Scientists may have found a clue to one of the most vexing questions in cancer care: How to determine which prostate tumors will return after surgery and spread aggressively, and which won’t.
A gene called SPARCL1 may be the switch that makes some prostate tumors more destructive than others, according to a study today in the Proceedings of the National Academy of Sciences. When the amount of protein secreted by the gene declined, cancer recurrence rose, researchers at the Johns Hopkins University medical school found.
Prostate malignancies are the second leading cause of cancer death in U.S. males, with more than 240,000 cases diagnosed yearly, according to the American Cancer Society. About 40 percent of cases carry a higher risk that the disease will spread after surgery, said Edward Schaeffer, a study author. Today’s report suggests doctors may one day be able to know early on which patients have the most aggressive disease.
“It’s very important to identify patients who are going to do really well after surgery, and maybe don’t need to worry so much about cancer recurrence,” said Schaeffer, an associate professor of urology and oncology at the Johns Hopkins University School of Medicine in Baltimore. “Those individuals who are at an increased risk may need closer follow up or more intensive interventions with treatments such as radiation.”
When the prostate is forming, SPARCL1 turns off to allow the gland cells to grow. It then turns itself back on after puberty to produce a steady level of its protein to a healthy prostate, Schaeffer said by telephone.
The researchers examined the DNA within the prostates of men who had the gland surgically removed, said Paula Hurley, the lead study author and an instructor of urology at Johns Hopkins. After identifying the SPARCL1 gene as a possible cancer culprit, they determined an 86 percent increased risk of recurrence over 10 years in men in whom the gene was shut off who had highly aggressive prostate cancer, Schaeffer said.
The researchers are now trying to design a test to look at SPARCL1 in men, he said.
“Although this work focused on prostate cancer, our work also suggests that it may play a role regulating other cancer recurrences as well,” Schaeffer said. “Mechanisms that regulate SPARCL1s expression are key next steps so this molecular pathway can be modulated.”
To contact the editor responsible for this story: Reg Gale at firstname.lastname@example.org