminate the false dichotomy between eating and weight disorders will help ensure that everyone receives the compassionate care that they deserve. Moreover, we need to continue to work on eliminating other barriers to treatment, including weight bias and stigma.”
Weight stigma — the devaluation of a person based on their weight — is rampant, the researchers note, citing previous research findings that more than half of health care providers attribute a patient’s being overweight or obese to a lack of willpower. This kind of fat-shaming only reinforces negative stereotypes, they say.

Genetic genealogy has become a popular hobby over the past several years, thanks to direct-to-consumer (DTC) genetic testing and relative-finder services offered by some DTC genetic testing companies. In a paper published February 24 in the American Journal of Human Genetics, researchers report results from a survey that asked people who had participated in these services what effect the discovery of previously unknown relatives had on their lives.
Among the most important findings were that identifying a genetic relative appeared to be somewhat common. Additionally, those discoveries were generally experienced as neutral or positive and didn’t appear to have a big impact on participants’ lives. However, some participants learned things that could be considered significant and destabilizing — such as that their biological parent wasn’t who they thought. These participants were especially vulnerable to negative outcomes.
“Everyone on our team is involved in studying the ethical, legal, and social implications of DTC genetic testing, and we’ve been paying attention to stories in the media about individuals who’ve made surprising family discoveries from these tests and relative-matching services,” says lead author Christi Guerrini of the Center for Medical Ethics and Health Policy at Baylor College of Medicine. “We wanted to understand if these and other kinds of discoveries are common, how they’re experienced by those making the discoveries, and what people are doing as a result.”
The investigators sent the survey to about one million DTC genetic testing customers and genetic genealogy database participants; more than 26,000 responded. The final sample for analysis consisted of 23,196 completed or substantially completed surveys. Among the reasons that respondents said they chose to participate in this type of testing were to learn more about their family or build their family trees; to search for a biological parent, child, or other relative; or to investigate a suspicion that they might not be genetically related to family members.
“It seems that many — perhaps most — are just curious about their families and interested in building out their family trees, but it’s clear that quite a lot of participants are looking for someone or hoping to confirm something in particular,” Guerrini says. “It might be that they’re adopted and looking for a biological parent, or that they’ve always felt out of place in their family and want to see if there’s something to that feeling. Or they might be looking for information about a branch of their family tree that’s unknown to them, or to confirm a family story that’s been passed down over the years.”
Most respondents (82%) reported that they learned the identity of at least one genetic relative. Among this subpopulation, 10% identified a biological grandparent, 10% identified a full or half- sibling, and 7% identified a biological father. The survey asked whether the participant had chosen to contact any of their newly identified relatives and, if so, the reasons for doing so. It also asked whether their discoveries resulted in any life changes, including changes in health-related behaviors.
Guerrini says that the high number of people overall who identified an unknown genetic relative was not unexpected, because many of those relatives could be very distant ones. But she acknowledges that the high number of participants who found close relatives could be skewed by the type of people who choose to undergo relative matching in the first place. “Unfortunately, we can’t answer that question with our data, but I’m very interested in trying to do so in future research,” she says.
She adds that although these experiences appear to be interesting and enjoyable to a large number of people, it’s clear that some who are participating in these services have experienced negative outcomes. “In future research, we’d like to better understand those outcomes and what resources could be helpful in managing them,” she says.
This research was supported by the National Human Genome Research Institute of the National Institutes of Health.
Story Source:
Materials provided by Cell Press. Note: Content may be edited for style and length.

