Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 15-20% of the employees in Europe and in the USA are engaged in shift work that involves night work. Some experimental and observational data indicate that this type of work might lead to circadian disruption, including disruption in the melatonin synthesis - a hormone of anticarcinogenic and antioxidative properties. A hypothesis that there is a potential link between exposure to light at night and the risk of breast cancer was formulated for the first time by Stevens in 1987. Since then, relatively few epidemiological studies have been carried out in this area (15 studies including 8 cohort and 7 case-control studies). All of them are reviewed in this article. The majority of the epidemiological studies performed to date have focused on the association between shift work and breast cancer risk, few studies have reported an increased risk of other cancers, including colorectal cancer, endometrial cancer, prostate cancer and non-Hodgkin's lymphoma. In six out of ten studies, a statistically significant association between night shift work and risk of breast cancer has been shown (OR = 2.2; 95% CI: 1.1-4.5 in nurses in Norway with > 30 years of night shift work). The increased cancer risk has been reported in nurses, radio-telephone operators, flight attendants, and women employed in the enterprises, in which 60% of employees work at night. Most of the analyses have been based on the data from the registries, with limited potential for the exposure assessment and confounders adjustment. Although some epidemiological studies suggest an increased risk of breast cancer among nurses, we are still far from drawing final conclusions. Therefore, further epidemiological studies are warranted.
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PMID:[Night shift work and cancer risk: a literature review]. 2187 Apr 22

Overweight and obese individuals frequently restrict caloric intake to lose weight. The resultant weight loss, however, typically is followed by an equal or greater weight gain, a phenomenon called weight cycling. Most attention to weight cycling has focused on identifying its detrimental effects, but preclinical experiments indicating that intermittent caloric restriction or fasting can reduce cancer risk have raised interest in potential benefits of weight cycling. Although hypothesized adverse effects of weight cycling on energy metabolism remain largely unsubstantiated, there is also a lack of epidemiologic evidence that intentional weight loss followed by regain of weight affects chronic-disease risk. In the limited studies of weight cycling and cancer, no independent effect on postmenopausal breast cancer but a modest enhancement of risk for renal cell carcinoma, endometrial cancer, and non-Hodgkin's lymphoma have been reported. An effect of either intermittent caloric restriction or fasting in protecting against cancer is not supported by the majority of rodent carcinogenesis experiments. Collectively, the data argue against weight cycling and indicate that the objective of energy balance-based approaches to reduce cancer risk should be to strive to prevent adult weight gain and maintain body weight within the normal range defined by body mass index.
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PMID:Weight cycling and cancer: weighing the evidence of intermittent caloric restriction and cancer risk. 2198 73

In recent years, rapidly accumulating evidence implicates forkhead box C1 (FOXC1) in cancer, especially in studies of basal-like breast cancer (BLBC). Other studies have followed suit, demonstrating that FOXC1 is not only a major player in this breast cancer subtype, but also in hepatocellular carcinoma (HCC), endometrial cancer, Hodgkin's lymphoma (HL), and non-Hodgkin's lymphoma (NHL). The FOXC1 gene encodes a transcription factor that is crucial to mesodermal, neural crest, and ocular development, and mutations found in FOXC1 have been found to cause dominantly inherited Axenfeld-Rieger Syndrome (ARS). Interestingly, while FOXC1 missense mutations that are associated with ARS usually reduce gene activity, increased FOXC1 function now appears to be often linked to more aggressive cancer phenotypes in BLBC, HCC, HL, and NHL. This review discusses not only the role of FOXC1 in cancer cell progression, proliferation, differentiation, and metastasis, but also the underlying mechanisms of how FOXC1 can contribute to aggressive cancer phenotypes.
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PMID:FOXC1, the new player in the cancer sandbox. 2948 24


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