Our laboratory investigates the mechanisms underlying the interaction between tumors and the brain in the context of cancer. Using viral tracing approaches such as PRV and AAV in combination with immunofluorescence imaging, we detect viral signals in central nervous system tissues to map neural circuits connecting tumors and the brain. Based on this circuit-level understanding, we aim to explore strategies to modulate and control cancer progression. Furthermore, we utilize various transgenic mouse models to identify neurons activated by cancer and to elucidate the neural circuits associated with cancer cachexia.

Our laboratory employs a multi-omics approach to investigate the interaction between systemic changes in cancer and the central nervous system. By conducting metabolomic analyses of the bloodstream, we track cancer-specific metabolic alterations, while simultaneously utilizing both bulk and single-cell RNA sequencing to analyze the sophisticated gene expression dynamics within the tumor microenvironment. Based on these multidimensional analyses, we provide in-depth interpretations of how the brain regulates and interacts with the physiological states of the tumor itself and peripheral organs, such as muscle and fat, during cancer progression. Through the integration of these multi-omics datasets, our primary research goal is to uncover the key pathways linking the tumor, the brain, and peripheral systems. 

Cancer cachexia is a complex metabolic syndrome characterized by persistent weight loss, muscle wasting (sarcopenia), and the depletion of adipose tissue, representing a critical clinical challenge that remains refractory to conventional nutritional support. Our laboratory aims to delineate the neurological networks between the brain and peripheral organs, such as muscle and fat, to analyze the correlation between tissue-specific metabolic reprogramming and the underlying neural circuits that govern these processes during cachexia progression. Ultimately, we seek to uncover the fundamental neurological mechanisms driving cancer-induced systemic metabolic collapse and propose next-generation therapeutic strategies to restore metabolic homeostasis.