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Researchers identify genetic marker that could guide brain cancer treatment

University of Kentucky Markey Cancer Center researchers have discovered a genetic biomarker that could help identify patients with glioblastoma most likely to benefit from the cancer drug bevacizumab.

The study, published in JCO Precision Oncology, found that brain tumors from patients treated with bevacizumab who lived longer were more likely to have a genetic change called CDK4 amplification. This suggests that testing for the could help oncologists identify patients most likely to respond well to bevacizumab treatment.

“The findings could help oncologists make more informed treatment decisions for , potentially sparing those unlikely to benefit from unnecessary side effects while ensuring those who might respond get access to the drug,” said John Villano, M.D., Ph.D., the study’s lead author and professor in the UK College of Medicine.

Key genes controlling brain tumor spread identified

The researchers identified three key factors involved in controlling the invasion routes. The gene ANXA1 was linked to invasion along blood vessels while HOPX and RFX4 was associated with diffuse infiltration in the brain. To evaluate the role of the genes, the researchers tested to knock them out in preclinical models, which resulted in a shift in the tumor’s invasion pattern. In several cases, the survival of the experimental animals was also prolonged.

The researchers also discovered proteins encoded by the identified genes in tissue samples from patients. In addition, they found that the presence of the ANXA1 and RFX4 correlated with poor survival. This indicates that these proteins could have a value as prognostic biomarkers.


An international research team has identified new mechanisms behind how the aggressive brain tumor glioblastoma spreads in the brain. Targeting the identified connection between the tumor invasion routes and the tumor cell states could be a potential new treatment strategy.

Glioblastoma is the most common and most lethal primary brain cancer in adults, known for its capacity to spread locally in the brain rather than forming distant metastases. The locally infiltrating cells are largely out of reach for current therapies and it is therefore crucial to determine how the spread in the brain is controlled.

In the current study, which was recently published in the journal Nature Communications, the researchers found that some tumor cells choose to grow along blood vessels in the brain whereas others spread diffusely in the brain tissue. This choice is controlled by the tumor cell states.

A new analysis of the neurocranium and mandible of the Skhūl I child: Taxonomic conclusions and cultural implications

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In a study published last week in the journal L’Anthropologie, researchers re-analyzed fragments of Skhūl I, the name for remains belonging to a likely female child between the ages of 3 and 5. While the individual is currently recognized as an anatomically modern human, Homo sapiens, its classification remains contentious, given that it has some Neanderthal-like features. Now, the new study suggests the child might have been a hybrid—and potentially had one Homo sapiens parent and one Neanderthal parent.

To reach this conclusion, the team conducted CT scans of the child’s neurocranium—the part of the skull that protects the brain—and jaw. They compared the resulting 3D models to remains of other Homo sapiens and Neanderthal children. In short, they found the neurocranium to be more similar to that of a modern human, while the jaw was more akin to a Neanderthal’s.

“The combination of features seen in Skhūl I may suggest that the child is a hybrid,” the researchers write in the study. “In the Middle Pleistocene, the Levant was the crossroad of gene flows between Indigenous lineages and other taxa from Africa and Eurasia, which is likely the explanation for Skhūl I anthropological.”

Their results align with genetic evidence indicating that modern humans and Neanderthals didn’t just cross paths—they interbred for thousands of years. In fact, some research has suggested Homo sapiens drove Neanderthals to extinction not with violence, but by absorbing them into their population through interbreeding. Regardless of the reason for Neanderthals’ demise, many humans have Neanderthal DNA today.

nouvelle analyse du neurocr ne et de la mandibule de l’enfant Skhūl I : conclusions taxonomiques et implications culturelles.


Scientists discover the receptor that helps your brain clean itself—and fight Alzheimer’s

Scientists at UCSF have uncovered how certain immune cells in the brain, called microglia, can effectively digest toxic amyloid beta plaques that cause Alzheimer’s. They identified a key receptor, ADGRG1, that enables this protective action. When microglia lack this receptor, plaque builds up quickly, causing memory loss and brain damage. But when the receptor is present, it seems to help keep Alzheimer's symptoms mild. Since ADGRG1 belongs to a drug-friendly family of receptors, this opens the door to future therapies that could enhance brain immunity and protect against Alzheimer’s in more people.

Next-Generation Proteomics of Brain Extracellular Vesicles in Schizophrenia Provide New Clues on the Altered Molecular Connectome

Extracellular vesicles (EVs) are tiny membranous structures that mediate intercellular communication. The role(s) of these vesicles have been widely investigated in the context of neurological diseases; however, their potential implications in the neuropathology subjacent to human psychiatric disorders remain mostly unknown. Here, by using next-generation discovery-driven proteomics, we investigate the potential role(s) of brain EVs (bEVs) in schizophrenia (SZ) by analyzing these vesicles from the three post-mortem anatomical brain regions: the prefrontal cortex (PFC), hippocampus (HC), and caudate (CAU). The results obtained indicate that bEVs from SZ-affected brains contain region-specific proteins that are associated with abnormal GABAergic and glutamatergic transmission.

Injured once, triggered forever? How the brain rewrites stress responses

A wound can leave a lasting imprint—even after it has healed. A new study in Current Biology finds that past injuries can quietly prime the body to overreact and be more sensitive to stress, pain and fear long after the damage is gone.

These findings may help explain how early injuries or trauma can set the stage for , where the remains hypersensitive long after the initial damage has healed. can set the stage for conditions, where the nervous system remains hypersensitive long after the initial damage has healed.

Researchers at the University of Toronto Mississauga discovered that mice with a history of responded more intensely to the scent of a predator, an extremely stressful event for mice. These mice showed exaggerated and developed long-lasting pain in both hind paws, including the uninjured side. Strikingly, the symptoms lasted more than six months, long after the original injury had physically healed.