Morbidly obese women with and without endometrial cancer: Are there differences in measured physical fitness, body composition, or hormones?

Modesitt, Susan C.; Geffel, Dyanna L.; Via, Jennifer; Weltman, Arthur

doi:10.1016/j.ygyno.2011.11.013

Cited by 29 publications

(41 citation statements)

References 57 publications

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“…Two other European studies have also identified a low serum adiponectin level as an independent risk factor for carcinogenesis, after adjusting for other confounding factors such as age and BMI (Dal Maso et al 2004, Cust et al 2007). On the other hand, a conflicting result was reported in a recent pilot study, where authors did not observe a significant difference between patients with and without endometrial cancer in terms of serum adiponectin levels (Modesitt et al 2012). Regardless, comparison of patients with endometrial cancer and those with benign endometrial conditions in our study revealed cancer patients to have significantly lower serum adiponectin levels (4.09 vs 17.13; P!0.0001), higher HOMA-IR values (2.93 vs 1.27; P!0.0001), as an indicator of insulin resistance, and lower QUICKI values (0.33 vs 0.37; P!0.0001), as an estimate of insulin sensitivity.…”

Section: Discussionmentioning

confidence: 85%

“…In a case-control study from Japan, investigators managed to demonstrate a significant correlation between adiponectin and HOMA-IR, but not with FINS (Ashizawa et al 2010). Recently, Modesitt et al (2012) did not observe any difference between patients with and without cancer in terms of insulin levels. We did not encounter any study in the English literature in which HOMA-IR and QUICKI were evaluated in patients with endometrial cancer.…”

Section: Discussionmentioning

confidence: 98%

“…Four hormonal mechanisms have been postulated; increased estrogen levels via conversion of circulating androgens in peripheral adipocytes, increased adrenal and ovarian secretion of androgens, increased free steroid hormone levels secondary to decreased sex hormone binding globulin production, and decreased progesterone production in premenopausal women secondary to decreased ovulation (Modesitt et al 2012). It remains a fact that not all obese women develop endometrial cancer, and not all patients with endometrial cancer are obese (Modesitt et al 2012). The role of other confounding factors in the carcinogenesis of endometrial cancer is currently under investigation.…”

Section: Discussionmentioning

confidence: 99%

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Evaluating vaspin and adiponectin in postmenopausal women with endometrial cancer

Erdoğan

Sezer

Başer

et al. 2013

Endocrine-Related Cancer

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Insulin resistance is a well-documented risk factor for the development of endometrial cancer. Adiponectin and vaspin are insulin-sensitizing proteins that are secreted from adipose tissue. A clear association between serum levels of adipokines and endometrial cancer has yet to be established. The study group consisted of postmenopausal women with confirmed endometrial cancer, whereas patients with benign endometrial conditions constituted the control group. The two groups were compared in terms of insulin resistance and serum levels of adiponectin and vaspin. A total of 60 patients with confirmed endometrial cancer and 70 controls with benign endometrial conditions (polyps and atrophy) were enrolled. Median homeostasis model assessment of insulin resistance value was significantly higher in the study group compared with the control group (2.93 vs 1.27, P!0.0001), whereas mean quantitative insulin sensitivity check index value was significantly lower (0.33G0.02 vs 0.37G0.37, P!0.0001). Median values for both adiponectin and vaspin were significantly lower in patients with endometrial cancer compared with the control group (4.09 vs 17.13 mg/ml, P!0.0001 and 0.21 vs 0.39 ng/ml, P!0.0001 respectively). Low levels of both adiponectin and vaspin were found to be significantly associated with an increased risk for endometrial cancer. Following adjustment for confounding factors, the respective odds ratios for endometrial cancer in patients in the first tertile compared with those in the third tertile were 10.80 (2.76-42.24; PZ0.001) and 13.23 (2.94-59.64; PZ0.001). Our results show that lower levels of circulating adiponectin and vaspin levels are associated with an increased risk of developing endometrial cancer.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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Evaluating vaspin and adiponectin in postmenopausal women with endometrial cancer

