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Leukemia stem cells cause treatments to fail, but findings open new avenues to overcome resistance

Scientists from the German Cancer Research Center (DKFZ) and the HI-STEM Stem Cell Institute have deciphered a key mechanism that contributes to treatment failure in acute myeloid leukemia (AML). They show that there are not just one, but four different subtypes of leukemia stem cells. This diversity could explain why one of the most important AML drugs does not work sufficiently in some patients or loses its effectiveness over time—resulting in the return of leukemia.

This discovery lays an important foundation for more precise and long-term successful treatment strategies that could specifically overcome resistance mechanisms. The findings are published in the journal Cell Stem Cell.

Acute myeloid leukemia (AML) is an aggressive form of blood cancer that primarily affects older people and often has a poor prognosis despite improved therapies. In recent years, the targeted drug venetoclax has significantly improved treatment. In combination with other drugs, venetoclax often shows good therapeutic success in AML and will, at least in part, replace highly aggressive chemotherapy in the future. However, AML returns in nearly all patients—usually because individual cancer stem cells become resistant to the drug.

Magnetic checkerboard separates microparticles by size and sends them along different paths

A team of researchers from the Universities of Tübingen, Bayreuth, and Kassel, and the Polish Academy of Sciences has developed a method for precisely controlling the movement of magnetic microparticles based on their size. These suspended particles, known as colloidal particles, range in size from a few tens of nanometers to several micrometers. Controlling them is important for applications such as drug delivery, medical laboratory tests, and the synthesis of new materials. The team’s study has now been published in Physical Review Letters.

The new method involves positioning microparticles above a magnetic layer that is patterned like a chessboard. In previous studies, magnetic transportation of the colloidal particles was limited to a specific height. At this distance, although the magnetic forces appear to balance each other out, the particles move regardless of their size. Therefore, it was not possible to control the particles specifically based on their size.

Mobile qubits on a chip move us a step closer to everyday quantum computers

For years, quantum computers have lived under a huge bubble of hype, promising to revolutionize numerous fields, from medicine and battery design to materials science and cybersecurity. But realizing their potential on any serious practical level will only be possible if large numbers of qubits (the basic units of information) can interact with each other with high precision and flexibility.

One of the main things holding that back is that traditional qubits are fixed in place, meaning they can only talk to their immediate neighbors. But in a new paper published in Nature, scientists describe how they overcame this limitation by using mobile qubits that can be moved around a chip. Lars R. Schreiber at the JARA-FIT Institute for Quantum Information in Germany has also published a News & Views piece in the same journal.

AI tool unifies fragmented cell maps into spatial atlases across tissues

A new computational method could dramatically accelerate efforts to map the body’s cells in space, according to a study published in Nature Genetics. Spatial multi-omics technologies—often described as ultra-high-resolution maps of tissues—allow scientists to see not only which genes or proteins are active in a cell, but exactly where that activity occurs. That spatial context is critical for understanding complex organs such as the brain, immune tissues and developing embryos.

Unfortunately, capturing multiple molecular layers at once remains expensive and technically challenging, said David Gate, Ph.D., assistant professor in the Ken and Ruth Davee Department of Neurology’s Division of Behavioral Neurology, who was a co-author of the study.

“In practice, investigators end up with ‘mosaic’ datasets: different slices or batches that each capture only some of the layers, often from different technologies or labs, with batch effects and missing pieces,” said Gate, who also leads the Abrams Research Center on Neurogenomics.

Humanity Will Change | Pantropy

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Imagine a civilization reaches something like a Type II level, advanced enough to move through interstellar space and keep large populations alive for generations. At that stage, the challenge is developing ships that can cross the void, and also making sure the people inside them can survive radiation, isolation, and extreme travel times. That could mean heavy genetic engineering before the journey begins, changing bone density, metabolism, resistance to disease, tolerance for low gravity, or even sensory systems and respiration. But when they finally arrive, they may still find that the planet is wrong for them, maybe the air is toxic, the gravity is crushing, the temperatures are extreme, or the native chemistry is incompatible with human biology.

At that point, they face two paths. One is terraforming, which means trying to remake an entire planet into something closer to Earth. That could involve thickening or thinning an atmosphere, warming a frozen world, cooling a hot one, importing water, altering soil chemistry, introducing engineered microbes, building orbital mirrors or shades, and managing the planet for centuries or even millennia. The scale of that project is absurdly expensive, not just in money but in energy, infrastructure, labor, time, and raw materials. You are not changing a city or even a continent, you are trying to rewrite a whole world.

