yifat Narinsky

A popular diet called the ketogenic diet (high fat, low carbs) causes the body to produce ketone bodies, which are natural energy sources. One of them, β-hydroxybutyrate (βHb), may affect how cancer cells behave.
We explored the connection between gut health and social behavior in stress-vulnerable mice. We evaluated the gut microbiome, gut barrier function, inflammation, immune markers, and behavior. We found that Submissive mice showed impaired gut health together with reduced sociability. Treatments that improved gut barrier function and reduced inflammation also improved behavioral outcomes, supporting the gut–brain axis as a promising target for stress-related social deficits.
Breast cancer is the leading cause of cancer-related deaths among women, and current treatments don't always work the same for everyone. One big challenge is that doctors often don't know in advance which chemotherapy will be most effective for each patient.
This project develops patient-derived tumor models that integrate epithelial, stromal, and immune components to better reflect human tumor biology. The platform preserves tumor heterogeneity and enables more accurate prediction of therapeutic responses and personalized treatment strategies across cancer types.
The ketogenic diet alters cancer cell metabolism by promoting ketone body utilization under low-glucose conditions. This study examines their dual role in signaling and energy supply, and their impact on breast cancer cell oncogenicity, survival, proliferation, and migration.
This project investigates how cancer cells adapt to glucose deprivation by shifting to oxidative metabolism. It focuses on metabolically flexible subpopulations, associated DNA damage and repair mechanisms, and chromatin changes that may support survival and resistance under nutrient stress conditions.
ALOS4 is a cyclic peptide with potent anti-cancer and anti-inflammatory effects. It inhibits tumor growth, reduces pro-inflammatory cytokines, modulates macrophage activity, and suppresses interferon-response pathways without observed toxicity.