20 articles
New research shows brief fasting periods can boost the effectiveness of cancer immunotherapy by reshaping tumor-fighting immune cells.
Peter Attia explains the science behind fasting as a tool to enhance chemotherapy efficacy while protecting healthy cells.
Eight-week study of weekday-only intermittent fasting in older breast cancer survivors with overweight demonstrates feasibility.
Specific gut microbes produce compounds that reprogram fat cells to enhance immune responses against cancer.
A growth factor called GDF11 reprograms pro-tumor macrophages by rewiring their metabolism, suppressing hepatocellular carcinoma growth.
Scientists discover D-cysteine selectively targets cancer cells by disrupting their energy production without harming normal cells.
New research reveals how a high-fat diet rewires tumor-to-nerve communication, accelerating cachexia — the devastating wasting syndrome that kills cancer patients.
AML stem cells produce BHB via autonomous ketogenesis to block ferroptosis, revealing a targetable metabolic vulnerability in leukemia.
Redirecting glucose metabolism during T cell expansion dramatically improves cancer immunotherapy effectiveness.
Tumor-infiltrating adipocytes release a lipid metabolite that triggers neutrophil cell death, suppressing CD8+ T cells in pancreatic cancer.
New research reveals how tumors hijack brain pathways through GDF15 protein to cause devastating weight loss in cancer patients.
Cancer cells that downregulate SMC4 enter a low-proliferation, diapause-like state that resists standard chemotherapy, revealing a dangerous survival mechanism.
A lipid metabolism enzyme called SMPD1 anchors the deadliest cancer mutation to the cell membrane — and blocking it may finally crack KRAS.
A pyruvate metabolism enzyme suppresses leucine catabolism to keep mTOR active in liver cancer — and blocking it shrinks tumors in vivo.
Researchers discovered why fibrolamellar carcinoma resists immunotherapy and found an existing drug can free trapped T cells to fight it.
Leukemic stem cells produce their own ketone bodies to block ferroptosis, revealing a metabolic weak point that could be targeted therapeutically.
GLP-1 receptor agonists may overcome Lenvatinib resistance in hepatocellular carcinoma by targeting a key glycolytic vulnerability.
Researchers respond to peer critique of risk-based, non-invasive hepatocellular carcinoma surveillance in metabolic liver disease patients.
Scientists discover how to reprogram cancer cells into harmless, non-dividing cells by targeting a nuclear enzyme pathway.
Researchers develop targeted drug that degrades FTO protein, disrupting ribosome production and protein synthesis in leukemia cells.
