Research Goals
Despite the advent of diverse therapeutic options such as chemotherapy, targeted therapy, and immunotherapy, the long-term efficacy of these treatments is often hindered by the emergence of drug resistance leading to frequent recurrence and metastasis. Our laboratory focuses on the critical determinants of survival that arise after initial cancer treatment by exploring the complex biological mechanisms of tumor progression and its terminal stages.
Our research is driven by a focus on the most lethal aspects of the cancer life cycle. We investigate tumor dormancy, which is the state where cancer cells evade treatment and persist as seeds for later recurrence, as well as cancer cachexia, a devastating metabolic syndrome responsible for approximately 40% of all cancer-related deaths. We believe that overcoming these late-stage challenges including resistance, dormancy, and cachexia is essential as they represent the primary causes of mortality in the modern era of oncology.
By asking why therapeutic efficacy fails to persist and what ultimately causes patient mortality, we aim to dissect the lethal tumor-host interactions from a systemic perspective. Our laboratory pursues translational research by integrating molecular biology and animal models for mechanistic validation with multi-omics and data analysis. By leveraging cutting-edge experimental technologies, we conduct integrated studies that link cellular models, animal experiments, and clinical patient samples to interpret complex biological networks. Through this approach, we strive to bridge the gap between fundamental biological discovery and clinical application to extend the lives of cancer patients.
Drug Resistance
While modern oncology has introduced highly innovative therapies, long-term clinical success is frequently challenged by the emergence of drug resistance. Even treatments that show exceptional initial responsiveness often encounter adaptive resistance in advanced stages, making it a primary barrier to sustained cancer survival. Once resistance emerges, clinical management often requires higher dosages, which inevitably leads to severe side effects and systemic toxicity. Ultimately, the inability of anticancer agents to control the disease results in rapid tumor progression. Our laboratory seeks to lower this survival hurdle by elucidating the fundamental mechanisms underlying resistance to various therapies and proposing novel therapeutic strategies to overcome them.
Key objectives
Elucidation of molecular mechanisms underlying anticancer drug resistance
Development of novel therapeutic strategies to overcome drug resistance
Identification of novel cell death pathways and therapeutic approaches to bypass resistance to chemotherapy, targeted therapy, and immunotherapy
Tumor Dormancy
There is often a significant temporal gap between the treatment of a primary tumor and the clinical manifestation of recurrence or metastasis. Cancer cells that have disseminated throughout the body can stop proliferating and remain in a quiescent state within distant organs for extended periods, only to "reawaken" at a later point to cause lethal relapse. Effectively managing these "sleeping" cancer cells is crucial for substantially reducing cancer mortality. Our laboratory addresses the core questions of why infinitely proliferating cancer cells enter dormancy in unfamiliar environments and what specific factors trigger their reawakening. We explore methods to detect these latent risks early and eliminate them at their source.
Key objectives
Investigation of the regulatory mechanisms controlling cancer cell entry into and exit from the quiescent state
Identification of molecular triggers and microenvironmental factors that induce the reawakening of dormant tumor cells
Development of early detection methods and targeted elimination strategies for latent disseminated tumor cells
Tumor-Host Interaction and Cancer Cachexia
Cancer is not a localized disease; it constantly interacts with various healthy organs throughout the patient’s body. By secreting a diverse array of factors, cancer cells communicate beyond the tumor microenvironment to exert systemic effects on skeletal muscle and adipose tissue. We specifically focus on cancer cachexia, a devastating syndrome of progressive muscle and fat wasting observed in late-stage cancer patients. Our research aims to characterize these tumor-host interaction axes at the molecular level using cellular and animal models to understand how they influence late-stage disease progression and ultimately dictate patient survival.
Key objectives
Characterization of systemic tumor-host interaction axes and inter-organ crosstalk at the molecular level
Deciphering the molecular pathways of muscle and adipose tissue wasting in late-stage cancer patients
Development of therapeutic interventions targeting systemic metabolic dysfunction to improve patient survival and quality of life