2,248 research outputs found
Serum levels of insulin-like growth factor-I, IGF-binding protein 1 and 3, and insulin and endometrial cancer risk
Relationship Between Plasma Glucose Levels and Malignant Uterine Cervical Neoplasias
Background There is a direct correlation between glycemic load and the risk of developing many malignant neoplasms. Aims The aim of this study was to determine the plasma glucose levels in women with cervical cancer. Methods The study included 177 women with anatomopathologically diagnosed uterine cervical cancer (stages 0–IV) treated between 1980 and 2008 at the Gynecology and Obstetrics outpatient service of the UFTM, Brazil. The plasma glucose levels of all patients were assayed at the time of diagnosis and correlated with tumor staging. Results We statistically compared the plasma glucose levels of group 1 (cervical intraepithelial neoplasia 2–3), group 2 (stage I–II), group 3 (stage III–IV), and group 4 (control group: leiomyomas). Patient groups with poor prognosis (groups 2 and 3) showed significantly higher plasma glucose levels ( P 90 mg/dl showed CIN versus I/II: P = 0.0753; OR = 2.018; (95% CI: 0.9236 to 4.410) and CIN versus III/IV: P = 0.0975; OR = 2.400; (95% CI: 0.8335 to 6.911). Conclusion We observed an association between high plasma glucose levels and cervical cancer cases with poor prognoses. Plasma glucose tests should be routinely used as additional prognostic parameters in patients with cervical neoplasias
Prediction of circulating adipokine levels based on body fat compartments and adipose tissue gene expression
BACKGROUND: Adipokines are hormones secreted from adipose tissue (AT), and a number of them have been established as risk factors for chronic diseases. However, it is not clear whether and to what extent adiposity, gene expression, and other factors determine their circulating levels. OBJECTIVES: To assess to what extent adiposity, as measured by the amount of subcutaneous AT (SAT) and visceral AT (VAT) using magnetic resonance imaging, and gene expression levels in SAT determine plasma concentrations of the adipokines adiponectin, leptin, soluble leptin receptor, resistin, interleukin 6, and fatty acid-binding protein 4 (FABP4). METHODS: We performed a cross-sectional analysis of 156 participants from the EPIC Potsdam cohort study and analyzed multiple regression models and partial correlation coefficients. RESULTS: For leptin and FABP4 concentrations, 81 and 45% variance were explained by SAT mass, VAT mass, and gene expression in SAT in multivariable regression models. For the remaining adipokines, AT mass and gene expression explained <16% variance of plasma concentrations. Gene expression in SAT was a less important predictor compared to AT mass. SAT mass was a better predictor than VAT mass for leptin (partial correlation r = 0.81, 95% confidence interval 0.75–0.86, vs. r = 0.58, 95% confidence interval 0.46–0.67), while differences between AT compartments were small for the other adipokines. CONLUSIONS: While plasma levels of leptin and FABP4 can be explained in a large and medium part by the amount of AT and SAT gene expression, surprisingly, these predictors explained only little variance for all other investigated adipokines
Bone versus breast density
The common link with oestrogen levels suggests that bone mineral density and mammographic density might also be linked. One study found weak support for this, but another study failed to provide confirmation. Overall, the relationship is very weak, if it exists at all. Other factors such as weight-bearing exercise, which have opposing impacts on these variables, may have a more dominant effect
Colorectal cancer: from epidemiology to current treatment
Colorectal cancer (CRC) was the second most frequent cancer in Europe in 2004, responsible for 13% (376,400) of all incident cancer cases. It is also the second most frequent cause of cancer mortality in Europe, with 11.9% (203,700) annual deaths. When localized, CRC is often a curable disease, but the overall prognosis is determined by the extent of local and particularly metastatic tumour spread. The disease outlook is relatively poor, because advanced disease is a significant cause of worldwide cancer-related mortality. Thus, estimated 5-year survival rates range from nearly 90% in stage I disease (Dukes’ A) to less than 10% in patients with metastatic disease (Dukes’ D). Comprehensive cancer care in the 21st century is dependent on a multidisciplinary approach to patients with malignant disease. Large bowel cancer is no exception, as there is increasing clinical trial data supporting multimodal treatment for both localized and advanced tumours. This review will focus on important aspects in CRC including the latest treatment strategies (chemotherapy, radiotherapy and the targeted therapies)
Bias in protein and potassium intake collected with 24-h recalls (EPIC-Soft) is rather comparable across European populations
Purpose: We investigated whether group-level bias of a 24-h recall estimate of protein and potassium intake, as compared to biomarkers, varied across European centers and whether this was influenced by characteristics of individuals or centers. Methods: The combined data from EFCOVAL and EPIC studies included 14 centers from 9 countries (n = 1,841). Dietary data were collected using a computerized 24-h recall (EPIC-Soft). Nitrogen and potassium in 24-h urine collections were used as reference method. Multilevel linear regression analysis was performed, including individual-level (e.g., BMI) and center-level (e.g., food pattern index) variables. Results: For protein intake, no between-center variation in bias was observed in men while it was 5.7% in women. For potassium intake, the between-center variation in bias was 8.9% in men and null in women. BMI was an important factor influencing the biases across centers (p <0.01 in all analyses). In addition, mode of administration (p = 0.06 in women) and day of the week (p = 0.03 in men and p = 0.06 in women) may have influenced the bias in protein intake across centers. After inclusion of these individual variables, between-center variation in bias in protein intake disappeared for women, whereas for potassium, it increased slightly in men (to 9.5%). Center-level variables did not influence the results. Conclusion: The results suggest that group-level bias in protein and potassium (for women) collected with 24-h recalls does not vary across centers and to a certain extent varies for potassium in men. BMI and study design aspects, rather than center-level characteristics, affected the biases across center
Premenopausal endogenous oestrogen levels and breast cancer risk: a meta-analysis.
