Endometrial changes in premenopausal obese women, an at-risk cohort

Authors: Dottino JA, Zhang Q, Loose DS, Fellman BM, Waters MS, McKenzie LJ, Yuan Y, Broaddus RR, Lu KH, Soliman PT, and Yates MS

Category: Early Detection & Risk Prediction
Conference Year: 2020

Abstract Body:
Background: Obesity is a well-known risk factor for endometrial cancer, yet mechanisms of obesity-related carcinogenesis are not well-defined, particularly for premenopausal women. Research has generally focused on obesity-mediated increased cancer risk via imbalance of estrogen/progesterone leading to endometrial proliferation. Despite the substantial increased risk at the population level, most obese women do not develop endometrial cancer. The molecular determinants for development of cancer are unknown for this high-risk cohort. Purpose: The prevalence of endometrial precancers (hyperplasia) was determined in obese premenopausal women. We also sought to evaluate whether obesity mediates changes in endometrial markers associated with altered estrogen/progesterone balance in premenopausal women. Methods: Premenopausal women with BMI ≥30 kg/m2 (n=97) or BMI ≤25 kg/m2 (n=33) were prospectively enrolled in a cross-sectional study, including assessment of serum metabolic markers and timed endometrial biopsy for pathology evaluation and hormone-regulated biomarker analysis. Medical and gynecologic history was obtained. Endometrial biomarkers were also compared by BMI groups in a previous cohort of premenopausal women with inherited cancer risk (Lynch syndrome). Results: Of 97 obese premenopausal women enrolled, one case of complex atypical hyperplasia was identified. In addition to known systemic metabolic changes, normal endometrium from obese women showed decreased expression of estrogen-induced genes (RALDH2, IGF-1, and survivin) compared to non-obese women. In contrast, obese women with Lynch syndrome had increased IGF-1. Obese women with insulin resistance had increased survivin expression. Conclusions: Endometrial markers in obese premenopausal women without inherited risk reflect a progesterone- dominant profile (decreased cancer risk). In describing premenopausal endometrial cancer risk, it may be insufficient to describe obesity alone as a high-risk state and additional risk factors (such as insulin resistance) may be required. However, in Lynch syndrome, endometrial biomarkers suggest that obesity further increases risk. Additional studies are needed to translate population-based observations to individualized risk assessment and prevention strategies.

Keywords: Obesity, endometrial cancer, premenopausal, Lynch syndrome