$50,000 Young Research Fellowship Grant Awarded to Dr. Ashleigh Poh, PhD.

$50,000 Research Fellowship was granted by Stupid Strong in partnership with Debbie’s Dream Foundation and AACR Gastric Cancer to Ashleigh Poh, PhD of Olivia Newton-John Cancer Research Institute in Melbourne, Australia. Dr. Poh is exploring co-targeting HCK as a combination therapy to treat gastric cancer.

Dr. Poh says, “I am extremely honored to be awarded this fellowship, and would like to express my sincere gratitude to Debbie’s Dream Foundation and AACR for their generous support of my research. This fellowship will enable me to further develop my scientific career in tumor immunology, and expand the breadth of my research by working with world renowned experts in gastric cancer.”

This Research Fellowship Grant was awarded in memory of Candace Netzer.


Scientific Statement of Research

The stromal compartment of gastric tumors is comprised of a heterogeneous collection of cells, of which macrophages are a major component. Tumor-associated macrophages are broadly classified into two main groups: classically-activated macrophages that mediate anti-tumor responses, or alternatively-activated macrophages that facilitate immunosuppression, invasion and metastasis. In human gastric cancer patients, the increased infiltration of alternatively-activated macrophages is associated with a poor clinical outcome. Thus, these cells represent promising targets for anti-cancer therapy. Elevated expression of the myeloid specific kinase, Hematopoietic Cell Kinase (HCK) is observed in most solid human malignancies including gastric cancer, and is associated with poor survival.

We have discovered that increased HCK activity enhances tumor progression by promoting the polarization of macrophages towards an alternatively-activated endotype. This project will explore HCK as a novel therapeutic target in early- and advanced stage gastric cancer. The outcomes of this project will provide novel molecular insights into therapeutically targetable mechanisms by which macrophages promote gastric tumor progression in pre-clinically validated mouse models.