Faculty Members

•  ericcheung@as.edu.tw
  ericcheunglab@gmail.com
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RESEARCH INTERESTS

Decoding the Dialogue Between Cancer and the Host

Cancer progression is not just a story about malignant cells; it's a story about a hostile takeover of the body. At the heart of this takeover is a fundamental rewiring of cellular metabolism. As cancer cells grow uncontrollably, they generate high levels of metabolic by-products called reactive oxygen species (ROS), leading to a state of oxidative stress. This stress can be a double-edged sword: while highly damaging, it can also trigger signaling pathways that cancer cells exploit to survive and spread. A critical question in cancer biology is how tumors manage this delicate balance.

Our laboratory operates on the central premise that cancer cells cannot solve this problem alone. They engage in a constant, dynamic dialogue with the non-cancerous cells and organs of the host. We believe that by decoding this communication, we can find new ways to cut the lines of support for tumors to grow and metastasize. Our research moves beyond the cancer-cell-centric view to investigate how these critical tumor-host interactions—both locally within the tumor microenvironment and systemically with distant organs—dictate the course of cancer.

To address these questions, we integrate sophisticated in vivo genetically-altered mouse models with advanced ex vivo organoid co-culture systems. These models are interrogated with powerful technologies, including single-cell RNA sequencing, CRISPR-based somatic genome editing, and metabolomics, allowing us to dissect these complex interactions with unprecedented resolution.

Ultimately, our goal is to translate our findings into more refined and effective cancer therapies. By including the host side of the tumor-host interaction as additional targets, we aim to develop novel strategies that disrupt the pro-tumor support network, creating a new therapeutic window to combat cancer progression and resistance.

Reactive oxygen species (ROS) affect tumour and stromal cells to either impede or promote cancer progression, depending on the integration of the response of all cells in the tumour microenvironment (TME).
From Cheung and Vousden 2022, Nature Review Cancer