Erdoğan

Sezer

Başer

et al. 2013

Endocrine-Related Cancer

View full text Add to dashboard Cite

show abstract

“…After checking the abstracts, 94 articles were firstly excluded because they were obvious irrelevant studies, reviews, or case reports. The left 11 articles were further evaluated by full-text, and five studies were excluded including 4 studies without usable data [24,25,26,27] and one study without relevant exposure [28]. Finally, 6 articles with a total of 3136 individuals were finally included into the meta-analysis [13,14,15,16,17].…”

Section: Resultsmentioning

confidence: 99%

High Leptin Level is an Independent Risk Factor of Endometrial Cancer: A Meta-Analysis

Wang

et al. 2014

Cell Physiol Biochem

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Background/Aims: Previous studies suggested that high leptin level might increase risk of endometrial cancer, but available data were conflicting and whether high leptin level was an independent risk factor of endometrial cancer was still unclear. Therefore, a meta-analysis was performed to assess whether high leptin level was an independent risk factor of endometrial cancer. Methods: PubMed, Web of Science, and Embase databases were searched for epidemiological studies published up to June 26, 2014. The pooled risk ratio (RR) with 95% confidence interval (95%CI) was used to assess the association between leptin level and risk of endometrial cancer. Results: Six studies with a total of 3136 individuals were finally included into the meta-analysis. Meta-analysis of total 6 studies showed that high leptin level was associated with increased risk of endometrial cancer (RR = 2.55, 95%CI 1.91-3.41, P < 0.001). After adjusting for confounding factors, high leptin level was also associated with increased risk of endometrial cancer (RR =1.59, 95%CI 1.27-1.98, P < 0.001). Sensitivity analysis proved the stability of the pooled estimates. The RR of endometrial cancer was 1.10 (95%CI, 1.03-1.18, P = 0.005) per 5 ng/mL increment in leptin levels. There was no obvious risk of publication bias (P Egger = 0.54). Conclusion: Our findings suggest that high leptin level is an independent risk factor of endometrial cancer. More prospective studies are needed to further confirm the association in the future.

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“…In our previous study comparing obese women with and without type I endometrial cancer, circulating glucose levels were higher in women with cancer (119.5 vs. 90.7 mg/dL for noncancer; P ¼ 0.049). However, other cancer-related parameters including estrogen and insulin were not significantly elevated in obese women with cancer (10). These findings suggested that, independent of adiposity and its associated hormonal changes, increased blood glucose levels may play an important role in the growth and/or development of type I endometrial cancer.…”

Section: Introductionmentioning

confidence: 82%

Metabolic Vulnerabilities in Endometrial Cancer

et al. 2014

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Women with metabolic disorders, including obesity and diabetes, have an increased risk of developing endometrial cancer. However, the metabolism of endometrial tumors themselves has been largely understudied. Comparing human endometrial tumors and cells with their nonmalignant counterparts, we found that upregulation of the glucose transporter GLUT6 was more closely associated with the cancer phenotype than other hallmark cancer genes, including hexokinase 2 and pyruvate kinase M2. Importantly, suppression of GLUT6 expression inhibited glycolysis and survival of endometrial cancer cells. Glycolysis and lipogenesis were also highly coupled with the cancer phenotype in patient samples and cells. To test whether targeting endometrial cancer metabolism could be exploited as a therapeutic strategy, we screened a panel of compounds known to target diverse metabolic pathways in endometrial cells. We identified that the glycolytic inhibitor, 3-bromopyruvate, is a powerful antagonist of lipogenesis through pyruvylation of CoA. We also provide evidence that 3-bromopyruvate promotes cell death via a necrotic mechanism that does not involve reactive oxygen species and that 3-bromopyruvate impaired the growth of endometrial cancer xenografts Cancer Res; 74(20); 5832-45. Ó2014 AACR.

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Morbidly obese women with and without endometrial cancer: Are there differences in measured physical fitness, body composition, or hormones?

Cited by 29 publications

References 57 publications

Evaluating vaspin and adiponectin in postmenopausal women with endometrial cancer

Evaluating vaspin and adiponectin in postmenopausal women with endometrial cancer

High Leptin Level is an Independent Risk Factor of Endometrial Cancer: A Meta-Analysis

Metabolic Vulnerabilities in Endometrial Cancer

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