Researchers from the Babraham Institute have today published their latest work in the journal Cell Stem Cell describing a new subset of human embryonic stem cells that closely resemble the cells present at the genomic ‘wake up call’ of the 8-cell embryo stage in humans. This new stem cell model will allow researchers to map out the key genomic changes during early development, and help move towards a better understanding of the implications of genome activation errors in developmental disorders and embryo loss.
In all mammals, the early embryo undergoes a number of molecular events just after fertilisation that set the stage for the rest of development. During this key ‘wake up call’ the genome of the embryo takes over control of the cell’s activities from the maternal genome. In humans, this happens at the 8-cell stage and is called zygotic genome activation (ZGA). Before the findings of this study, investigating the details of human ZGA could only be done in human embryos; existing human stem cell models represented the embryo only at later stages of the developmental process. In the UK, experiments using embryos are permitted but highly regulated, meaning that research into early development relied in part on alternative, non-human models.
In 2012, cells representing the genome activation stage of development were found in mouse embryonic stem cells (ESCs), allowing researchers to learn more about mammalian ZGA. Almost a decade later, the Reik lab at the Institute have found a human equivalent. The lab’s discovery opens up a way to advance our knowledge of the earliest events during preimplantation development.
Dr Jasmin Taubenschmid-Stowers, lead author and Research Fellow in the Reik lab, part of the Institute’s Epigenetics research programme , commented: “Studying mouse embryonic stem cells has allowed researchers to learn about the general process of genome activation, but we could learn even more about this important step in human development thanks to our discovery of a human stem cell counterpart.”
In order to function, cells take copies of the genome in the form of an RNA code which is translated into proteins. The RNA code output is called the transcriptome and it can be used to identify different populations of cells. In this study, researchers used existing human data sets and information from mouse ESC studies to identify characteristic transcriptome marks that could be linked to genome activation. Using single cell techniques, they started the search for similar cells in their population of human ESCs.
The team found a subset of human ESCs with the right transcriptome marks to be a potential match for the 8-cell stage, when the major wave of genome activation occurs. They called these cells ‘8-cell like cells’ or 8CLCs and used the published human data to further validate and confirm that these cells shared the same molecular outputs indicative of genome activation and could be pursued as a reliable model for future studies.
To further explore the extent of the similarities between their 8CLCs and 8-cell stage in human embryos, the team worked with Professor Jennifer Nichols from the Wellcome — MRC Cambridge Stem Cell Institute. Together they were able to select and search for proteins present in both sets of cells that were indicative of ZGA. Their results showed that the ZGA-associated proteins of 8CLCs closely matched those seen in human 8-cell embryos.
As Jasmin explains: “The collaboration with Professor Nichols and her team was vital as we could identify selected proteins and really look at those in real, fixed human 8-cell stage embryo cells compared to our new stem cell counterparts. This work confirmed that our 8C-like cells matched at the protein level too, in additional to the transcriptomics data, providing validation that the 8-cell like cells matched embryo cells across multiple molecular layers.”
“Our focus is now to characterise these cells and understand their unique properties so that we can use 8-cell like cells as a tool to ask questions about the molecular changes that may cause developmental issues at this early stage.” said Professor Wolf Reik, Babraham Institute group leader.
Story Source:
Materials provided by Babraham Institute. Note: Content may be edited for style and length.

Researchers at the Francis Crick Institute have uncovered how a process involved in the regeneration of tissue damaged by radiation can aid the spread of cancer.
The spread of cancer around the body is a complex process and understanding more about how it happens is vital to the development of new treatments.
In their study, published in Nature Cancer today (Thursday), the scientists investigated the relationship between healthy tissue repair and cancer growth.
They exposed healthy mouse lungs, a site where it is common for many cancers to spread, to a high dose of radiation in order to damage the tissue. They then tested the potential of breast cancer cells to grow in the damaged area in comparison to the uninjured lungs. More cancer cells spread to the lungs and began forming secondary tumours in mice that had been injured by radiation compared to the mice who had not.
Further experiments revealed that this is due to the signalling of neutrophils, a type of immune cell, which help repair tissue damage. When the researchers blocked signalling from the neutrophils in the injured lungs, secondary tumours were greatly reduced.
Emma Nolan, first author and postdoc in the Tumour-Host Interaction Laboratory at the Crick, says: “This is a situation where tissue damage sets the stage for the spread of cancer and, in trying to repair the damaged tissue, the immune system inadvertently aids the cancer. This role of neutrophils in supporting cancer spread is something which needs further research and could potentially help to identify new ways to treat the disease.”
Ilaria Malanchi, author and group leader of the Tumour-Host Interaction Laboratory at the Crick, says: “The relationship between cancer cells, the immune system and the organ where cancer takes hold is highly complex. And it’s by untangling aspects of this web that we can better understand why cancer is able to spread, what predisposes organ to the arrival of cancer cells and ultimately how we can try to stop this.”
It is important to note that the radiation that was given to the mice in this study was a higher dose than is used for radiotherapy treatment in hospital and targeted a significantly larger proportion of the tissue. Thanks to advancing technology, the exposure to radiation is now restricted to cancerous tissue and indeed radiotherapy represents a powerful weapon to control cancer disease.
Ilaria adds: “Unrevealing the new responses of neutrophils to radiation we described here, could further enhance the efficacy of this highly-regarded treatment for cancer.”
Story Source:
Materials provided by The Francis Crick Institute. Note: Content may be edited for style and length.

A new variant of the Hendra virus has been identified by Sydney-led research as a cause of fatal illness in Australian horses, and of risk for virus spillover into humans.
A second case of the variant was confirmed by the NSW Department of Primary Industries near Newcastle in October 2021, using updated testing methods made possible by the research.
The story of its discovery serves as a case study on how ongoing disease surveillance programs are crucial to detecting emerging diseases.
Hendra virus circulates among flying foxes and is fatal to horses and humans. All flying-fox species in Australia are capable of being infected with the virus and may transmit it to humans via spillover infection of domestic animals. Flying foxes are a protected species, critical to our environment because they pollinate our native trees and spread seeds.
Flying foxes transmit the virus to horses via exposure to virus-laden fluids such as urine when horses graze near or below trees with feeding bats.
Since 1994 there have been seven human cases, four of which were fatal, and all had been exposed to horses infected with Hendra.