SOURCE: Massachusetts General Hospital, news release, Feb. 12, 2016
FRIDAY, Feb. 19, 2016 (HealthDay News) -- Researchers believe they've unlocked at least one way that obesity may promote the progression of pancreatic and breast cancers.
The finding could eventually lead to preventive treatments for those cancers, and maybe other cancers as well, the researchers said.
"The fact that this new mechanism underlies obesity's impact on two types of cancer suggests that it may be a common mechanism of tumor induction that could apply to other cancer types," said study co-senior author Rakesh Jain. Director of the Laboratory of Tumor Biology at Massachusetts General Hospital in Boston, Jain made his comments in a hospital news release.
More than half of people diagnosed with breast and pancreatic cancers are overweight or obese, the researchers said. Previous studies have linked obesity with an increased risk of death from these and other types of cancer, they added.
However, the reason for the link between obesity and pancreatic and breast cancer was unclear.
In animal and laboratory experiments with cells and patient tumor samples, the researchers identified an association between obesity and high levels of a protein called placental growth factor (PlGF).
They also found that PlGF's binding to its receptor VEGFR-1 promotes tumor progression. VEGFR-1 affects the activity of immune cells within tumors, the study authors said.
The findings suggest that targeting the PlGF/VEGFR-1 pathway might be a way to prevent cancer in obese patients, the researchers said.
However, it's important to note that research in laboratories and with animals doesn't always produce similar results in humans.
"We found that obesity increased infiltration of tumor-promoting immune cells and the growth and metastasis [spread] of pancreatic cancers," said study co-senior author Dr. Dai Fukumura. He's also with the Laboratory of Tumor Biology as well as the department of radiation oncology at Massachusetts General Hospital.
When the researchers blocked VEGFR-1, they saw a shift toward prevention of tumor progression in obese mice for both pancreatic and breast cancer models. But, they didn't see the same prevention in lean mice, Fukumura said.
"We also found that PlGF was present in excess in obesity and that reduction of PlGF produced similar results to VEGFR-1 inhibition in the tumors of obese mice," Fukumura added.
The study was published online recently in the journal Clinical Cancer Research.
The U.S. National Cancer Institute has more on obesity and cancer risk.