All Posts in "News Team"

Insect vision inspires noninvasive method for deep tissue molecular mapping

The journal Advanced Materials recently published a study introducing a new method for monitoring molecular processes deep within tissue. Developed at the Technion–Israel Institute of Technology, the innovation is expected to accelerate key advancements in personalized medicine, cancer diagnosis, and early disease detection.

The research was led by Prof. Hossam Haick, postdoctoral fellow Dr. Arnab Maity, and Ph.D. student Vivian Darsa Maidantchik from the Wolfson Faculty of Chemical Engineering at the Technion. The study also involved Dr. Dalit Barkan, research assistant Dr. Keren Weidenfeld, and Prof. Sarit Larisch from the University of Haifa’s Faculty of Natural Sciences.

The Technion researchers’ method enables functional and molecular mapping of organoids—three-dimensional cell-based models that replicate the structural and functional characteristics of natural tissues. Organoids play a critical role in biomedical research by allowing scientists to study health and disease states and assess the effects of various treatments on organs and tissues.

Despite their potential, organoids face major technological challenges, particularly in monitoring internal tissue processes. Current methods are expensive and have the following significant limitations:

  • Some techniques destroy the tissue (e.g., RNA sequencing)
  • Others are blind to deep-tissue processes (e.g., confocal microscopy)

Technion’s breakthrough overcomes these limitations with a low-cost, accurate, and non-invasive approach that allows for continuous monitoring of structural and molecular changes within organoids.

Chemical tomography: New method in deep-tissue monitoring

The researchers’ new method, called chemical tomography, provides insights into tissue function by analyzing volatile organic compounds (VOCs). These molecules are present in exhaled breath, saliva, sweat, and other bodily fluids. Prof. Haick is a leading global expert in the use of VOCs for early disease detection. His prior research has led to the development of multiple diagnostic technologies based on VOC analysis.

In this study, VOC monitoring enabled the dynamic molecular and functional mapping of a human breast tissue organoid, revealing key protein and genomic data associated with the transformation of healthy breast tissue into cancerous tissue.

The system detects VOCs using a graphene-based sensor array, with the collected data analyzed through generative artificial intelligence (AI). The inspiration for this technology comes from the compound eye of insects—a structure composed of multiple small eyes that send numerous images to the insect’s brain for analysis. In the system, the graphene sensors function as the compound eye, while AI acts as the brain, processing and interpreting the data.

The new system provides real-time, dynamic mapping of organoids at a significantly lower cost than existing alternatives, without damaging the tested tissue. This method enables researchers to:

  • Track cancer progression at different stages
  • Gain a deeper understanding of cancer biology
  • Map biochemical pathways, metabolic markers, and molecular processes involved in cancer development

Using this new approach, the researchers identified six biochemical pathways responsible for producing 12 different types of VOCs, which could serve as biomarkers for disease states.

According to Prof. Haick, “Beyond cancer applications, our system has the potential to diagnose issues in various organs, including the kidneys, brain, and liver. It could also transmit real-time internal health data to an external monitoring system via an antenna, enabling continuous tracking of tissue health and early disease warnings. This is a breakthrough in integrating artificial intelligence into medicine, particularly in personalized health care.”

News Team by — March 08, 2025 By News Team in Biotechnology Daily
Scientists develop advanced forest monitoring systems: Will forests monitor themselves in the future?

KTU researchers are proposing an innovative forest regeneration model and a sound analysis system that can predict forest conditions and detect environmental changes in real time.

“Forests are among the most important ecosystems in nature, constantly evolving, yet their monitoring is often delayed,” says Rytis Maskeliūnas, a professor at Kaunas University of Technology (KTU). Climate change, pests, and human activity are transforming forests faster than we can track them—some changes become apparent only when the damage is already irreversible.

Forest management today is increasingly challenged by environmental changes that have intensified in recent years. “Forests, especially in regions like Lithuania, are highly sensitive to rising winter temperatures. A combination of factors is causing trees to weaken, making them more vulnerable to pests,” says Maskeliūnas.

According to the scientist, traditional monitoring methods such as foresters’ visual inspections or trap-based monitoring are no longer sufficient. “We will never have enough people to continuously observe what is happening in forests,” he explains.

To improve forest protection, KTU researchers have employed artificial intelligence (AI) and data analysis. These technologies enable not only real-time forest monitoring but also predictive analysis, allowing early intervention in response to environmental changes.

Spruce trees are particularly affected by climate change

One key solution is the forest regeneration dynamics model, which forecasts how forests will grow and change over time. The model tracks tree age groups and calculates probabilities for tree transitions from one age group to another by analyzing growth and mortality rates. Details of this model are published in the journal Forests.

Head of the Real time computer center (RLKSC), data analysis expert, Prof. Robertas Damaševičius, identifies core advantages of the model: it can identify which tree species are best suited to different environments and where they should be planted.

“It can assist in planning mixed forest replanting to enhance resilience against climate change, as well as predict where and when certain species might become more vulnerable to pests, enabling preventive measures. This tool supports forest conservation, biodiversity maintenance, and ecosystem services by optimizing funding allocation and compensation for forest owners,” says Maskeliūnas.

