Research conducted in part by Northwestern’s Feinberg School of Medicine explained one more clue about the spread of ovarian cancer, the fifth-leading cause of cancer-related deaths among women.
The authors of the study, published in Nature Medicine on Sunday, were researchers from NU, the University of Chicago and the University of Texas’ MD Anderson Cancer Center. They discovered fat cells from the omentum, a patch of fat in the abdomen, can accelerate the spread of ovarian cancer.
This finding is important because ovarian cancer spreads to the omentum nearly 80 percent of the time, said Kristin Nieman, a postdoctoral fellow at the University of Chicago and co-author of the paper.
In one part of the study, researchers injected ovarian cancer cells into non-cancerous cells from surgery patients’ omentums. The results showed the omentum cells increased in metabolism, growth and fat uptake, which altogether fueled the growth of the cancer cells.
Nieman explained metastasis, or spread, to the omentum is taxing on the body.
“The omentum, in some cases, can grow tumors that are even greater in size than the primary tumor (in the ovaries) itself,” Nieman said.
In another part of the study, researchers injected ovarian cancer cells into mice. The ovarian cancer cells reached the omentum in 20 minutes, the authors of the paper stated.
Marcus Peter, a professor of medicine at NU’s Feinberg School of Medicineand co-author of the study, played a large role in determining why omentum cells fuel cancer growth, Nieman said. Peter narrowed down the specific chemical to a protein called FABP4.
Peter declined to comment, deferring questions about the study to his co-authors.
To measure FABP4’s effect on the cancer cells, researchers injected cancer cells into a genetically modified mouse that didn’t produce any FABP4.
“The cancer spread, but it did not spread as well, did not grow in the sites it spread to and did not grow as well in the primary cells,” Nieman said.
The metabolism finding is important in fields beyond oncology, said Dr. Diljeet Singh, co-director of the NU Ovarian Cancer Early Detection and Prevention Program.
Because fat cells in the omentum are now linked to cancer, Singh said it also sheds light on the connection between obesity and cancer.
Nieman said this research is the first of its kind to identify FABP4 as a link between cancer cell metastasis and fat cells. She also said her team believes it may play a larger role in therapy for breast, gastric and colon cancer, which are all concentrated around regions of high fat. If scientists can “turn off” FABP4, then they may be able to slow down and isolate each cancer’s metastasis, she added.
Although Singh is optimistic about the potential of the study, she is hesitant about whether the discovery can be translated to human subjects at this point.
“Can we actually cause an FABP4 deficiency in a way that’s meaningful?” Singh said.
However, Ernst Lengyel, a professor of obstetrics/gynecology at the University of Chicago and the lead author of the study, said ongoing diabetes research is attempting to deactivate certain proteins such as FABP4. This research, he said, could possibly help researchers “turn off” FABP4 in cancer cases.
“I think for the first time, we now understand,” Lengyel said. “You cannot treat if you do not understand, and now that we understand, we know what the enemy is.”
