SALT LAKE CITY, Utah (News4Utah) — Roughly 60,000 women in the United States are diagnosed every year with endometrial cancer. It is the most common form of uterine cancer and the numbers are growing.
Researchers at Huntsman Cancer Institute are hoping to stop that trend. They found a surprising link between levels of estrogen and cortisol may contribute to more aggressive endometrial cancer tumors.
“In general, cortisol is an immune suppressive, that’s its major role, that’s why it was so surprising that we found it was helping these tumors grow and to be more aggressive,” said Dr. Jay Gertz, HCI researcher.
Tara McKee had to have a hysterectomy. She ignored the signs of endometrial cancer for two years.
“I didn’t realize the signs at the time,” said McKee.
Researchers say signs include: post menopausal bleeding and irregular and abnormal bleeding.
They also say the number of cases of endometrial cancer is rising and shifting toward younger women.
“The more we find these nuances, we can customize how we want to approach this,” said Dr. Maggie Janat-Amsbury, HCI researcher.
Estrogen is needed for overall reproductive health. It can also cause tumors to grow. But researchers at Huntsman say, the other element they’ve found, is that cortisol, drives the more aggressive tumors.
Endometrial cancer is the 4th most diagnosed cancer in women.
“The follow up we’re trying to do is find ways to block both estrogen and cortisol signaling that would be the most effective treatment for these patients,” said Dr. Gertz.
“This is the goal of studies like this, to advance and go past molecular data sets and animal studies that it advances to clinical trials and probably new ways to tackle this cancer will be made available to patients,” said Dr. Janat-Amsbury.
Both hormones, estrogen and cortisol exist naturally in the body but keeping the levels in balance can be tricky. Researchers recommend checking with your doctor for any abnormal symptoms.
The study was published in the medical journal, Cell Reports: http://www.cell.com/cell-reports/fulltext/S2211-1247(18)30271-7