The model is based on advanced statistical methods. The Markov chain model calculates how a forest transitions from one state to another, based on current conditions and probabilistic growth and mortality rates.

“This allows us to predict how many young trees will survive or die due to diseases or pests, helping to make more informed forest management decisions,” explains KTU’s Faculty of Informatics professor.

Additionally, a multidirectional time series decomposition distinguishes long-term trends in forest growth from seasonal changes or unexpected environmental factors such as droughts or pest outbreaks. Combining these methods provides a more comprehensive view of forest ecosystems, allowing for more accurate forecasting under different environmental conditions.

The model has also been applied to assess Lithuania’s forest situation, revealing that spruce trees are particularly affected by climate change, becoming increasingly vulnerable due to longer dry periods in summer and warmer winters.

“Spruce trees, although they grow rapidly in young forests, experience higher mortality rates in later life stages. This is linked to reduced resistance to environmental stress,” says Maskeliūnas.

News Team by — March 08, 2025 By News Team in Biotechnology Daily
Transposons Hijack Telomeres to Persist in Bacterial DNA

Transposons are critical drivers of bacterial evolution that have been studied for many decades and have been the subject of Nobel Prize winning research. Now, researchers from Cornell University have uncovered mechanisms by which these mobile genetic elements integrate into the chromosomes of bacteria with linear genomes.

Their findings, published in Science in a paper titled, “Telomeric transposons are pervasive in linear bacterial genomes,“ reveal that transposons can target and insert themselves into chromosome ends, or telomeres, a strategy that influences genome stability and bacterial adaptation.

“Bacteria are like these little tinkerers,” noted Joseph Peters, PhD, professor of microbiology at Cornell University. “They’re always collecting these mobile DNA pieces, and they’re making new functions all the time—everything in antibiotic resistance is really about mobile genetic elements and almost always transposons that can move between bacteria.”

Bacterial telomeres

While most bacterial DNA is in the form of plasmids, there are some that have linear DNA that contain telomeres. Though the presence of telomeres at the ends of the linear DNA is similar to eukaryotes, the structure and maintenance of these DNA ends are unique. This study utilized two different types of bacteria, each representing a different type of telomere: hairpin-shaped telomeres or telomeres with a terminal protein.   

Cyanobacteria transposons have hairpin-shaped telomers, which, as Peters puts it, “solves the replication problem” of a double-end break, allowing the polymerase to wrap around the end of the DNA during replication. This prevents the need for telomerase to maintain the length of the telomere. 

He continued that the second telomeric transposon mechanism is found in Streptomyces, which has aided in the development of many antibiotics. Their telomeres “have an end binding protein that binds to the end, so that makes it not look like a double-strand break, and it itself is able to recruit or make its own primer and recruit a polymerase to solve the end replication problem.” 

“In each one of these cases, whether it’s a hairpin or these end binding, they have cis-acting sequences that that system recognizes,” Peters concluded. “So, it’s independent to each individual telomere.” 

Tracking transposons in telomeres

The research group focuses on how pieces of DNA move around. Their exploration of transposon movement into telomeres was realized by data mining transposon sequences in relation to telomere sequences in Genbank. Leveraging advanced sequencing technologies, the researchers identified several families of transposons in cyanobacteria and Streptomyces.  

Typically, transposons have protein-binding sequences on either end. However, the researchers found that these telomeric transposons have single-sided binding sequences and replace the bacterium’s own telomere. This effectively allows the transposon to function as the telomere, making it an essential component of the bacterial genome.  

The team is the first to document these telomeric transposons in bacteria. Peters explained that transposons are insidious, utilizing the telomeres as a safety net for the bacterium to not remove the transposon. “It’s the ultimate parasite because the cell can’t get rid of the transposon because it controls the end. If it killed the transposon, it would lose the telomere, and it would die,” he told GEN. 

Modern tech to study ancient systems 

Advancements in artificial intelligence (AI) and bioinformatics have played a key role in the team’s discoveries. Peters’ team is excited about the progress in computational tools available for researchers. “We absolutely use AlphaFold all the way,” Peters said about the AI system.  

Additional new computational tools have revolutionized genomic analyses. Peters described how his team has used programs including BLAST searches and HHpred because, compared with humans (and with other programs over time), their algorithms are “much, much better at finding matches, even when there’s almost no amino acid sequence, because somehow it’s able to predict something.” 

As technology advances, DNA synthesis accessibility has become a game-changer in the field. In the not-so-distant past, the process of creating novel sequences and inserting them into plasmids was technically and financially challenging.  

“Another huge thing that I think isn’t really said enough is this idea of DNA synthesis has really been coming down in price,” Peters explained. “Now you can go to one of these biotech companies, and you can get it made and it’s already in plasmids!”  

This, he noted, makes the process of moving from hypothesis building to experimentation much faster.  

From bacterial immunity to human health 

Beyond an advance in understanding evolution, these findings could have practical applications in biotechnology and medicine. The study uncovered a subfamily of telomere-targeting transposons that had utilized a CRISPR system. While CRISPR is typically utilized in bacteria to fight off viral attacks, this subfamily of transposons uses CRISPR to target and integrate into chromosome ends, further supporting prior research from Peters’ lab. 

