UK health officials say no one factor linking all the cases has been identified so far.
Monkeypox outbreak mostly in young men in London
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Scientists Find World’s Largest Plant In Australia And It’s 4,500 Years Old
Researchers have made a startling discovery beneath the waters off Western Australia. A meadow of sea grass stretching more than 110 miles long was actually a single plant that had spent the past 4,500 years cloning itself to carpet an area three times larger than Manhattan.
The findings, published Wednesday in the Proceedings of the Royal Society B, make the colony of Posidonia australis, or ribbon weed, the largest known plant on Earth, scientists said.
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Elizabeth Sinclair, a senior research fellow at the University of Western Australia and a lead author of the study, said her team has been testing seagrass meadows around Australia for genetic diversity for years to see how they respond to climate change. When her team visited an area known as Shark Bay, a relatively pristine landscape untouched by development, they went beneath the waves to collect samples of seagrass to see what types of plants were growing across the ocean floor.
The answer was one.
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“It’s quite bizarre when you think about it, there’s this plant in one end of the bay and then you move 100 kilometres down to the other end and it’s the same plant,” Sinclair said.
Rachel Austin/University of Western Australia
Her team hypothesised that thousands of years ago, a single seagrass seedling landed in the bay. It was particularly suited to survive in different oceanic environments due to its unusual genome.
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Most comparable plant offspring contain 50% of each parent’s genes. But Posidonia australis has 100% from each parent, making it a polyploid, meaning it has double the usual number of chromosomes.
“Polyploid plants often reside in places with extreme environmental conditions, are often sterile, but can continue to grow if left undisturbed, and this giant seagrass has done just that,” Sinclair said in a statement. “Even without successful flowering and seed production, it appears to be really resilient, experiencing a wide range of temperatures and salinities plus extreme high light conditions, which together would typically be highly stressful for most plants.”
The ribbon weed has slowly grown through a series of runners — like a normal turf lawn — to stretch nearly 80 square miles. The researchers estimate its age at about 4,500 years, based on the species’ size and growth rate.
Like other delicate oceanic structures, namely corals, seagrass meadows are susceptible to climate change. A severe heat wave in 2010 and 2011 sparked widespread damage to the Shark Bay meadows, killing about a third of the seagrasses. Underwater meadows are also home to many different species and serve a key role in an area’s biodiversity.
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Angela Rossen // University of Western Australia
“You lose a plant that creates this whole environment and you lose all the biodiversity that goes with it,” Sinclair said, adding that the 2010-2011 event had calamitous effects. “The turtles were going hungry, the dolphins weren’t getting enough fish, the whole network is connected.”
Although the ribbon weed has already begun to recover and spread since that event, Sinclair cautioned that climate change still poses a threat to region.
She also noted that it was “scary” how researchers had only just discovered the remarkable colony hiding beneath the waves, noting climate change could rip such species away before humans had a chance to discover them.
“It’s scary because we might lose it before we find out about it,” Sinclair said. “It might be gone before we even know.”
Star Wars Defends Moses Ingram Against Racist Attacks From Obi-Wan Kenobi Viewers
After Obi-Wan Kenobi actor Moses Ingram revealed on social media the onslaught of racist harassment she’s received since the Disney+ series premiered last week, the Star Wars franchise stepped up Monday to show support for Ingram.
Moses plays Reva Sevander, also known as the Third Sister, who is hunting Obi-Wan Kenobi for Darth Vader in the new series.
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The Emmy-nominated actor shared on her Instagram the hateful messages fired at her from fans of the series, including atrocious messages using the N-word and claims that she’s part of the show only as a “diversity hire.”
“There’s nothing anybody can do about this. There’s nothing anybody can do to stop this hate,” Ingram said in a video posted to her Instagram story. “I question my purposes in even being here in front of you saying that this is happening. I don’t really know.”
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She spoke on the pain of being targeted by racist harassment and thanked supporters who have stuck by her: “The thing that bothers me is this feeling inside of myself, that no one has told me, but this feeling that I have to shut up and take it, that I have to grin and bear it. And I’m not built like that. So, I wanted to come on and say thank you to the people who show up for me in the comments and the places that I’m not going to put myself. And to the rest of y’all, y’all weird.”
The official social media accounts for Star Wars issued a statement late on Monday backing Moses against the abominable online attacks.
