Mikhail Kolonin, Ph.D., talks to GEN about the recent Cancer Research study.

While about a decade of research has suggested a link between obesity and several forms of cancer, a preclinical study published this week has begun to shed light on just how fat progenitor cells may contribute to the deadly disease beyond the effects of diet and exercise.

Researchers from the University of Texas Health Science Center at Houston (UTHealth) found that tumors emit a signal that attracts progenitor cells from white adipose tissue in mouse models of cancer. These cells in turn support the network of blood vessels associated with tumor angiogenesis.

Obese mice had far more of the white adipose tissue stromal progenitor cells than did lean mice. And while both types of mice were fed the same diet, tumors grew much faster in the obese mice than they did on the lean ones.

“The mechanisms are not clear as to why obesity is linked with cancer. We have a partial answer to that now,” Mikhail Kolonin, Ph.D., an associate professor at the Center for Stem Cell & Regenerative Medicine at The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, part of the UTHealth Medical School, told GEN.

Dr. Kolonin is corresponding author for the study, published Monday in Cancer Research. He is also a faculty member of the graduate school and holder of the Jerold B. Katz Distinguished Professorship in Stem Cell Research at UTHealth.

“It is the excess of the adipose tissue that does something to tumors. And what we found out is that cells from fat tissue travel and they help tumors grow,” Dr. Kolonin added.

According to the study, some of the adipose stromal cells developed into fat cells within tumors, while others were incorporated into tumor-associated blood vessels, which support tumor growth by bringing in the oxygen and nutrients needed for cancer cells to survive and proliferate.

While the growth of fat tissue and migration of adipose stromal cells to tumors was shown to be associated with cancer progression, the study cannot answer whether fat tissue cells trigger cancer.

“Obesity is linked to incidence of some cancers and progression of others. We only looked at progression. We didn’t look at risk. We cannot say anything about the risk. It could be that cells from fat tissue are also responsible for cancer risk, but we don’t have the data,” Dr. Kolonin said.

He added the results shouldn’t be read as downplaying the importance of diet and exercise in helping prevent obesity and reduce the risk of certain cancers associated with obesity, such as endometrial, colorectal, and breast cancer.

Future avenues for research, Dr. Kolonin said, include identifying the signals that cause the adipose stromal cells to be recruited into tumors, then finding ways to block them that could serve as future cancer treatments.

“Future research will test whether trafficking of adipose cells that we discovered in animal models is clinically relevant. The relative importance of adipose cell action from within the tumors, as opposed to signaling from distant fat tissue depots, will need to be assessed,” Dr. Kolonin said.

“It will be important to understand the major mechanisms through which obesity drives cancer risk and cancer progression. And then it will be important to come up with therapeutic strategies on how to break these links.”

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