“These transposons captured CRISPR-Cas systems to be able to use them as ways to identify and self-program to sites they really want to go into,” Peters told GEN. “It was this totally ingenious way that they evolved on their own.” 

As interest in harnessing transposon systems for gene-editing applications grows, researchers recognize both the promise and the challenges ahead. “It’s a good inspiration for ideas.” However, he added that it doesn’t solve all of the problems. Nor can it be put into humans to cure everything.  

He described how gene editing comes in three groups: base editing, prime editing, and large-program gene delivery. Transposons, he said, are a good inspiration for the third group: “These elements are just really ready for that.” 

Looking ahead, he hopes to apply transposon-based systems to gene editing. Peters explained that many genetic diseases have single nucleotide errors in the DNA sequence. Based on the current path to creating disease treatments, each individual genetic change through base or prime editing would require a unique set of trials. Instead, Peters emphasizes that broadening the scope of genetic replacement would be a better and more streamlined solution. “You really want to replace that exon, because then you can cure a hundred diseases at one time.”  

However, delivery systems remain a key challenge. “To really meet the potential for all these, you really need some kind of delivery [mechanism] that can allow this cargo range,” Peters noted. “I think it is safe to say that a lot of these things are aspirational, and that we are going to make a great machine that we don’t know how to deliver yet.” 

Despite these hurdles, Peters remains optimistic. “That’s still a challenge. There’s a lot of money and a lot of companies going into that. So, I think that is something that will be solved.” 

News Team by — March 08, 2025 By News Team in Bio Business News
Gut Microbe Composition During Infancy May Protect Against Diabetes in Later Life

Scientists headed by a team at the University of Utah Health have reported on research in mice suggesting that microbiome composition during infancy can shape development of pancreatic insulin-producing cells, leading to long-term changes in metabolism and impacting on diabetes risk later in life. The study, reported in Science by research co-lead June Round, PhD, professor of pathology at University of Utah Health, and colleagues, identified what the team describes as “a critical neonatal window in mice when microbiota disruption results in lifelong metabolic consequences stemming from reduced β cell development.”

Round suggests that understanding how the microbiome impacts metabolism could potentially lead to microbe-based treatments to prevent type 1 diabetes. “What I hope will eventually happen is that we’re going to identify these important microbes, and we’ll be able to give them to infants so that we can perhaps prevent this disease from happening altogether.”

In their published paper, titled “Neonatal fungi promote lifelong metabolic health through macrophage-dependent β cell development,” the team concluded that their results “… identify fungi as critical early-life commensals that promote long-term metabolic health …”

“Loss of early-life microbial diversity is correlated with diabetes, yet mechanisms by which microbes influence disease remain elusive,” the scientists explained. The body’s control of blood sugar depends on the hormone insulin, which is produced solely by pancreatic β cells, and diabetes develops when there is insufficient insulin. “Loss of insulin production or responsiveness is the basis of diabetes,” they stated.

β cell mass expands rapidly after birth, the team continued, and coincident with this postnatal β cell expansion, “… the composition of gut microbiota during the postnatal period also diversifies in phases, with each new phase dominated by distinct taxa.” Acquiring a sufficiently diverse microbiota appears to protect against childhood diabetes, the team further stated, “… however, the mechanisms involved are not known, and we cannot yet attribute specific mechanisms of disease susceptibility or protection to specific microbes.”
For their newly reported study, the team sought to test the hypothesis that mouse postnatal β cell development is linked to the presence of specific microbes during defined windows of microbial colonization. They systematically deleted and restored microbiota during certain windows of pre- and postnatal life in mice. The results identified a 10-day period before weaning when the resident microbes are required to establish normal β cell mass. “These observations were replicated using antibiotic and antifungal drugs, indicating that both bacteria and fungi promote host β cells,” the team noted in their research article summary.
The results indicated that mice exposed to broad-spectrum antibiotics in early life have worse metabolic health in the long term. If the mice received antibiotics during the 10-day window shortly after birth, they developed fewer β cells. The antibiotic-treated mice also had higher levels of blood sugar and lower levels of insulin in adulthood. “This, to me, was shocking and a bit scary,” said Round. “It showed how important the microbiota is during this very short early period of development.” 

The investigators in addition found that fecal samples from human infants, 7 to 12 months of age, stimulated mouse β cell mass, whereas samples from other age groups did not. “Mice that were colonized with samples obtained from children between 7 and 12 months of age had significantly more insulin-expressing tissue and serum insulin than did mice colonized from donors of any other age group.” This finding suggests that humans may also exhibit a window of colonization by β cell–promoting microbes, the authors suggested.

By testing in mice a variety of antibiotics that affect different types of microbes, the researchers pinpointed several specific microorganisms that increased the amount of insulin-producing tissue and the level of insulin in the blood. Intriguingly, they found one of these metabolism-boosting microbes to be a largely unstudied fungus called Candida dubliniensis, which isn’t found in healthy human adults but may be more common in infants.