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“We are proud to welcome Moses Ingram to the Star Wars family and excited for Reva’s story to unfold. If anyone intends to make her feel in any way unwelcome, we have only one thing to say: we resist,” the statement said.
“There are more than 20 million sentient species in the Star Wars galaxy, don’t choose to be a racist,” the message concluded.
Other actors of colour in the franchise, including Kelly Marie Train and John Boyega, also experienced toxic and racist backlash from fans when they joined the cast.
Before Obi-Wan aired on Disney+, the Baltimore actor told The Independent that executives on the show cautioned her that racist “Star Wars” trolls could be on the horizon.
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“It was something that Lucasfilm actually got in front of and said, ‘This is a thing that, unfortunately, likely will happen. But we are here to help you; you can let us know when it happens,’” Moses said at the time.
She added: “‘Obi-Wan’ is going to bring the most diversity I think we’ve ever seen in the galaxy before. To me, it’s long overdue. If you’ve got talking droids and aliens but no people of color, it doesn’t make any sense. It’s 2022, you know. So we’re just at the beginning of that change. But I think to start that change is better than never having started it.”
Star Trek: Strange New Worlds actor Anson Mount also headed to social media on Tuesday to share his support for Ingram.
“This is Moses Ingram. She is a singular talent and a recent addition to the @starwars universe. She has also been targeted by racists pretending to be fans because her mere existence threatens a skewed, dystopian fantasy that selectively omits the likes of @therealbillydee and others. We, the Trek Family, have her back,” he wrote.
New episodes of Obi-Wan Kenobi stream on Wednesdays on Disney+.
Tory Elections Guru Lord Hayward Predicts Boris Johnson Will Face Confidence Vote
To mount a leadership challenge, 54 have to submit a letter to Sir Graham Brady who leads the 1922 committee of backbench Conservative MPs.
Only Brady knows how many have submitted letters and he keeps it a secret until the threshold is reached.
Analysis by Sky News shows 41 MPs have publicly questioned Johnson’s position, while 28 have confirmed they have sent in letters.
Hayward said it was striking that a lot of the MPs who have admitted submitting letters recently had experienced local elections in their constituencies, adding: “They have spent more time asking people for support on behalf of their councillors, their candidates, than other people.
“In the local elections, the Tories did reasonably in being a party of government against the Labour Party in the Midlands of the North.
“But they did far worse than expected in parts of London and in the southeast in the middle class, the what’s described as the gravel drive, Waitrose shopping areas.
“And that has clearly unsettled MPs who had, with their associations, to go out and campaign and what we’re seeing now is that feeding off the losses of May 5.”
Asked if Johnson would lose a confidence vote, Hayward replied: “That is very difficult to say. I think if it were held today, no he wouldn’t.
“But there are these series of hurdles – we’ve got Lord Geidt’s comments yesterday, which have come completely out of the blue nobody was expecting this to have happened and therefore the reset is not proving to be the calming experience that most people at No.10 and within the organisation behind Boris would actually have wanted it to.
“So there is the prospect, but it’s worth remembering Theresa May won a vote of confidence, in theory that gave her another year, but she was out of office within seven months.”
He said a vote of confidence, even if you win, is not a guarantee that you will continue as the party leader because losing support is an “attritional process”.
In order to oust him, 180 MPs would have to vote against Johnson in the confidence vote.
If it gets to that stage, the odds are in the PM’s favour with around 140 MPs on the “payroll” alone including ministers and aides.
Shanghai lockdown: China eases Covid restrictions after two months
China’s biggest city, a vital global trade hub, begins to relax crippling Covid restrictions.
Violent incidents at GP surgeries double in five years
A senior GP warns that the steep rise is likely to have a “significant impact” on doctors and staff.
Spaceflight: Microgravity analog culture profoundly affects microbial infection process in 3-D human tissue models
Infectious microbes have evolved sophisticated means to invade host cells, outwit the body’s defenses and cause disease. While researchers have tried to puzzle out the complicated interactions between microorganisms and the host cells they infect, one facet of the disease process has often been overlooked — the physical forces that impact host-pathogen interactions and disease outcomes.
In a new study, corresponding authors Cheryl Nickerson, Jennifer Barrila and their colleagues demonstrate that under low fluid shear force conditions that simulate those found in microgravity culture during spaceflight, the foodborne pathogen Salmonella infects 3-D models of human intestinal tissue at much higher levels, and induces unique alterations in gene expression.