The other option is pantropy. Instead of forcing the planet to become Earth-like, the colonists change themselves to fit the planet. They might alter their lungs to breathe a different atmospheric mix, redesign their skin to handle harsher radiation, reduce their size for lower resource use, strengthen their bodies for higher gravity, or even become something so biologically different that they no longer look fully human. That is the core idea of pantropy, adapting the colonists to the world rather than adapting the world to the colonists.

The term was coined by James Blish, and he used it in connection with the stories collected in The Seedling Stars, especially “Surface Tension.” which was first published in 1952 in Galaxy Science Fiction.

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Hantavirus in humans: a review of clinical aspects and management

Hantavirus infections are part of the broad group of viral haemorrhagic fevers. They are also recognised as a distinct model of an emergent zoonotic infection with a global distribution. Many factors influence their epidemiology and transmission, such as climate, environment, social development, ecology of rodent hosts, and human behaviour in endemic regions. Transmission to humans occurs by exposure to infected rodents in endemic areas; however, Andes hantavirus is unique in that it can be transmitted from person to person.

FDA Approves Novel Weekly Basal Insulin for T2D

The FDA has approved once-weekly insulin icodec-abae (Awiqli; Novo Nordisk) for use in adults with type 2 diabetes (T2D), with a current projected launch in the second half of 20,261 for the 700-units/mL dose. This novel treatment option is a first-in-its-class therapeutic, freeing patients living with T2D from their strict schedule of daily basal insulin injections and reducing total injections from 7 to 1 for each 7-day period.

Its indication is as an adjunct to diet and exercise for improved glycemic control, as well as for patients also taking mealtime insulin or another common oral antidiabetic agent and/or a glucagon-like peptide-1 receptor agonist. A prescription is required, and administration is with or without food via a prefilled FlexTouch device on the same day each week.

Data from 4 of the trials in the phase 3a ONWARDS program and 2,680 adult patients with uncontrolled T2D support this approval; their primary end point of interest was reduction in hemoglobin A1c. Overall, the ONWARDS program encompasses 6 phase 3a trials and more than 4,000 adults with type 1 diabetes (T1D) or T2D.


Insulin icodec-abae (Awiqli; Novo Nordisk) is now approved for use in the US, Canada, European Union, Switzerland, and 12 other countries.

Gene Therapy Pioneers Win 2026 Breakthrough Prize

Genetic diseases impact almost 70–80 million people worldwide. Oftentimes, there are limited treatments that doctors can provide, leaving patients with few interventions to manage symptoms.

Recently, though, gene therapy has completely shifted the potential to care for many diseases. Advances in knowledge of responsible genes and nucleic acid technology have revolutionized the ability to specifically edit regions of the genome to correct mutations.

Today (April 18), the Breakthrough Prize Foundation awarded the Life Sciences prize to two teams of five researchers who pioneered gene therapies for two different types of genetic diseases. Physician scientist Jean Bennett, retinal surgeon Albert Maguire, and physician scientist Katherine High from the University of Pennsylvania developed a treatment to cure retinal blindness that is currently in use in the US, Canada, Australia, and Switzerland. Separately, clinical investigator Swee Lay Thein, now at the National Heart, Lung, and Blood Institute, tracked down the gene responsible for continued production of fetal hemoglobin in beta thalassemia and sickle cell disease and, with the help of physician scientist Stuart Orkin at Harvard University, brought this finding from the bench to the bedside.

A brain reward circuit inhibited by next-generation weight-loss drugs in mice

New research using humanized mouse models has finally pulled back the curtain on how these small-molecule drugs work in the brain, revealing that they don’t just tell the body it’s full—they actually change how we perceive “treats.”

1. The Homeostatic Circuit: This is the body’s fuel gauge. It involves the hypothalamus and hindbrain, which manage basic hunger and energy levels. It’s the circuit that tells you, “I’ve had enough calories for today.”

These new weight-loss pills do more than just settle your stomach; they speak directly to the brain’s reward center to help quiet the “food noise” that leads to overeating.

This is a “proof of concept” study. It proves the mechanism exists, but it doesn’t yet guarantee that a pill will be a side-effect-free “cure” for overeating in humans.


Humanized glucagon-like peptide 1 receptor (GLP1R) mouse models are used to investigate the neural circuitry through which small-molecule GLP1R agonists modulate feeding, with implications for how these orally delivered weight-loss drugs engage brain reward circuits.

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