Dr. Keith Syson Chan received his BSc in Life Sciences from Queen’s University in Kingston, Ontario, Canada, and his PhD from the University of Texas Graduate School of Biomedical Sciences at MD Anderson Cancer Center in Houston. He received his postdoctoral training in cancer stem cells and immune evasion at the Institute for Stem Cell Biology and Regenerative Medicine at Stanford University in California. Dr. Chan most recently relocated to Houston Methodist with a $6 million Established Investigator recruitment grant from the Cancer Prevention and Research Institute of Texas (CPRIT).

1. Tumor microenvironment: Immune checkpoint blockade therapy is emerging as a major treatment modality for cancer patients. However, a large fraction of patients remain non-responders. Ongoing projects is further characterizing the resistance mechanisms, e.g., i) how to turn cold tumors into hot tumors, via modulating dying cancer cell-released DAMPs and iDAMP and dendritic cell cross priming of CD8+ T cells, ii) cancer cell modulation of the immunosuppressive immune microenvironment etc

2. Cell death-induced biology: Most anti-cancer therapeutics designate cell death as the end goal, we serendipitously discovered drug-induced dying cells play a major role in inducing residual tumor cell repopulation and immunosuppression. And thus, driving therapeutic resistance. Proteomics discovery identified novel protein complexes associated with various forms of programmed cell death mechanisms. Ongoing studies will further dissect these molecular mechanisms.

3. Metastatic niche: We recently identified collagen-rich airway smooth muscle cells as a metastatic niche for cancer cell colonization in the lung. Ongoing projects will further characterize its interaction with other immune cells in the microenvironment (e.g. neutrophils, NK cells) to facilitate the process. We are building on existing RNAseq data profiling the niche and cancer cells, functionally integrating with microfluidics system in vitro and established in vivo models to study their mechanistic interactions