The experiments showed that C. dubliniensis exposure in early life also dramatically reduced the risk of type 1 diabetes in at-risk male mice. When male mice that were genetically predisposed to develop type 1 diabetes were colonized by a metabolically “neutral” microbe in infancy, they developed the disease 90% of the time. In contrast, mice that were colonized with the C. dubliniensis fungus developed diabetes less than 15% of the time.

Exposure to C. dubliniensis could even help a damaged pancreas recover, the study results suggested. When researchers introduced the fungus to adult mice in which insulin-producing cells had been killed off, the insulin-producing cells regenerated and metabolic function improved. The researchers emphasized that this is highly unusual, as this kind of cell normally doesn’t grow during adulthood.

The C. dubliniensis fungus appears to support insulin-producing cells via its effects on the immune system. Previous research has shown that immune cells in the pancreas can promote the development of their insulin-producing neighbors. The researchers found that mice without a microbiome have fewer immune cells in the pancreas and worse metabolic function in adulthood.

When such mice were given a booster of C. dubliniensis in early life, both their pancreatic immune cells and their metabolic function were restored back to normal. The studies showed that C. dubliniensis could only promote the growth of insulin-producing cells in mice that have macrophages, showing that the fungus promotes metabolic health by affecting the immune system. “Here we identify a previously unknown microbiota-mediated mechanism to influence β cell development through macrophage seeding of the islet,” they stated, noting that the results indicated that it is increased numbers of islet macrophages, rather than their functional state, that drive β cell proliferation.

The scientists emphasized that there are probably other microbes that confer similar benefits as C. dubliniensis. The new insights could help scientists better understand how similar health cues from other microbes might function. “We don’t know a lot about how the microbiome is impacting early-life health,” said Jennifer Hill, PhD, first author on the study, who led the research as a postdoctoral scientist in the Round Lab at the U. Hill is now an assistant professor in molecular, cellular, and developmental biology at University of Colorado Boulder. “But we’re finding that these early-life signals do impact early development, and then, on top of that, have long-term consequences for metabolic health.”

The newly reported findings, the researchers suggest, could ultimately help doctors reduce the risk of type 1 diabetes—or potentially even restore lost metabolic function in adulthood—by providing specific gut microbes that help the pancreas grow and heal.

If the benefits seen in mice hold true in humans, microbe-derived molecules might eventually help restore pancreatic function in people with diabetes. Hill added, “One possibility in the far future is that maybe signals like these could be harnessed not only as a preventative but also as a therapeutic to help later in life.” However, Hill also cautions that treatments that help β cells regenerate in mice historically have not led to improvements in human health.

News Team by — March 08, 2025 By News Team in Bio Business News
Federal judge stops compounded copies of Eli Lilly weight loss, diabetes drugs

A federal judge has effectively ended the ability of compounding pharmacies to make their own copies of Eli Lilly’s weight loss and diabetes drugs Zepbound and Mounjaro.

In a sealed decision filed late Wednesday, Judge Mark Pittman of the Northern District of Texas declined to issue an injunction to stop the Food and Drug Administration (FDA) from declaring there was no longer a shortage of the medicines’ active ingredient, tirzepatide.

The lawsuit against FDA was brought in October by a trade organization representing compounding industry groups. The Outsourcing Facilities Association (OFA) alleged the agency was “abruptly depriving patients of much needed treatment and artificially raising drug prices.”

Compounders had been allowed to produce and sell hundreds of thousands of their own versions of popular anti-obesity drugs, so long as the FDA considered them in shortage.

Compounded drugs are sold at vastly lower prices than the branded versions, but drug companies and some obesity specialists have expressed concerns that some compounded products aren’t FDA-approved.

After the suit was filed, the FDA temporarily paused to reconsider the declaration to end the shortage but ultimately reaffirmed its decision in December. The agency said it would not take any enforcement action against compounders before the court ruled.

The agency at the time gave drug compounders a transition period to avoid patient care disruption. Smaller state-licensed pharmacies had until Feb. 18 and now must immediately stop producing their own copies of the drugs.

Larger outsourcing facilities, which are FDA-regulated and can create prescription-specific compounded drugs as well as bulk orders, must cease compounding, distributing or dispensing tirzepatide injections by March 19.

OFA’s lawsuit said FDA made its decision to remove tirzepatide from the shortage list based only on statements from the manufacturer, “without notice, without soliciting input from affected parties and the public, and without meaningful rationale.”

In a statement to The Hill on Thursday, OFA Chair Lee Rosebush said the group “is considering all of its options regarding the judgment, including an appeal.”

Rosebush said he couldn’t comment on specifics of the decision until the court unseals it.

Eli Lilly in a statement said the decision “marks the end of the road for mass compounding of risky, unapproved knockoffs that threaten the health and safety of Americans.”

Any company that continues mass compounding tirzepatide “is breaking the law, and we will work with regulators and law enforcement to stop it,” a company spokesperson said.

A similar OFA lawsuit against FDA for removing semaglutide, the active ingredient in Ozempic, from the shortage list is pending.