This study advances previous work by the same team showing that physical forces of fluid shear acting on both the pathogen and host can transform the landscape of infection.
Understanding this subtle interplay of host and pathogen during infection is critical to ensuring astronaut health, particularly on extended space missions. Such research also sheds new light on the still largely mysterious processes of infection on earth, as low fluid shear forces are also found in certain tissues in our bodies that pathogens infect, including the intestinal tract.
While the team has extensively characterized the interaction between conventionally grown shake flask cultures of Salmonella Typhimurium and 3-D intestinal models, this study marks the first time that S. Typhimurium has been grown under the low fluid shear conditions of simulated microgravity and then used to infect a 3-D model of human intestinal epithelium co-cultured with macrophage immune cells, key cell types targeted by Salmonella during infection.
The 3-D co-culture intestinal model used in this study more faithfully replicates the structure and behavior of the same tissue within the human body and is more predictive of responses to infection, as compared with conventional laboratory cell cultures.
Results showed dramatic changes in gene expression of 3-D intestinal cells following infection with both wild-type and mutant S. Typhimurium strains grown under simulated microgravity conditions. Many of these changes occurred in genes known to be intimately involved with S. Typhimurium’s prodigious ability to invade and colonize host cells and escape surveillance and destruction by the host’s immune system.
“A major challenge limiting human exploration of space is the lack of a comprehensive understanding of the impact of space travel on crew health,” Nickerson says. “This challenge will negatively impact both deep space exploration by professional astronauts, as well as civilians participating in the rapidly expanding commercial space market in low Earth orbit. Since microbes accompany humans wherever they travel and are essential for controlling the balance between health and disease, understanding the relationship between spaceflight, immune cell function, and microorganisms will be essential to understand infectious disease risk for humans.”
Nickerson, who co-directed the new study with Jennifer Barrila, is a researcher in the Biodesign Center for Fundamental and Applied Microbiomics and is also a professor with ASU’s School of Life Sciences. The research appears in the current issue of the journal Frontiers in Cellular and Infection Microbiology
Life-altering force
Life on earth has diversified into an almost incomprehensibly vast array of forms, evolving under wildly dissimilar environmental conditions. Yet one parameter has remained constant. Throughout the 3.7-billion-year history of life on earth, all living organisms evolved under, and respond to, the pull of Earth’s gravity.
For more than 20 years, Nickerson has been a pioneer in exploring the effects of the reduced microgravity environment of spaceflight on a range of pathogenic microbes and the impact on interactions with human cells and animals they infect. She and her colleagues have doggedly pursued this research in both land-based and spaceflight settings, the results of which helped lay the foundation for the rapidly growing research field, mechanobiology of infectious disease, the study of how physical forces impact infection and disease outcomes.
Among their important findings is that the low fluid shear conditions associated with the reduced gravity environment of spaceflight and spaceflight analog culture are similar to those encountered by pathogens inside the infected host, and that these conditions can induce unique changes in the ability of pathogenic microbes like Salmonella to aggressively infect host cells and exacerbate disease, a property known as virulence.
The infectious agent explored in the new study, Salmonella Typhimurium, is a bacterial pathogen responsible for gastrointestinal disease in humans and animals. Salmonella is the leading cause of death from food-borne illness in the United States. According to the CDC, Salmonella bacteria cause about 1.35 million infections, 26,500 hospitalizations, and 420 deaths in the United States each year. Foods contaminated by the bacteria are the primary source for most of these illnesses.
Salmonella infection typically causes diarrhea, fever, and stomach cramps, beginning 6 hours to 6 days after infection. Illness from the disease usually lasts 4 to 7 days. In severe cases, hospitalization may be required.
‘Shear’ probability?
Cells in mammalian organisms, including humans, as well as the bacterial cells that infect them, are exposed to extracellular fluid flowing over their outer surfaces. Just as a gentle downstream current will affect the pebbles in the underlying streambed differently than a raging torrent, so the force of fluid gliding over cell surfaces can cause changes to affected cells. This liquid abrasion of cell surfaces is known as fluid shear.
