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New study reveals CRISPR enzyme that responds to human DNA methylation

Cancer cells excel at evading detection, but subtle chemical differences set them apart from healthy cells. Now, a team of scientists from Wageningen University & Research and Van Andel Institute has identified a way to exploit this distinction. Using a variant of CRISPR, a modern tool for editing DNA, they distinguished tumor DNA from healthy DNA and selectively cut only the former. The study, published today in Nature, is an early but promising step toward a cancer therapy that targets and destroys tumor cells with high precision.

The new method relies on methyl groups, small chemical tags attached to DNA that regulate whether genes are on or off. This process, called DNA methylation, is altered in cancer cells and can act as a molecular “fingerprint” that differentiates malignant cells from healthy ones.

Survival strategies of Rhinocladiella similis in perchlorate-rich Mars like environments

Fungi can live on mars face_with_colon_three

Dos Santos, A., Schultz, J., Souza, F.O. et al. Survival strategies of Rhinocladiella similis in perchlorate-rich Mars like environments. npj Microgravity 11, 18 (2025). https://doi.org/10.1038/s41526-025-00475-y.

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Secondary causes of diabetes: a crossroad of endocrinology and oncology

Cancer and diabetes share a bidirectional relationship, with cancer increasingly recognised as an associated factor of diabetes, both from the disease itself and its treatments. In this Review, we aim to: summarise the distinct mechanisms of dysglycaemia arising from cancer and neuroendocrine tumour treatments, including targeted therapies such as PI3K–AKT–mTOR inhibitors, antibody–drug conjugates, immune checkpoint inhibitors, corticosteroids, and somatostatin receptor ligands; examine the often overlooked aspect of the secondary cause of diabetes as an early manifestation of cancer; and highlight research gaps and encourage a collaborative care approach to manage the rising rate of dysglycaemia as a result of cancer and its evolving treatments.

The autoantigen TRIM21 assembles proinflammatory immune complexes after lytic cell death

Proinflammatory lytic cell death releases cytosolic TRIM21, which binds to circulating antibodies and is internalized by macrophages, stimulating cross-antigen presentation and inflammation in Sjögren’s disease.

Learn more in Science Immunology.

TRIM21/Ro52 assembles proinflammatory immune complexes.

De novo fast motion computation in the primate visual cortex

He et al. suggest that MT and MST neurons can generate velocity selectivity anew by integrating sequential visuotopic activations from the V1 rather than by simple inheritance, as the V1 is no longer direction selective at high speeds. This de novo velocity computation provides a parsimonious explanation for fast motion processing in the primate brain.

Mechanical Thrombectomy and Final Infarct Volume in Patients With Stroke

In Stroke due to medium or distal vessel occlusion, endovascular treatment plus best medical treatment preserved more brain tissue and was linked to improved imaging outcomes and better clinical recovery compared with medical treatment alone.

Interventions EVT plus BMT compared with BMT alone.

Main Outcomes and Measures Primary outcome was calculated as the difference in volume of tissue at risk and the final infarct volume divided by the tissue at risk (change in Vrel). We defined a Vrel of 0.8 or greater as a good imaging outcome, meaning that at least 80% of the brain tissue initially at risk was not infarcted at 24 hours. Additionally, the association between brain tissue preserved and clinical outcome at 90 days was investigated.

Results From the 447 patients (252 [56.4%] male; median [IQR] age, 77.0 [68.0–84.0] years) included in this secondary analysis, 226 received EVT plus BMT and 221 received BMT alone. Median (IQR) time of the follow-up imaging was 22.9 (19.2−25.5) hours. Median (IQR) Time to maximum less than 6 seconds (Tmax6) volume was 34.0 (20.0−50.0) mL. Median follow-up infarct volume was 7.0 (1.0−22.9) mL. The median (IQR) change in absolute volume in the EVT plus BMT group was 23.6 (5.7−38.9) mL and 14.8 (0−30.3) mL in the BMT group. Median (IQR) change in Vrel was 0.8 (0.2−1.0) in the EVT plus BMT group and 0.6 (0−0.9) in the BMT group. Odds for reaching a change in Vrel of 0.8 or greater were higher in the EVT plus BMT group compared with BMT (adjusted odds ratio [aOR], 1.6; 95% CI, 1.1−2.3) and with successful reperfusion compared with no successful reperfusion (aOR, 2.5; 95% CI, 1.3−4.8). Patients with a change in Vrel of 0.8 or greater had a better clinical outcome at 90 days.

Scientists discover skincare compound that kills drug-resistant bacteria

A popular Korean skincare ingredient may be far more powerful than anyone realized. Scientists have discovered that madecassic acid—derived from the herb Centella asiatica—can stop antibiotic-resistant bacteria in their tracks, including dangerous strains of E. coli. By targeting a bacterial protein that humans don’t have, the compound disrupts the microbes’ ability to survive, making it a promising new type of antibiotic.

Our Universe Might Be a Giant Brain, According to New Theories

There’s something quietly unsettling about placing a photograph of a human neuron next to a simulated image of the large-scale cosmic web. The two look almost identical: delicate, branching filaments connecting dense clusters, with vast open spaces in between. One fits inside your skull. The other stretches across billions of light-years. The resemblance is hard to dismiss, and for a growing number of researchers, it’s far more than a visual coincidence.

What started as a striking observation in cosmology and neuroscience has evolved into a serious theoretical question. Could the universe, at its most fundamental level, operate the way a brain does? The ideas being put forward aren’t purely philosophical. Some of them come with testable mathematics, published peer-reviewed papers, and the names of well-regarded physicists attached. What follows is an honest look at where the science currently stands.

The estimated 200 billion detectable galaxies aren’t distributed randomly, but are lumped together by gravity into clusters that form even larger clusters, which are connected to one another by “galactic filaments,” long thin threads of galaxies. This vast architecture is what scientists call the cosmic web. When you zoom far enough out, the structure of the entire observable universe begins to take on a shape that looks startlingly familiar.

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