News Team by — March 07, 2025 By News Team in Trending Now
FDA blasts Edenbridge over ‘misleading’ exhibit booth panel

The FDA has sent its first untitled letter of 2025, hitting Edenbridge Pharmaceuticals with a notice after assessing an exhibit booth panel’s compliance with the rules on promoting prescription drugs.

Edenbridge, which rebranded as Dexcel Pharma in October, created the panel to communicate data on its multiple myeloma drug Hemady. The product is an oral formulation of the steroid dexamethasone. By including 20 mg of dexamethasone in each tablet, rather than the 4 mg found in some other products, the company has cut the number of pills multiple myeloma patients need to take.

The exhibit displays data on the claimed advantages of Hemady. However, the FDA, having reviewed the panel and a complaint made via the Bad Ad program, found fault with some information Edenbridge left out and the robustness of a study that underpinned some of the claims.

The panel’s omission of risk information is one focus of the FDA’s letter. The exhibit states that Hemady can cut the number of dexamethasone tablets multiple myeloma patients take by 80%. However, the panel is misleading, according to the FDA, because it presents those data but “entirely omits all risk information.” The agency said the lack of risk information creates a misleading impression about the safety of the drug.

The FDA also took aim at a retrospective, real-world comparison of adherence to Hemady and generic dexamethasone. Edenbridge presented the findings of the analysis in a table on the exhibit. The table compares the medication possession rate (MPR), a measure of adherence, and the percentage of people with an MPR of at least 80% for 4 mg dexamethasone and Hemady.

The ratio and percentage of patients with an MPR of at least 80% are higher in the Hemady cohort than in the 4-mg arm, according to Edenbridge. The company compared the cohorts, generating p-values of 0.0002 and 0.007. P-values of 0.05 and lower are typically considered statistically significant.

Yet, the FDA said the study “does not support conclusions regarding comparative adherence” to the two formulations because of design and methodology limitations. The agency listed problems with patient selection, noting that the study had failed to verify whether people on Hemady actually had been diagnosed with multiple myeloma and had included both newly diagnosed and relapsed or refractory patients in the 4 mg dexamethasone cohort, without distinguishing between the different phases of disease.

The FDA also highlighted the “notably unbalanced sample size”: The 4 mg dexamethasone arm contained 3,775 patients, but there were only 43 people in the Hemady group. The FDA said “such unbalanced sample sizes can lead to overestimation of adherence in favor of the Hemady group.”

Citing such issues, the agency said the study did not establish that adherence was better on Hemady than 4 mg dexamethasone.

The FDA sent the letter on Feb. 3 and gave Edenbridge 15 working days to respond. The agency asked Edenbridge to list all promotional communications that contain representations like those described in the letter.

The Hemady website for healthcare professionals used to display results from the adherence study, but Edenbridge removed that page some time after Dec. 3, 2024, per snapshots saved in the Internet Archive.

News Team by — March 07, 2025 By News Team in Trending Now
Woolly mice are cute and impressive—but they won’t bring back mammoths or save endangered species

US company Colossal Biosciences has announced the creation of a “woolly mouse”—a laboratory mouse with a series of genetic modifications that lead to a woolly coat. The company claims this is the first step toward “de-extincting” the woolly mammoth.

The successful genetic modification of a laboratory mouse is a testament to the progress science has made in understanding gene function, developmental biology and genome editing. But does a woolly mouse really teach us anything about the woolly mammoth?

What has been genetically modified?

Woolly mammoths were cold-adapted members of the elephant family, which disappeared from mainland Siberia at the end of the last Ice Age around 10,000 years ago. The last surviving population, on Wrangel Island in the Arctic Ocean, went extinct about 4,000 years ago.

The house mouse (Mus musculus) is a far more familiar creature, which most of us know as a kitchen pest. It is also one of the most studied organisms in biology and medical research. We know more about this laboratory mouse than perhaps any other mammal besides humans.

Colossal details its new research in a pre-print paper, which has not yet been peer-reviewed. According to the paper, the researchers disrupted the normal function of seven different genes in laboratory mice via gene editing.

Six of these genes were targeted because a large body of existing research on the mouse model had already demonstrated their roles in hair-related traits, such as coat color, texture and thickness.

The modifications in a seventh gene—FABP2—was based on evidence from the woolly mammoth genome. The gene is involved in the transport of fats in the body.

Woolly mammoths had a slightly shorter version of the gene, which the researchers believe may have contributed to its adaptation to life in cold climates. However, the “woolly mice” with the mammoth-style variant of FABP2 did not show significant differences in body mass compared to regular lab mice.

What would it mean to de-extinct a species?

This work shows the promise of targeted editing of genes of known function in mice. After further testing, this technology may have a future place in conservation efforts. But it’s a long way from holding promise for de-extinction.

Colossal Biosciences claims it is on track to produce a genetically modified “mammoth-like” elephant by 2028, but what makes a mammoth unique is more than skin-deep.

De-extinction would need to go beyond modifying an existing species to show superficial traits from an extinct relative. Many aspects of an extinct species’ biology remain unknown. A woolly coat is one thing. Recreating the entire suite of adaptations, including genetic, epigenetic and behavioral traits that allowed mammoths to thrive in ice age environments, is another.