Since spaceflight experiments are rare and access to the space research platform is currently limited, researchers often simulate the low fluid shear conditions that microbes encounter during culture in spaceflight by growing cells in liquid growth media within a device known as a rotating wall vessel bioreactor or RWV. As the cylindrical reactor rotates, cells are maintained in suspension, gently and continuously tumbling in their surrounding culture medium. This process mimics the low fluid shear conditions of microgravity that cells experience during culture in spaceflight.
The team has also shown that this fluid shear level is relevant to conditions that microbial cells encounter in the human intestine and other tissues during infection, triggering changes in gene expression that can help some pathogens better colonize host cells and evade the immune system’s efforts to destroy them.
Portrait of an intruder
The study found significant changes in both gene expression and ability to infect 3-D intestinal models by Salmonella bacteria cultured in the RWV bioreactor. These experiments involved two S. Typhimurium strains, one unaltered or wild type strain and one mutant strain.
The mutant strain was otherwise identical to the wild type but lacked an important protein known as Hfq, a major stress response regulator in Salmonella. In earlier research, Nickerson and her team discovered that Hfq acts as a master regulator of Salmonella’s infection process in both spaceflight and spaceflight analog culture. They later discovered additional pathogens that also use Hfq to regulate their responses to these same conditions.
Unexpectedly, in the current study, the hfq mutant strain was still able to attach, invade into, and survive within 3-D tissue models at levels comparable to the wild type strain. In agreement with this finding, many genes responsible for Salmonella’s ability to colonize human cells, including those associated with cell adherence, motility, and invasion were still activated in the mutant strain under simulated microgravity conditions, despite the removal of Hfq.
From the host perspective, the 3-D intestinal co-culture model responded to Salmonella infection by upregulating genes involved in inflammation, tissue remodeling, and wound healing at higher levels when the bacteria were grown under simulated microgravity conditions prior to use in infection studies. This was observed for both wild type and hfq mutant strains of the pathogen.
Data from this new spaceflight analog study reinforces previous findings from the team’s 2006, 2008 and 2010 Space Shuttle experiments. In particular, the 2010 flight experiment conducted aboard Space Shuttle Discovery, called STL-IMMUNE, used the same wild type strain of S. Typhimurium to infect a 3-D model of human intestinal tissue made from the same epithelial cells used in the new study.
Several commonalities were observed between host cell responses to infection in the new spaceflight analog study and those previously reported when infections took place in true spaceflight during the STL-IMMUNE experiment. These results further reinforce the RWV as a predictive ground-based spaceflight analogue culture system that mimics key aspects of microbial responses to true spaceflight culture.
“During STL-IMMUNE, we discovered that infection of a human 3-D intestinal epithelial model by Salmonella during spaceflight induced key transcriptional and proteomic biosignatures that were consistent with enhanced infection by the pathogen,” Barrila says. “However, due to the technical challenges of performing in-flight infections, we could not quantify whether the bacteria were actually attaching and invading into the tissue at higher levels. The use of the RWV bioreactor as a spaceflight analog culture system in our current study has been a powerful tool which allowed us to explore this experimental question at a deeper level.”
New horizons
Astronauts face a double risk from infectious disease during their missions far from earth. The combined rigors of spaceflight act to weaken their immune systems. At the same time, some pathogens like Salmonella may be triggered by low fluid shear conditions induced by microgravity to become more effective infectious agents.
With longer spaceflight missions in the advanced planning stages and the advent of civilian space travel rapidly emerging, safeguarding space travelers from infectious disease is vital.
Studies like the current one are also helping to pull back the curtain on the infection process, revealing foundational details with broad relevance for the battle against diseases, on Earth and beyond.
Immune recognition of self and non-self explored in new study
Unless you are an identical twin, you probably aren’t often mistaken for someone else. Likewise, our own sense of self as distinct from all other humans is deeply ingrained since early childhood.
The immune system, however, faces far greater challenges in distinguishing self from non-self. Should this complex surveillance network fail to identify a foreign intruder, like a bacterium or virus, the result may be serious, unchecked disease.
Under certain circumstances, however, the immune system can become over-vigilant, identifying our own tissues as foreign and targeting them for destruction, resulting in autoimmune disease. Autoimmune responses are also associated with some cancers.
In a new study, Arizona State University researcher Joshua LaBaer and his colleagues explore components of the immune system known as autoantibodies. While they have been implicated as central players in a range of serious autoimmune diseases, the study observes that autoantibodies are also found in healthy individuals.
