Giaccia and his collaborators found that human pancreatic cancer cells expressing high levels of CCN2 grew robustly when injected under the skin of mice.
Cancer cells expressing high levels of CCN2 formed tumors that grew more rapidly and metastasized more aggressively than did those expressing lower levels, and the mice died sooner than others injected with cancer cells expressing less CCN2.
The researchers wondered if CCN2 played a role in keeping tumor cells alive in hypoxic conditions.
Many other cellular conditions can also kick-start CCN2 expression, including the presence of CCN2 itself.
A phase-1 clinical trial testing the safety of an antibody that binds CCN2 and blocks its activity in a small number of patients began in December at Stanford and Dartmouth-Hitchcock Medical Center.