Inflammation of the endometrium.

The results led to the hypothesis that an unfavorable adipokines profile with a reduction of adipokines with anti-inflammatory or anti-tumor activity could provide a comprehensive insight into the understanding of the molecular mechanisms involved in carcinogenesis related to obesity. This can provide the specific targets that are involved in those mechanisms whereby obesity leads to tumor progression. In conclusion, in obese subjects may become useful to follow a path to preventing cancer and its progression reduction plan to stop the inflammatory cascade, improve insulin sensitivity and contrast the factors that induce hypoxia.

Inflammation and endometrial cancer: a hypothesis.

(2005) Inflammation and endometrial cancer: a hypothesis

Obesity, inflammatory markers, and endometrial cancer …

Chronic inflammation may play an etiologic role in ovarian and endometrial cancer, and it is hypothesized that nonsteroidal anti-inflammatory drugs (NSAIDs) decrease the risk of developing these malignancies. No prospective study with a large multiethnic population has explored this hypothesis.

Obesity, inflammatory markers, and endometrial cancer risk: ..

Chronic inflammation has been postulated to contribute to ovarian and endometrial carcinogenesis through various pathophysiological pathways (–). Chronic inflammation, including elevations in cytokines, prostaglandins and cyclooxygenase (COX) with concomitant oxidative stress, induces rapid cell division and DNA damage which increase the risk of malignancy (). Specific exposures, such as perineal talc use or medical conditions associated with inflammation, including endometriosis and pelvic inflammatory disease, have been reported to increase ovarian cancer risk (–). Elevated serum levels of C-reactive protein, a biological marker of chronic systemic inflammation, has likewise been associated with increased risk of ovarian and endometrial cancers (–). These epidemiologic observations are supported by in vitro studies showing that aspirin and other analgesic drugs with anti-inflammatory properties inhibit tumor growth and induce apoptosis in ovarian and endometrial cancer cell lines (–).

15/04/2013 · Inflammation and endometrial cancer: a hypothesis, ..
A prospective study of inflammation markers and endometrial cancer risk in …

Program | 12th Congress of the European Society of …

We did not collect information on the reason for NSAID use. The most common reason for use of non-prescription NSAIDs is relief of pain (). To reduce the influence of reverse causation, we excluded the first year of follow-up among all participants to ensure the prospective nature of our exposure. As expected given the large number of early-stage tumors in our study, results remained similar to the main analyses. We also were concerned about aspirin use taken for cardiovascular health benefits because inflammation is a key factor in cardiovascular health (), and thus aspirin use for secondary prevention of cardiovascular disease might obscure a protective association with endometrial cancer risk. In analyses restricted to individuals without a self-reported history of heart disease, hypertension, or diabetes, results generally were similar to the main analyses.

assessed the relationship between inflammation factors and endometrial cancer

Body Fatness and Cancer — Viewpoint of the IARC Working Group

Although the genetics of endometrial cancer are poorly understood, its heritability of approximately 0.5 indicates that there is a strong genetic component for disease risk (, ). A number of lines of experimental and epidemiological evidence have indicated that inflammation may play an important role in the transition from normal endometrium to malignancy. Of the many risk factors associated with endometrial cancer, several -- including use of unopposed estrogen (), anovulation (), endometriosis (), early age at menarche (), late age at menopause (), nulliparity (, ), polycystic ovary syndrome (PCOS) (), and obesity () -- may contribute to a state of prolonged exposure to inflammation (). Chronic inflammation can result in derangement of cellular processes, leading to excessive mitosis, decreased apoptosis, the accumulation of DNA damage, and thus initiate and promote neoplastic transformation (, ). Given that inflammatory process are influenced by inflammation-related genes, we hypothesized that common genetic polymorphisms in inflammatory pathway genes may also influence the risk of endometrial cancer.

Ness RB, Chen C, Weiss NS: Inflammation and endometrial cancer: a hypothesis.

A R T I C L E Aspirin, brain, and cancer

Actions of inflammatory triad. Obesity causes chronic silent inflammation with subsequent increased secretion of inflammatory triad cytokines and decreased production of adiponectin that make unable adipose tissue to store the surplus of free fatty acids contributing to a development of insulin resistance, type 2 diabetes, and obesity-related cardiovascular disease. The mitogenic and anti-apoptotic environment caused by elevated levels of insulin in obesity accelerates the stepwise accumulation of mutations and, hence, favor carcinogenesis. TNF-a, IL-6 and IL-1 signaling, enhancing carcinogenesis by increasing cell proliferation and neoangiogenic cell properties. In addition, the inflammatory enhancing expression of VEGF, ICAM-1 and VCAM-1 by endothelial cells.