"These models represent a new frontier in cancer research because they give us a better insight into what specific genes really do in a live mammal," he said. "The mice give us a highly reproducible glimpse at the earliest forms of cancer those rarely seen in the clinic and therefore can be used to develop new markers for detection as well as new strategies for prevention and early intervention."
Prostate cancer is the second leading cause of death for men in the United States. This year, more than 230,000 men will be diagnosed with the disease, in large part due to widespread screening with the prostate-specific antigen, or PSA, test. The test has been controversial because it cannot distinguish between men who have non-progressing forms of the disease that may never cause harm and those who have aggressive cancers that require treatment. Researchers are eager to develop tests that can stratify early stage prostate cancers by their likelihood to worsen, an achievement that could spare many men from unnecessary surgery or radiation therapy.
With this in mind, Greenberg said his next goal is to identify the additional mutations - such as occur in p53 or other tumor suppressor genes - that must collaborate with Rb to drive the benign condition to cancer. Ideally, blood or other simple tests to detect these mutations could be developed that reveal predictive information about a man's type of cancer well before he is in danger.
"The idea is to set the bar for detection as early as possible," Greenberg said. "Ideally, we'd hope that a man diagnosed at an early age with prostate cancer could be assured that his cancer wasn't likely to progress or that he needed early intervention that could save his life."
The study, funded by the National Cancer Institute and the Prostate Cancer Foundation, was led by Lisette Maddison, Ph.D., a former graduate student of Greenberg's who is now a postdoctoral fellow at Oregon Health and Scien
Contact: Dean Forbes
Fred Hutchinson Cancer Research Center