Unlike the thylacine (or Tasmanian tiger)—another species Colossal aims to resurrect—the mammoth has a close living relative in the modern Asian elephant. The closer connections between the genomes of these two species may make mammoth de-extinction more technically feasible than that of the thylacine.

But whether or not a woolly mouse brings us any closer to that prospect, this story forces us to consider some important ethical questions. Even if we could bring back the woolly mammoth, should we? Is the motivation behind this effort conservation, or entertainment? Is it ethical to bring a species back into an environment that may no longer sustain it?

News Team by — March 07, 2025 By News Team in Biotechnology Daily
Uncovering Aspirin’s Mechanism to Reduce Cancer Metastasis in Mice

An international research team headed by scientists at the University of Cambridge has uncovered a mechanism that may underpin how aspirin could reduce the metastasis of some cancers by preventing an immunosuppressive pathway that limits T-cell immunity. Reporting in Nature on their studies, including tests in mouse models of cancer, the researchers suggest that discovering the mechanism will support ongoing clinical trials, and could lead to the targeted use of aspirin to prevent the spread of susceptible types of cancer, and to the development of more effective immunotherapies to prevent cancer metastasis.

Research lead Rahul Roychoudhuri, PhD, at the University of Cambridge, said, “Most immunotherapies are developed to treat patients with established metastatic cancer, but when cancer first spreads there’s a unique therapeutic window of opportunity when cancer cells are particularly vulnerable to immune attack. We hope that therapies that target this window of vulnerability will have tremendous scope in preventing recurrence in patients with early cancer at risk of recurrence.”

The researchers described their work in a paper titled, “Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity,” in which they say that their findings, “… reveal a novel immunosuppressive pathway that limits T-cell immunity to cancer metastasis, providing mechanistic insights into the anti-metastatic activity of aspirin and paving the way for more effective anti-metastatic immunotherapies.”

Metastasis is the spread of cancer cells from primary tumors to distant organs and is the cause of 90% of cancer deaths globally,” the authors wrote. Roychoudhuri further noted, “Despite advances in cancer treatment, many patients with early-stage cancers receive treatments, such as surgical removal of the tumor, which have the potential to be curative, but later relapse due to the eventual growth of micrometastases—cancer cells that have seeded other parts of the body but remain in a latent state.”

Studies of people with cancer have previously observed that those taking daily low-dose aspirin have a reduction in the spread of some cancers, such as breast, bowel, and prostate cancers, and this has led to ongoing clinical trials. “Meta-analyses of large randomized controlled trials have shown that daily aspirin treatment is associated with reduction in metastasis at multiple sites in individuals with cancer,” the investigators wrote. However, until now it wasn’t known exactly how aspirin could prevent metastases.
In their newly reported study, the University of Cambridge-led team acknowledged that the discovery of how aspirin reduces cancer metastasis was serendipitous. The researchers were investigating the process of metastasis, and wanted to better understand how the immune system responds to metastasis, because when individual cancer cells break away from their originating tumor and spread to another part of the body, they are particularly vulnerable to immune attack. The immune system can recognize and kill these lone cancer cells more effectively than cancer cells within larger originating tumors, which have often developed an environment that suppresses the immune system. “Metastasizing cancer cells are uniquely vulnerable to immune attack, as they are initially deprived of the immunosuppressive microenvironment found within established tumors,” they noted.
The researchers previously screened 810 genes in mice and found 15 that had an effect on cancer metastasis. In particular, they found that mice lacking a gene that produces a protein called ARHGEF1 had fewer metastases of various primary cancers to the lungs and liver.
The researchers determined that ARHGEF1 suppresses T cells that can recognize and kill metastatic cancer cells. The collective results of their experiments, they reported, “… show that ARHGEF1 functions intrinsically in T cells to limit effector functions and anti-metastatic immunity in vivo.”
To develop treatments that may take advantage of this discovery, the investigators needed to find a way for drugs to target it. “We sought to define upstream receptors and ligands that drive the immunosuppressive function of ARHGEF1 in T cells so as to reveal extracellular components of the pathway that might be amenable to therapeutic targeting,” they wrote.
The scientists traced signals in the cell to determine that ARHGEF1 is switched on when T cells are exposed to a clotting factor called thromboxane A2 (TXA2). This was an unexpected revelation for the scientists because TXA2 is already well-known and linked to how aspirin works. The findings, they commented “… suggest that ARHGEF1 has a critical role in transducing TXA2 signaling in T cells, limiting T cell activation and proliferation in response to T cell receptor (TCR) signaling.”
TXA2 is produced by platelets in the circulation that help blood to clot, preventing wounds from bleeding, but occasionally causing heart attacks and strokes. Aspirin reduces the production of TXA2, leading to the anti-clotting effects, which underlies its ability to prevent heart attacks and strokes. “The biosynthesis of TXA2 is blocked by inhibitors of COX enzymes, including aspirin,” the team explained. “Our observation that TXA2 limits T cell activation in an ARHGEF1-dependent manner in vitro led us to hypothesize that aspirin exerts an anti-metastatic effect by releasing T cells from TXA2-driven suppression mediated by ARHGEF1 in vivo.”
Their studies did then find that aspirin prevents cancers from spreading by decreasing TXA2 and releasing T cells from suppression. They used a mouse model of melanoma to show that in animals given aspirin, the frequency of metastases was reduced compared to control mice, and this was dependent on releasing T cells from suppression by TXA2.

