The body’s cells respond to stress—toxins, mutations, starvation or other assaults—by pausing normal functions to focus on conserving energy, repairing damaged components and boosting defenses.

If the stress is manageable, cells resume normal activity; if not, they self-destruct.

Scientists have believed for decades this response happens as a linear chain of events: sensors in the cell “sound an alarm” and modify a key protein, which then changes a second protein that slows or shuts down the cell’s normal function.

But in a new study published today in the journal Nature, researchers at Case Western Reserve University have discovered a cell’s response is more nuanced and compartmentalized—not fixed or rigid, as previously thought.

Research conducted by the National Cancer Research Centre (CNIO), published today in ‘Nature’, reveals a mechanism in mice that is triggered just minutes after acute liver damage occurs.

This finding opens up avenues for future treatments of serious liver damage to include a diet enriched with the amino acid glutamate.

Glutamate supplementation can promote liver regeneration and benefit patients in recovery following hepatectomy or awaiting a transplant, the authors write in ‘Nature’.

Activating liver regeneration is key to treating diseases that involve severe liver damage, which are becoming increasingly frequent and are associated with poor dietary habits and alcohol consumption.

The FDA approval was based on results from the CABINET study, a phase 3 pivotal trial evaluating cabozantinib compared with placebo in two groups of patients with previously treated NETs: advanced pancreatic NETs and advanced extra-pancreatic NETs. The study was led by Jennifer Chan, MD, MPH, clinical director of the gastrointestinal cancer center and director of the program in carcinoid and neuroendocrine tumors at Dana-Farber Cancer Institute.

New research from Memorial Sloan Kettering Cancer Center (MSK) develops a new tool for studying mitochondrial DNA deletions; uncovers mechanisms of histiocytosis-associated neurodegeneration; and investigates how mutant stem cells co-opt regeneration to make tumors grow.

Researchers at City of Hope have found that cell mutations are necessary but not always sufficient for tumors to form. Instead, they suggest that additional risk factors that promote tumor growth, like chronic inflammation, are a key trigger for tumor formation. The study findings, published this month in Cancer Discovery, answer a question that scientists have long asked: Are cell mutations alone — whether genetically inherited or acquired through lifestyle choices — enough to cause cancer?

A critical analysis of the latest literature data on changes in the viability of cancer cells under the influence of terahertz radiation was reported.