Mouse Amh(Muellerian-inhibiting factor) ELISA Kit

Background: Reproductive factors, including parity, breastfeeding, and contraceptive use, affect lifetime ovulatory cycles and cumulative exposure to gonadotropins and are associated with ovarian cancer. To understand the role of ovulation-regulating hormones in the etiology of ovarian cancer, we prospectively analyzed the association of anti-Mullerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B with ovarian cancer risk. Methods: Our study included 370 women from the Janus Serum Bank, including 54 type I and 82 type II invasive epithelial ovarian cancers, 49 borderline tumors, and 185 age-matched controls. We used conditional logistic regression to assess the relationship between hormones and risk of ovarian cancer overall and by subtype (types I and II). Results: Inhibin B was associated with increased risk of ovarian cancer overall [OR, 1.97; 95% confidence interval (CI), 1.14-3.39; P-trend = 0.05] and with type I ovarian (OR, 3.10; 95% CI, 1.04-9.23; P-trend = 0.06). FSH was not associated with ovarian cancer risk overall, but higher FSH was associated with type II ovarian cancers (OR, 2.78; 95% CI, 1.05-7.38). AMH was not associated with ovarian cancer risk. Conclusions: FSHand inhibin B may be associated with increased risk in different ovarian cancer subtypes, suggesting that gonadotropin exposure may influence risk of ovarian cancer differently across subtypes. Impact: Associations between prospectively collected AMH, FSH, and inhibin B levels with risk of ovarian cancer provide novel insight on the influence of premenopausal markers of ovarian reserve and gonadotropin signaling. Heterogeneity of inhibin B and FSH effects in different tumor types may be informative of tumor etiology.

Background: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. Anti-Mullerian hormone (AMH) is a valid indicator of ovarian function and is used for PCOS diagnosis. Some studies have shown that adipokines affect the synthesis of AMH, and therefore they are somehow related in function. The aim of the present study was to determine the relationship between serum levels of AMH, adiponectin and oxidative stress markers in PCOS patients. Materials and Methods: In this cross-sectional study, PCOS patients and healthy women (80 cases in total) were investigated. Serum levels of AMH, adiponectin, gonadotropins, androgens, total antioxidant capacity (TAC), nitric oxide (NO) and insulin resistance (IR) were measured by standard methods. An independent t test was used to compare the two groups and Pearson correlation coefficient was used to determine the relationship between variables. Results: There was a significant difference between the means of AMH (5.16 +/- 5.3 vs. 2.44 +/- 2.5 ng/mL) (P=0.007) and adiponectin (24.55 +/- 9.41 vs. 30.57 +/- 14.2 mu g/L) (P=0.029) among the PCOS and control groups, respectively. The correlation between AMH and adiponectin in the control group was statistically significant and negative (P=0.028, r=-0.35), while in the PCOS group it was not significant (P=0.11, r=-0.25). Conclusion: Various biochemical and hormonal factors differ between PCOS and healthy women. Different factors can influence AMH and adiponectin levels independently of PCOS in women of reproductive age.