 

Co-author Jie Yang, PhD, at the University of Cambridge, said: “It was a Eureka moment when we found TXA2 was the molecular signal that activates this suppressive effect on T cells. Before this, we had not been aware of the implication of our findings in understanding the anti-metastatic activity of aspirin. It was an entirely unexpected finding which sent us down quite a different path of inquiry than we had anticipated … Aspirin, or other drugs that could target this pathway, have the potential to be less expensive than antibody-based therapies, and therefore more accessible globally.”

In their paper, the team concluded: “This work establishes TXA2 as a regulator of T-cell immunity, with implications for cancer prevention and therapy. The identification of this pathway provides mechanistic insights into the anti-metastatic effects of aspirin, a potential basis for its more targeted use, and targets for development of new therapeutic strategies for preventing metastatic disease.”

In the future, the researchers plan to help the translation of their work into potential clinical practice by collaborating with Ruth Langley, MD, professor of oncology & clinical trials at the MRC Clinical Trials Unit at University College London, and who is leading the Add-Aspirin clinical trial, to find out if aspirin can stop or delay early stage cancers from coming back. Langley, who was not involved in the newly reported study, commented, “This is an important discovery. It will enable us to interpret the results of ongoing clinical trials and work out who is most likely to benefit from aspirin after a cancer diagnosis.”

The scientists caution that, in some people, aspirin can have serious side effects and clinical trials are underway to determine how to use it safely and effectively to prevent cancer spread, so people should consult their doctor before starting to take it. “In a small proportion of people, aspirin can cause serious side effects, including bleeding or stomach ulcers,” Langley said. “Therefore, it is important to understand which people with cancer are likely to benefit and always talk to your doctor before starting aspirin.”

News Team by — March 07, 2025 By News Team in Biotechnology Daily
Jazz to Acquire Chimerix for $935M, Expanding Rare Oncology Portfolio

Jazz Pharmaceuticals has agreed to acquire Chimerix for approximately $935 million, the companies said Wednesday, in a deal designed to bolster the buyer’s rare oncology portfolio with a treatment under FDA Priority Review and potential approval this summer for a form of glioma.

Chimerix’s lead clinical pipeline candidate is dordaviprone, a first-in-class small molecule treatment designed to selectively target the mitochondrial protease ClpP and dopamine receptor D2 (DRD2). Dordaviprone is being developed for H3 K27M-mutant diffuse glioma, a rare, high-grade brain tumor that most commonly affects children and young adults.

The FDA has set a target Prescription Drug User Fee Act (PDUFA) action date of August 18 for dordaviprone after the agency accepted the company’s New Drug Application (NDA) under Priority Review for accelerated approval.

If approved, dordaprivone would be the first FDA-approved drug for recurrent H3 K27M-mutant diffuse glioma, with the current standard of care now limited to radiation therapy.

“Adding dordaviprone to our oncology R&D pipeline will further diversify our portfolio with a medicine that addresses a significant unmet need with no other FDA-approved therapies and limited treatment options for this patient population,” Bruce Cozadd, Jazz’s co-founder, chairperson, and CEO, said in a statement.

He added that dordaviprone could also contribute durable revenue beginning in the near-term. Chimerix projected in 2001 that the drug—then known as ONC201—would generate more than $500 million in global peak sales in H3 K27M-mutant diffuse glioma, the first of several potential indications.

Chimerix revealed that projection in January 2021 when it announced it had acquired the drug and the rest of the pipeline of Oncoceutics for $78 million upfront—half in Chimerix stock, the other half in cash—plus up to $360 million in payments for ONC201 and two other programs tied to achieving development, regulatory, and sales milestones.

“We are encouraged by the dordaviprone clinical trial results to date and look forward to closing the proposed acquisition and working with our new colleagues from Chimerix to fully leverage our combined R&D and commercial expertise to deliver this novel therapy to patients, beginning as early as the second half of this year,” Cozadd added.

That could be one of Cozadd’s last major acts at the day-to-day helm of Jazz. In December, Cozadd told Jazz’s board that he intends to retire as CEO once it chooses a successor, something expected by the end of this year.

The board is undertaking a formal search process to identify a new CEO—though Cozadd would continue to serve as chairperson of the board of directors. Cozadd co-founded Jazz in 2003, serving as executive chairman until being appointed chairperson and CEO in 2009.

“Durable growth driver”

“We see this acquisition adding a durable growth driver to JAZZ’s oncology franchise,” Jessica Fye, an analyst with J.P. Morgan, wrote Wednesday in a research note. “We also see the deal as consistent with JAZZ’s recent commentary signaling BD [business development] as an area of (continued) high priority, even with the CEO transition on the horizon.”

