Tobias Janowitz

This study shows that caloric restriction before tumor induction delays cancer cachexia by reducing systemic inflammation and preserving lean mass.

The paper identifies altered tryptophan metabolism in cancer cachexia, showing serotonin depletion and kynurenine accumulation, which drive behavioral dysfunction but not wasting.

This study shows that JAK1/2 inhibition with ruxolitinib improves survival and body weight in lung cancer models by increasing food intake and restoring metabolic function.

The paper identifies a cytokine-lipid axis that links systemic inflammation to hepatic autophagy dysfunction in cancer across species.

This study identifies sustained glucose turnover flux as a distinguishing metabolic feature of cancer cachexia compared to nutrient limitation under controlled food intake.

This paper shows autophagy prevents cachexia by suppressing CCL2, which damages appetite-promoting neurons, leading to lethal weight loss in mice.

The paper shows that tumor-secreted cytokines induce hepatic gluconeogenesis, contributing to hyperglycemia and poor prognosis in cancer cachexia using Drosophila and mouse models.

This study identifies area postrema neurons as mediators of IL-6 function in cancer-associated cachexia, showing that targeting these neurons can prevent cachexia and prolong lifespan in mice.

This study identifies Neurotensin-expressing neurons in the mouse IPAC that regulate energy balance by modulating feeding behavior and physical activity.