Seed Grant Recipient Charts Progress in Pursuit of New Approaches to H. Pylori-Driven Gastric Cancer
When Zheng Chen, MD, PhD, was awarded a $100,000 seed grant from the Gastric Cancer Foundation a year ago, his goal was to understand how a particular network of proteins contributes to raising the risk of the disease in people with the gut bacterial infection Helicobacter pylori (H. pylori). Thanks to our support, Chen has made significant progress in reaching that goal – and raised additional funding that he hopes to use to develop novel therapies based on his findings.
One of the priorities of the Gastric Cancer Foundation is to bridge the funding gap for researchers like Chen, who are in the early and mid-stages of their careers. Our hope is that this funding will allow researchers to gather valuable data they can use to apply for larger grants. We believe this is a crucial funding mechanism that supports the early development of novel diagnostics and treatments.
Chen, who is assistant professor of surgery at the University of Miami’s Miller School of Medicine, is focusing on the WEE1-STAT3 protein signaling axis, which is active in H. pylori-driven gastric cancer. His research centers around the hypothesis that WEE1-STAT3 promotes the growth of gastric cancer cells, in part by suppressing the ability of the immune system to fight the disease.
In studies supported by the Gastric Cancer Foundation, Chen discovered that WEE1 is overexpressed in gastric cancer. What’s more, the protein exists largely outside of the cell’s nucleus – in the cytoplasm. That location allows it to activate and stabilize STAT3 signaling, promoting tumor survival and predicting poor patient outcomes, he and his colleagues discovered. Chen was the principal investigator of a paper on the potential of WEE1 inhibition in gastric cancer, which was published in July in the journal Critical Reviews in Oncology/Hematology.
In subsequent studies, Chen’s team found that high levels of WEE1 activate an oncogene called MYC, which helps tumors resist cancer therapies. He believes that blocking WEE1 could inhibit MYC, thereby reversing drug resistance. This could “potentially make these aggressive cancers more responsive to treatment,” he said.
The next step for Chen and his team is to investigate whether removing WEE1 prevents the development of gastric cancer. Using a new mouse model of gastric cancer that they developed, they plan to test combinations of WEE1 inhibitors with other drugs, including immunotherapies.
Chen credits the Foundation’s funding for helping him to attract additional grant money for his project. In 2025, he was awarded $250,000 from the Mark Foundation for Cancer Research and $100,000 from the DeGregorio Family Foundation for Gastric and Esophageal Cancer Research.
None of this would have been possible without the support of the Gastric Cancer Foundation, Chen said:
“This funding is very important for early-stage investigators like me. It builds preliminary data that we need to get bigger grants. Because of this award, we can seek out more opportunities to support this research – and to try to improve outcomes for gastric cancer patients.”