In addition, dordaviprone is also being developed for newly diagnosed, non-recurrent H3 K27M-mutant diffuse glioma following radiation treatment, for which the treatment is under study in the ongoing Phase III ACTION trial (NCT05580562). Should dordaprivone win approval for that indication, it would potentially extend use of the drug into the front-line setting.

At $8.55 per share cash, the purchase price marks a 72% premium from Chimerix’s closing price Tuesday of $4.96. Investors reacted to news of the company’s acquisition by Jazz Pharma with a buying surge that sent Chimerix shares soaring 70% to $8.44 Wednesday in late trading as of 3:40 p.m. ET.

Shares of Chimerix have zoomed nearly 10-fold since December, when the company announced plans to seek accelerated approval for dordaviprone. Chimerix also said at the time that it intended to pursue a rare pediatric disease priority review voucher. A 2024 study has pegged the average value of a PRV at $100 million, though individual vouchers have sold for between $67.5 million and $350 million.

Jazz said it will begin an all-cash tender offer to acquire all outstanding shares of Chimerix’s common stock. Upon successful completion of the tender offer, Jazz said, it would acquire all shares not acquired in the tender through a second-step merger for the same price per share as was paid in the tender offer.

Jazz expects to fund the transaction through existing cash and investments. The company finished 2024 with $2.413 billion in cash and cash equivalents, plus $580 million in investments—nearly double the $1.6 billion in cash, cash equivalents, and investments the company reported at the end of 2023.

Both Jazz and Chimerix have approved the acquisition deal, which is expected to close in the second quarter. The deal is subject to customary closing conditions that include the tender of a majority of the outstanding shares of Chimerix’s voting common stock.

“We are excited to reach this agreement with Jazz Pharmaceuticals as they bring global scale to broaden our dordaviprone commercial strategy,” stated Mike Andriole, Chimerix’s president and CEO. “This announcement is the culmination of years of scientific work by our incredibly talented team and will deliver significant and certain value to our shareholders.”

News Team by — March 07, 2025 By News Team in Bio Business News
Solanum Pan-Genome Unveils Paralogs’ Role in Genome Engineered Crops

Advancements in genomics, next-generation sequencing, and genome editing are driving forward a new era of crop breeding. About 75% of the world’s food comes from 12 plants. However, scientists estimate up to 30,000 species are edible. One opportunity in broadening our food supply lies in exchanging genotype-to-phenotype knowledge between globally and locally cultivated crops. However, many genetic variants are species-specific. And methods of selecting for advantageous traits can produce different results in related species.

“There’s a lot of wonderful food crops out there,” said Zachary Lippman, PhD, Cold Spring Harbor Laboratory (CSHL) professor & HHMI investigator. “How many of them have not received the attention they would benefit from, compared to ‘major’ crops?”

Now, CSHL researchers and colleagues around the globe have established a pan-genome of the crop-rich genus Solanum. The team sequenced dozens of complete genomes for the plant genus that includes tomatoes, potatoes, and eggplants. The new, high-quality pan-genome was then used to map the genes behind specific traits of agricultural significance across the genus, and target those genes to create desirable mutations.

This work is published in Nature in the paper, “Solanum pan-genetics reveals paralogues as contingencies in crop engineering.”

The team’s research reveals the importance of understanding the evolution of paralog genes in predicting genome editing outcomes. How paralogs relate to physical changes across species has not been deeply studied—until now. And, in this study, the biggest breakthroughs came from the African eggplant: a tomato relative indigenous to the sub-Saharan region, African eggplant varies highly in fruit shape, color, and size.

The authors wrote, “Despite broad conservation of gene macrosynteny among chromosome-scale references for 22 species, including 13 indigenous crops, thousands of gene duplications, particularly within key domestication gene families, exhibited dynamic trajectories in sequence, expression, and function. By augmenting our pan-genome with African eggplant cultivars and applying quantitative genetics and genome editing, we dissected an intricate history of paralogue evolution affecting fruit size.”

Lippman and longtime collaborator Michael Schatz, PhD, professor of computational biology and oncology at Johns Hopkins University, turned to a breeder in Uganda to exchange ideas and expertise. Mapping tens of thousands of paralogs, the team identified a previously unknown gene in African eggplant that affects fruit size. The paralog has the same function in tomatoes. The researchers discovered they could influence tomato size by editing it.

“Reciprocal exchange between indigenous and major crops creates new, predictable paths for better breeding,” said Benoit. “This is key to boost the diversity and resilience of the food system.”

The findings, the authors suggest, demonstrate that “paralogue diversifications over short timescales are underexplored contingencies in trait evolvability. Exposing and navigating these contingencies is crucial for translating genotype-to-phenotype relationships across species.”

“Crop diversity benefits nutrition, choice, and health,” Lippman added. “Determining how related paralogs function across species could help improve crop yields, flowering times, and food selection. In other words, it’s a win-win-win for scientists, farmers, and consumers everywhere.”

News Team by — March 07, 2025 By News Team in Bio Business News
error: Content is protected !!