This fact may make the diagnostic use of autoantibodies as sentinels of autoimmune disease more challenging, hence the importance of such investigations.
An improved awareness of the pervasiveness and role of autoantibodies in human health and disease may ultimately help in the design of better diagnostics and therapeutics against a range of illnesses.
“Historically, we looked for autoantibodies present only in disease, but we’ve always been intrigued because our healthy controls always had autoantibodies too,” LaBaer says. “So, we decided to see if any of these “healthy autoantibodies” were common in healthy people and sure enough many of them were. Knowing about these will help us avoid confusion in future studies.”
Dr. LaBaer is the executive director of ASU’s Biodesign Institute as well as the director of the Biodesign Virginia G. Piper Center for Personalized Diagnostics.
The research findings appear in the current issue of the journal Cell Reports.
Biological civil war
Autoimmune diseases are a widespread phenomenon, affecting roughly 23 million Americans. Researchers have identified more than 80 autoimmune diseases, including both common ailments like type 1 diabetes, lupus, multiple sclerosis and rheumatoid arthritis, as well as more obscure ailments, which often prove challenging to properly diagnose. Nearly 80% of autoimmune diseases occur in women, for reasons researchers are still trying to puzzle out.
Science has much to learn about the underlying mechanisms responsible for autoimmune reactions. Often such illnesses arise following infections. Two primary components of the so-called adaptive immune system also play important roles in autoimmunity. These are the are white blood cells or lymphocytes, known as T cells and B cells. Lymphocytes are crucial for maintaining health and are essential to survival. These sentries, ceaselessly patrolling the bloodstream, are alerted by the presence of foreign entities known as antigens.
T cells guard against infection from pathogens like bacteria, viruses and fungi. They can also attack and destroy cancerous cells. B cells secrete proteins known as antibodies that either disrupt interactions or target infected cells so that other cells can come in to destroy them. Antibodies operate by binding with pathogens or foreign substances, including toxins, and neutralizing their harmful effects. If an antibody binds with a virus, for example, it may prevent the intruder from entering a normal cell to cause infection. B cells can also recruit other specialized immune cells to migrate to the sites of infected cells and help destroy them.
The immune system’s defensive arsenal is exquisitely sensitive to foreign proteins, peptides, enzyme complexes, RNA and DNA. When these are encountered, B cells can swing into action, producing antibodies directed against these foreign entities.
Mutinous immunity
The immune system, however, faces a formidable challenge. B and T cells must be able to accurately target threats to the body while remaining harmless to host cells and tissues. Immune cells are not born with this knowledge, they learn it over a matter of weeks, receiving training in a kind of biological classroom, where they undergo two rounds of careful screening.
The B and T cells that successfully graduate from their training sessions exhibit two kinds of immune tolerance, central immune tolerance, which develops in the bone marrow and peripheral immune tolerance, which matures in the lymph nodes.
After their training, cells displaying immune tolerance, a kind of non-aggression pact with healthy tissues — are preserved in the body for future use. Immune cells that flunk out of their training and present a risk of autoimmunity are sequestered or destroyed.
Yet sometimes, pathogens or cancers can produce antigens that bear such a close resemblance in terms of sequence or structure to features found in normal tissues in the body that the host tissues are mistaken for disease antigens and targeted by antibodies. Such features are known as self-antigens and the antibodies produced to target them are known as autoantibodies.
The mistaken targeting of self-antigens due to their similarities with disease antigens is known as molecular mimicry and is implicated in many autoimmune disorders, from rheumatoid arthritis to multiple sclerosis.
Scavenger hunt for antibodies
The new study explores common autoantibodies — those occurring in healthy individuals. Though these common autoantibodies don’t appear to cause disease, they nevertheless appear in as many as 40% of the people tested. It is likely that at least some of these common autoantibodies have been mistakenly identified as disease antibodies.
The researchers performed a meta-analysis of 9 datasets. The tool of choice for exploring the common autoantibodies is a device known as a protein microarray. Here, thousands of individual proteins are affixed to a glass slide. When a sample of blood is spread over the microarray, antibodies, (in this case, autoantibodies) bind with specific protein antigens.
The microarrays were subjected to two rounds of screening. In the first round, 182 blood samples from healthy individuals were screened against 7,653 human proteins. In the second round, 90 blood samples were screened against 1,666 human proteins. The experiments identified a total of 77 common autoantibodies.
