Explore the role of genetic instability in cancer, its impact on progression, and emerging treatment strategies targeting these mechanisms.

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 molecular marker could help oncologists identify patients most likely to respond well to bevacizumab treatment.

“The findings could help oncologists make more informed treatment decisions for glioblastoma patients, 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.

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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.

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This is a sci-fi documentary looking at the future of genetic engineering and how it applies to space exploration, astronauts, terraforming planets and even Earth.

What is DNA, and how can it be engineered. What is CRISPR, and the future technology used in genetic engineering and biotechnology.

Personal inspiration in creating this video came from: Jurassic Park (the book), and The Expanse TV show (the protomolecule).

Other topics in the video include: how genetic engineering can change food allergies, cryosleep astronauts using hibernation biology borrowed from bears, squirrels and hedgehogs, engineering plants for terraforming other planets, and entries from The Encyclopedia of the Future.

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Researchers from Columbia Engineering have established a framework for the design of bioactive injectable hydrogels formulated with extracellular vesicles (EVs) for tissue engineering and regenerative medicine applications.

Published in Matter, Santiago Correa, assistant professor of biomedical engineering at Columbia Engineering, and his collaborators describe an injectable hydrogel platform that uses EVs from milk to address longstanding barriers in the development of biomaterials for regenerative medicine.

EVs are particles naturally secreted by cells and carry hundreds of biological signals, like proteins and genetic material, enabling sophisticated cellular communication that synthetic materials cannot easily replicate.

For a few individuals, scientists found genetic material from cancerous tumors in blood samples taken years before they were diagnosed through traditional methods

The researchers developed what is called an “ageing clock”, a computational tool designed to measure the biological age of cells, as opposed to their chronological age. Indeed, the organs and tissues of people of the same age can evolve differently over time depending on genetic and environmental factors, leading to different biological ages. These clocks are therefore useful tools to assess ageing at the molecular level and can help in understanding its causes and consequences.

The clock designed by the LCSB and CIC bioGune researchers is specific to the brain and uses gene expression information from 365 genes to make predictions. Using a machine learning approach, it was trained on data from healthy individuals, aged from 20 to 97, and could accurately predict their age. Further tests showed that the clock is able to estimate the biological age of different cell types in the brain, especially neurons. Lastly, by looking at the predicted biological ages for healthy individuals and for patients with neurological conditions, the researchers observed that patients exhibited a higher biological age.

“Our results tell us that the biological age of the brain cells calculated by our clock reflects the decline in brain function experienced by the patients, especially between 60 and 70, and is even correlated with the degree of neurodegeneration,” explains Dr Guillem Santamaria, first author of the study. “It supports the view of neurodegeneration as a form of accelerated ageing but, more importantly, the positive association between neurodegeneration and biological age suggests that the rejuvenating interventions identified by the clock could serve as neuroprotective agents.”

The aim of the researchers was to use the clock to find genetic or chemical interventions that would significantly shift back the biological age of brain cells. They explored the effect of thousands of compounds on neural progenitor cells and neurons and identified 453 unique rejuvenating interventions.

Among the identified compounds that have the potential to reverse the biological age of the two types of brain cells, several are known to extend lifespan in animal models and some are already used to treat neurological disorders, but the vast majority has not yet been studied in the context of health-or lifespan extension. “On the one hand, the fact that our computational platform identified drugs that have a known effect on brain function supports the idea that using the predicted effect of a compound on the biological age is an efficient way to evaluate its neuroprotective potential,” details Prof. Antonio Del Sol, head of the Computational Biology groups at the LCSB and CIC BioGUNE. “On the other, the results also highlight that our clock can help us find many new candidates that haven’t been studied before for their rejuvenating properties. It opens up a lot of new avenues.”

As a proof of concept of their approach, the researchers then tested three of the predicted compounds in mice, in collaboration with the team of Prof. Rubén Nogueiras at the Centre for Research in Molecular Medicine and Chronic Diseases. The administration of these drugs significantly reduced anxiety and slightly increased spatial memory in older mice, addressing two well-known symptoms associated with ageing. An analysis of gene expression showed that the combination of these compounds also led to a shift toward a younger phenotype. Altogether, these results show that a selection of compounds predicted to rejuvenate the brain did produce rejuvenation at the molecular level in the cortex of aged mice and had an impact on behavioural and cognitive functions.

Globally, the study, recently published in the journal Advanced Science, highlights the computational ageing clock developed by the researchers as a valuable resource for identifying brain-rejuvenating interventions with therapeutic potential in neurodegenerative diseases. It provides a strong foundation for further research. “The hundreds of compounds predicted by our platform require validation across multiple biological systems to assess their efficacy and safety, offering extensive opportunities for future therapeutic development,” concludes Prof. Antonio Del Sol.

Bipolar disorder is a mental health condition characterized by extreme mood swings, with alternating periods of depression and manic episodes. Past research suggests that bipolar disorder has a strong genetic component and is among the most heritable psychiatric disorders.

To better understand the genetic factors that increase the risk of developing this mental health disorder, neuroscientists and geneticists have carried out various genome-wide association studies (GWAS). These are essentially studies aimed at identifying specific regions of the human genome that are linked with an increased risk of having bipolar disorder, also referred to as bipolar risk loci.

While earlier works have identified many of these regions, causal single nucleotide polymorphisms (SNPs) for the disorder are largely unknown. These are essentially genetic variants that primarily contribute to bipolar disorder risk, as opposed to just being mere markers of it.

The team took publicly available data from three studies of the Alzheimer’s brain that measured single-cell gene expression in brain cells from deceased donors with or without Alzheimer’s disease. They used this data to produce gene expression signatures for Alzheimer’s disease in neurons and glia.

The researchers compared these signatures with those found in the Connectivity Map, a database of results from testing the effects of thousands of drugs on gene expression in human cells.

Out of 1,300 drugs, 86 reversed the Alzheimer’s disease gene expression signature in one cell type, and 25 reversed the signature in several cell types in the brain. But just 10 had already been approved by the FDA for use in humans.

Poring through records housed in the UC Health Data Warehouse, which includes anonymized health information on 1.4 million people over the age of 65, the group found that several of these drugs seemed to have reduced the risk of developing Alzheimer’s disease over time.

“Thanks to all these existing data sources, we went from 1,300 drugs, to 86, to 10, to just 5,” said the lead author of the paper.

The authors chose 2 cancer drugs out of the top 5 drug candidates for laboratory testing. They predicted one drug, letrozole, would remedy Alzheimer’s in neurons; and another, irinotecan, would help glia. Letrozole is usually used to treat breast cancer; irinotecan is usually used to treat colon and lung cancer.

The team used a mouse model of aggressive Alzheimer’s disease with multiple disease-related mutations. As the mice aged, symptoms resembling Alzheimer’s emerged, and they were treated with one or both drugs.