Researchers have identified the molecular trigger of the uterin fibroid tumor, a single stem cell that develops a mutation, starts to grow uncontrollably and activates other cells to join its expansion.
The stem cell initiating the tumor carries a mutation called MED12. Once the mutation kicks off the abnormal expansion, the tumors grow in response to steroid hormones, particularly progesterone.
"No one knew how these came about before," said Serdar Bulun, M.D., chair of obstetrics and gynecology at Northwestern University Feinberg School of Medicine and Northwestern Memorial Hospital. "These stem cells
Researchers, lead by Masanori Ono, M.D., a post-doctoral student in Bulun's lab, examined the behavior of human fibroid stem cells when grafted into a mouse. Tumors originating from the fibroid stem cell population grew 10 times larger compared to tumors initiated with the main cell population, suggesting a key role of these tumor stem cells is to initiate and sustain tumor growth.
Fibroid uterine tumors affect an estimated 15 million women in the United States, causing irregular bleeding, anemia, pain and infertility. Despite the high prevalence of the tumors, which occur in 60 percent of women by age 45, the molecular cause has been unknown.
"Understanding how this mutation directs the tumor growth gives us a new direction to develop therapies," said Bulun, also the George H. Gardner Professor of Clinical Gynecology.
Adapted from the Northwestern University announcement.