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Inducing cell death in pancreatic cancer cells

Researchers have discovered a previously unknown mechanism that makes most pancreatic cancer cells susceptible to a form of programmed cell death. The team showed that cancer cells with mutations in the KRAS gene develop a vulnerability which can be used to eliminate tumor cells in preclinical models. The findings open up new perspectives for treating pancreatic cancer. The study was published in the journal Nature Communications.

Pancreatic cancer is one of the most aggressive forms of cancer and has so far shown only limited response to available treatments. In approximately 90 percent of cases, these tumors carry mutations in the KRAS gene that drive cancer growth. Due to the ageing population and the lack of effective therapies, physicians, clinicians, and researchers expect pancreatic carcinoma to become one of the leading causes of cancer-related deaths worldwide in the coming years. With the discovery of this newly identified vulnerability, a therapeutically promising approach has now been identified for treating this disease following future clinical trials.

The researchers discovered that KRAS-mutated tumor cells continuously activate signals from the innate immune system. This primes the cancer cells for an inflammatory form of cell death known as necroptosis. In order to survive, tumor cells rely heavily on the protein caspase-8, which usually inhibits necroptosis. If caspase-8 is blocked, the tumor cells die. “KRAS-mutated tumors have a previously unknown Achilles heel,” says the senior author of the study. “By switching off the tumor cells’ defence mechanisms, we can significantly kill these tumors.”

Vascular Control Of Aging And Regeneration (Featuring Anjali Kusumbe, PhD)

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Light-triggered arrhythmia reveals rapid brain oxygen shifts in mice

An irregular heartbeat, or arrhythmia, leads to inefficient pumping of blood by the heart, which then prevents blood and oxygen from getting to the body’s other organs. When blood and oxygen flow poorly to the brain, the risk of stroke and cognitive decline increases.

A team of researchers based at Washington University in St. Louis used cardiac optogenetics to noninvasively study arrhythmia and its impact on the brain. Using highly sensitive imaging in a mouse model, they found that arrhythmia in a mouse heart alters oxygen concentration in the brain during and after arrhythmia.

Results of the research are published in Science Advances.

Fragile X deficits in mice respond to gene therapy

A gene therapy designed to replace a missing brain protein restored normal brain activity and improved behavior in a mouse model of fragile X syndrome (FXS), according to a study led by researchers at the University of California, Riverside. The findings, published in Molecular Therapy Nucleic Acids, suggest that gene therapy may one day address the underlying cause of FXS rather than simply treating its symptoms.

FXS affects approximately 2–3% of individuals diagnosed with autism and is one of the best-defined genetic causes of neurodevelopmental disability. The condition occurs when a mutation in the FMR1 gene prevents the production of fragile X messenger ribonucleoprotein (FMRP), a protein that regulates communication between brain cells.

“In a typical brain, FMRP acts like a brake or a volume control,” said Iryna Ethell, the paper’s senior author and a professor of biomedical sciences in the UCR School of Medicine. “Without it, neural circuits become overactive and less efficient, which contributes to many of the developmental and behavioral challenges associated with FXS.”

Scientists uncover a genetic ‘shield’ that lowers the risk of colorectal cancer

A team of scientists from the Barbara Ann Karmanos Cancer Institute, Wayne State University and institutions across the U.S. have published a new paper on the role of TGFBR1*6A, a naturally occurring genetic mutation in the TGFBR1 gene found in approximately 14% of the general population.

The study, “TGFBR1*6A and risk for colorectal cancer,” published June 9, 2026, in Cancer Communications, focuses on TGFBR1*6A and how it influences a person’s risk of developing colorectal cancer. Dr. Boris Pasche, president and CEO of the Karmanos Cancer Institute and chair of the Wayne State University Department of Oncology, was the first to discover TGFBR1*6A as a cancer risk allele.

“This mutation has often been overlooked by genome-wide association study chips, which cannot detect TGFBR1*6A, and is commonly missed by next-generation sequencing platforms due to the complexity of the region,” said Dr. Allan Johansen, a postdoctoral fellow and first author of the paper.

Quantum-inspired AI could tailor patients’ cancer treatment to their entire molecular background

For a child diagnosed with neuroblastoma—the most common infant cancer, occurring when early nerve cells grow out of control—the path to treatment isn’t simple. Some types of neuroblastoma resolve on their own, while others require aggressive intervention. Researchers have tried matching treatments to patients based on one-gene mutations with limited success. This is because patients’ outcomes depend on their entire molecular background, containing millions or even billions of features, such as DNA and RNA from tissues and blood.

“It’s much more than just one gene—everything that’s happening in the cells of the patient matters,” said Orly Alter, an associate professor of biomedical engineering at the University of Utah’s Scientific Computing & Imaging Institute.

Current artificial intelligence and machine learning (AI/ML) approaches require massive amounts of training data and, specifically, vastly more patient samples than genetic features.

Intracellular mechanisms promote tumor survival during hypoxia

Northwestern Medicine scientists have, for the first time, described the underlying mechanisms that regulate how cells rapidly change gene expression in response to hypoxia, a key feature of many treatment-resistant tumors, according to a recent study published in Science Advances.

Ali Shilatifard, Ph.D., the chair and Robert Francis Furchgott Professor of Biochemistry and Molecular Genetics, was the senior author of the study.

Scientists found an 8-year-old Neanderthal child in a Belgian cave, and the molar DNA found is said to be the oldest human genetic code ever sequenced, turning one hillside into a rare window on our deep past

Scientists have uncovered the oldest human genetic code from an 8-year-old Neanderthal child in Belgium, offering profound insights into our evolutionary past and Neanderthal development.

Breastfeeding may protect against ADHD symptoms

A new study from the University of Bergen shows an association between breastfeeding up to 6 months of age and a reduced risk of ADHD symptoms from ages 3 to 8.

Breast milk is the primary source of nutrition for infants. It is uniquely tailored for the child and contains numerous components beneficial for growth and brain development, including long-chain fatty acids, amino acids, antibodies and beneficial bacteria.

“It is well established that psychiatric symptoms and disorders can be influenced by both genetic and environmental factors,” says Berit Skretting Solberg, psychiatrist and researcher at the Department of Biomedicine, University of Bergen, and senior consultant at Betanien Hospital.

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