“UCLA researchers have discovered that the Chinese practice of tai chi can reduce inflammation in people who have had breast cancer, thereby reducing a risk factor for the recurrence of the cancer.
“Current research indicates that women diagnosed with breast cancer in the past 10 years are three times more likely to suffer from lack of sleep. Insomnia can lead to increases in inflammation, which places breast cancer survivors at risk for cancer recurrence as well as cardiovascular disease.
“Led by UCLA Jonsson Comprehensive Cancer Center member Dr. Michael Irwin, researchers conducted a five-year randomized clinical trial from April 2007 to August 2013. His team analyzed blood samples from 90 participants between 30 to 85 years old, before and after they started the tai chi routine.
” ‘When people practice tai chi, there is a decrease in the stress hormones produced by the sympathetic nervous system,’ said Irwin, who is professor of psychiatry and biobehavioral sciences at UCLA.
“Irwin and his colleagues also discovered that tai chi relaxes the body to a certain point that it can reduce inflammation, which is commonly seen in most breast cancer survivors after treatment.”
“Men who show signs of chronic inflammation in non-cancerous prostate tissue may have nearly twice the risk of actually having prostate cancer than those with no inflammation, according to results of a new study. The link between persistent inflammation and cancer was even stronger for men with so-called high-grade prostate cancer — those with a Gleason score between 7 and 10 — indicating the presence of the most aggressive and rapidly growing prostate cancers.”
“Men with early stage prostate cancer who ate a low-fat diet supplemented with fish oil had lower amounts of proinflammation molecules in their blood and lower prostate tumor cell proliferation compared with men who ate a high-fat Western diet. Men on the low-fat fish oil diet had lower serum levels of omega-6 fatty acids and high levels of serum omega-3 fatty acids compared with the prostate cancer patients who consumed a Western diet. The experimental group also had lower levels of the proinflammatory eicosanoid 15(S)-hydroxyeicosatetraenoic acid, or 15(S)-HETE, which has been previously shown to be associated with cancer. The decline in mean 15(S)-HETE was 7.2% in the low-fat diet group compared with 24.7% in the high-fat diet group (P = .02). The men in the low-fat diet group also had a lower cell cycle progression score, a marker for the aggressiveness of a cancer.”
Increased inflammation may be a warning of elevated lung cancer risk. A recent study analyzed blood samples taken from over 1,000 patients getting screened for lung cancer. Half of the patients went on to develop lung cancer in the following years. Eleven chemical markers of inflammation in the patients’ blood were associated with an increased risk of developing lung cancer. The researchers developed an inflammation score based on the levels of four of these inflammation markers. Patients with the highest inflammation score were 2.8 times more likely to develop lung cancer than those with the lowest score (3.4 times more likely if the patients were current smokers). This inflammation score may therefore serve to identify high-risk patients in the future.
“Doctors at the North Shore-LIJ Health System have discovered that increased inflammation in the prostate may predict reduced risk for prostate cancer. The findings are published online in Cancer. Prostate cancer is one of the most common cancers in men, with an estimated 240,000 new cases diagnosed every year–it kills approximately 30,000 men annually. The prostate is a small gland that produces fluid that nourishes and transports sperm. When the cancer is detected early while still confined to the prostate gland, there is a much better chance of successful treatment–according to the American Cancer Society, a 5-year relative survival rate is 100% when prostate cancer is detected early and there is no sign that the cancer has spread outside of the prostate. Previous studies have found that chronic inflammation contributes to several forms of cancer–an estimated 20% of adult cancers can be attributed to chronic inflammatory conditions. To evaluate if inflammation in the prostate increases the risk of cancer in the gland, Daniel Moreira, MD, a urologist at the North Shore-LIJ Health System, and his colleagues conducted a clinical trial.”
“Men with prostate cancer who ate a low-fat diet and took fish oil supplements had lower levels of pro-inflammatory substances in their blood and a lower cell cycle progression score, a measure used to predict cancer recurrence, than men who ate a typical Western diet, UCLA researchers found. The findings are important because lowering the cell cycle progression (CCP) score may help prevent prostate cancers from becoming more aggressive, said study lead author William Aronson, a clinical professor of urology at UCLA and chief of urologic oncology at the West Los Angeles Veterans Affairs Medical Center.”
While inflammation is part of the normal immune response, chronic inflammation is linked to many diseases, including cancer. Now, new research shows that white blood cells near non-small cell lung cancers have high levels of a protein that amplifies inflammation. Called TREM-1, this protein is not found in white blood cells from normal lung tissue. These findings were presented at the 2013 meeting of the American College of Chest Physicians. TREM-1 has also been linked to liver cancer and some breast cancers; researchers suspect that this protein helps tumor cells invade tissue and spread to other parts of the body. In addition, recent research shows that TREM-1 can be inhibited with prostaglandins, which are antiinflammatory biomolecules that promote healing.
Stewart CA, Metheny H, Iida N, Smith L, et al. The Journal of Clinical Investigation. Oct 8, 2013.
“The capacity of IL-10 and Tregs in the inflammatory tumor microenvironment to impair anticancer Th1 immunity makes them attractive targets for cancer immunotherapy. IL-10 and Tregs also suppress Th17 activity, which is associated with poor prognosis in several cancers. However, previous studies have overlooked their potential contribution to the regulation of pathogenic cancer-associated inflammation. In this study, we investigated the origin and function of IL-10–producing cells in the tumor microenvironment using transplantable tumor models in mice. The majority of tumor-associated IL-10 was produced by an activated Treg population. IL-10 production by Tregs was required to restrain Th17-type inflammation. Accumulation of activated IL-10+ Tregs in the tumor required type I IFN signaling but not inflammatory signaling pathways that depend on TLR adapter protein MyD88 or IL-12 family cytokines. IL-10 production limited Th17 cell numbers in both spleen and tumor. However, type I IFN was required to limit Th17 cells specifically in the tumor microenvironment, reflecting selective control of tumor-associated Tregs by type I IFN. Thus, the interplay of type I IFN, Tregs, and IL-10 is required to negatively regulate Th17 inflammation in the tumor microenvironment. Therapeutic interference of this network could therefore have the undesirable consequence of promoting Th17 inflammation and cancer growth.”
Akbay EA, Koyama S, Carretero J, Altabef A, et al. Cancer Discovery. Sept 27, 2013.
The success in lung cancer therapy with Programmed Death (PD)-1 blockade suggests that immune escape mechanisms contribute to lung tumor pathogenesis. We identified a correlation between Epidermal Growth Factor Receptor (EGFR) pathway activation and a signature of immunosuppression manifested by upregulation of PD-1, PD-L1, cytotoxic T lymphocyte antigen-4 (CTLA-4), and multiple tumor-promoting inflammatory cytokines. Our data suggest that oncogenic EGFR signaling remodels the tumor microenvironment to trigger immune escape, and mechanistically link treatment response to PD-1 inhibition.