BACKGROUND: Many of the established risk factors for breast cancer implicate circulating hormone levels in the aetiology of the disease. Increased levels of postmenopausal endogenous oestradiol (E2) have been found to increase the risk of breast cancer, but no such association has been confirmed in premenopausal women. We carried out a meta-analysis to summarise the available evidence in women before the menopause. METHODS: We identified seven prospective studies of premenopausal endogenous E2 and breast cancer risk, including 693 breast cancer cases. From each study we extracted odds ratios of breast cancer between quantiles of endogenous E2, or for unit or s.d. increases in (log transformed) E2, or (where odds ratios were unavailable) summary statistics for the distributions of E2 in breast cancer cases and unaffected controls. Estimates for a doubling of endogenous E2 were obtained from these extracted estimates, and random-effect meta-analysis was used to obtain a pooled estimate across the studies. RESULTS: Overall, we found weak evidence of a positive association between circulating E2 levels and the risk of breast cancer, with a doubling of E2 associated with an odds ratio of 1.10 (95% CI: 0.96, 1.27). CONCLUSION: Our findings are consistent with the hypothesis of a positive association between premenopausal endogenous E2 and breast cancer risk
Promoting Effects of Sucrose-rich Diet on N-Nitrosobis (2-oxopropyl) amine-induced Pancreatic Carcinogenesis in Hamsters
It has been reported that there is an association between pancreatic cancer
and obesity, impaired glucose metabolism and diabetes based on excess
dietary fat and sugar intakes. A number of studies have suggested that a
high-fat diet increases development of carcinomas in various organs and
possible risk factors for pancreatic cancer. However, how an excess sugar
intake promotes pancreatic carcinogenesis is still unknown. In the present
study, we investigated the influence of an excess sugar intake on
pancreatic carcinogenesis by administration of a sucrose-rich diet in which
starch was replaced by sucrose in order to contain the same calories and
other nutrients. Two similar experiments were performed. Six-week-old male
Syrian golden hamsters were given N-nitrosobis (2-oxopropyl) amine (BOP) at
a dose of 50 and 20 mg/kg body weight as a carcinogen in Week 0 and 1,
respectively. In Week 2, the animals were divided into control and
experimental groups. In experiment 1, 15 animals received a control diet or
sucrose-rich diet in which 100% of the starch was replaced by sucrose,
respectively. Since five animals fed on the sucrose-rich diet died by Week
12, the diet was changed to a sucrose-rich diet in which 50% of the starch
was replaced by sucrose. In experiment 2, 15 animals received a control
diet or sucrose-rich diet in which 50 or 20% of the starch was replaced by
sucrose, respectively. All animals were sacrificed 25 weeks after the start
of the experiment, and histological examination of the pancreas was
performed. No significant difference was seen in the body weight at the end
of the experiment. There were no significant differences in the
glycosylated hemoglobin (HbA1c) and serum triglyceride, total cholesterol
and HDL-cholesterol levels between the control and sucrose-rich diet groups
in experiments 1 and 2. The incidence and number of carcinomas increased in
hamsters fed the sucrose-rich diet compared with the control diet in
experiments 1 and 2. These results suggest that an excess sucrose intake
may promote the development of pancreatic cancer in hamsters
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