The blood samples came from healthy individuals of both sexes, ranging in age from infancy to 84 years old. The results showed that the number of autoantibodies increased from birth up to the age of adolescence and then plateaued. Further, the number of autoantibodies detected was the same regardless of sex, a surprising outcome given the large disparity between men and women in the prevalence of autoimmune disease.
Another underlying enigma is why common autoantibodies fail to produce autoimmune disease. Although such antibodies appear to have evaded the screening process leading to immune tolerance, their occurrence in the body remains benign. It is believed that autoimmune pathology requires autoantibodies to bind and form complexes with autoantigens, and this may be blocked in the case of common autoantibodies.
Future research promises to unlock many more secrets concerning the nature of autoantibodies. The current study examined less than half of all human proteins. Most likely, additional common autoantibodies remain to be uncovered.
Women can safely have fewer smears thanks to HPV test
Cervical screening is changing, but fewer checks will not mean more cancers missed, a study confirms.
Investigational drug attacks synovial sarcoma, a rare type of tumor
Researchers at Washington University School of Medicine in St. Louis have developed a way to attack synovial sarcoma — a rare tumor of soft tissues, such as ligaments and muscles — using an investigational drug that triggers cell death. The drug was developed by Washington University researchers who are planning a phase 1 clinical trial to investigate its safety and effectiveness in patients who have synovial sarcoma that has spread beyond the original tumor site.
The study is available online in the journal Clinical Cancer Research.
Synovial sarcoma is rare, with 900 to 1,000 new cases diagnosed annually, and is most typically diagnosed during adolescence and into young and middle adulthood. Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine is a major center for the treatment of sarcomas nationwide, as is Siteman Kids at St. Louis Children’s Hospital.
“Synovial sarcoma is responsible for about 10% of all sarcomas, and because sarcoma in general is rare, a lot of these patients — pediatric and adult — travel from all over the country to receive treatment at our specialized Sarcoma Center,” said oncologist Brian A. Van Tine, MD, PhD, a professor of medicine. “If it’s diagnosed early, this cancer can be cured with standard care — surgery, radiation and chemotherapy. But once it spreads, we have no effective curative therapies, so we’re looking for new treatment strategies that take advantage of the genetic quirks of this rare tumor.”
The researchers found that synovial sarcoma is missing an important protein that most tumors rely on to drive their energy metabolism. The absence of this key protein — called malic enzyme 1 (ME1) — forces synovial sarcoma tumors to rely on a different metabolic pathway, which makes it uniquely vulnerable to the inhibition of that alternate pathway. The investigational drug ACXT-3102 interferes with this alternate route. The interference causes volatile waste compounds called reactive oxygen species to build up inside the cancer cells. When enough reactive oxygen species build up inside, the cell dies.
“Because they’re missing ME1, these tumor cells are already crippled in their ability to fight damage from reactive oxygen species,” said Van Tine, who leads the sarcoma program at Siteman. “So, we asked if we could use this broken defense against this cancer. When levels of these compounds skyrocket inside the cells, they die very quickly.”
The drug ACXT-3102 was developed by William G. Hawkins, MD, the Neidorff Family and Robert C. Packman Professor of Surgery, and his team, to treat pancreatic cancer. Because most pancreatic cancers still have ME1, researchers will need to find a second way to attack that tumor type. But because the metabolism of synovial sarcoma is unusual and consistent across patients — the cancer’s defining genetic mistake is present in 90% to 95% of all cases — the researchers suspect that this rare tumor could be treatable with ACXT-3102 alone.
“Synovial sarcoma is caused by a very specific genetic mutation, so it’s a relatively clean cancer, meaning it has a single specific genetic mistake that can be exploited, unlike other cancers that have a complex accumulation of many mutations whose effects are difficult to unravel,” Van Tine said. “Because of this single mutation, it’s harder for synovial sarcoma cells to adapt to an attack on their energy metabolism. Finding a weakness in cancer that we can exploit based on the biology of a rare tumor is really exciting.”
The drug ACXT-3102 was licensed to a Washington University startup company called Accuronix Therapeutics that was co-founded by Hawkins to develop new cancer therapies.
Story Source:
Materials provided by Washington University School of Medicine. Original written by Julia Evangelou Strait. Note: Content may be edited for style and length.
