SAN FRANCISCO, July 8 (UPI) -- Low levels of inflammation, called parainflammation, play an early role in the development of cancer, including increased mortality in some forms of the disease, researchers in California report in a new study.
Recognizing parainflammation could help identify the potential for cancer earlier, as well as find the patients most likely to respond well to the anti-inflammatory aspirin, say researchers at the University of California San Francisco.
Aspirin and other non-steroidal anti-inflammatory drugs have been shown in previous studies to reduce the risk of colorectal cancer, breast cancer and some others, though the effect wasn't clearly understood because these cancers often show little to no signs of inflammation.
The same group of UCSF researchers has previously found non-immune cells could activate cellular pathways used by the immune system to induce low levels of inflammation.
The inflammation can often be controlled by the protein p53, a regulator of cellular division credited with better cancer prognosis when found in tumors. When the protein is mutated, however, parainflammation becomes dangerous and can lead to the development of cancer.
In a large review of patient data, UCSF researchers found higher levels of p53 mutation is linked to higher levels parainflammation, which is present faster-growing cancers such as those of the pancreas and bladder.
"This paper shows how years of research data can be reused to study cancer immunology, one of the newest areas of cancer therapeutics," Dr. Atul Butte, director of the Institute for Computational Health Sciences at the University of California San Francisco, said in a press release. "More importantly, it shows the benefits of our efforts to connect research models of cancer, like cell lines and mouse models, with actual cancer therapy in humans, which remains a major challenge in cancer immunology."
For the study, published in the journal Genome Biology, researchers reviewed data on 6,523 tumors in 18 types of cancer collected as part of the Cancer Genome Atlas, finding higher levels of parainflammation was linked to higher levels of mutated p53.
The data review showed NSAIDs lowered parainflammation in mouse intestinal tumors and human cancer cell lines of oral, pancreatic and colorectal cancers, which the researchers say could help predict patients most likely to respond to aspirin or other NSAID treatment.
"Understanding the initial triggers of tumor formation is one of the main challenges in cancer research," said Dr. Dvir Aran, a postdoctoral scholar at the University of California San Francisco. "We think parainflammation could be a big part of this puzzle."