Prevalence of Endometrial Abnormalities In Obese Women

NCT00500591UNKNOWNOBSERVATIONAL

Summary

Key Facts

Lead Sponsor

M.D. Anderson Cancer Center

Enrollment

200

Start Date

2004-06-01

Completion Date

2021-06-01

Study Type

OBSERVATIONAL

Official Title

Prevalence of Endometrial Abnormalities In Obese Women

Interventions

Questionnaire

Conditions

Obesity

Eligibility

Age Range

30 Years – 55 Years

Sex

FEMALE

Inclusion Criteria:

1. Patients must have a measured BMI greater than or equal to 30 kg/m2 (obese) or less than or equal to 25 kg/m2 (lean) at the time of enrollment.
2. Patients must be between the ages of 30 and 55 years old at the time of enrollment.
3. Patients must not have taken any birth control (including pills, patch, injectables) for at least three months prior to enrollment.
4. Patients may not be pregnant at the time of enrollment (defined by negative urine pregnancy test).
5. Patients must have signed an informed consent indicating they are aware of the investigational nature of this study.
6. Patients with a history of non-metastatic cancer may be included if they have not undergone cancer treatment for at least six months prior to enrollment.

Exclusion Criteria:

1. Patients who have had a prior hysterectomy.
2. Patients who are pregnant or have a positive pregnancy test.
3. Patients with a prior history of endometrial hyperplasia or endometrial cancer.
4. Patients who are currently on birth control (including pills, patch, or injectable birth control).
5. Patients who are postmenopausal (have not had a menstrual cycle in greater than or equal to one year).
6. Patients who have ever been on selective estrogen receptor modulators (SERMs) in the past including Tamoxifen and Raloxifene.
7. Patients with a history of metastatic cancer (any type).
8. Patients with a history of non-metastatic cancer who are currently undergoing therapy for that cancer or who have received therapy within six months of enrollment.
9. Patients with a history of non-metastatic cancer who have received any type of hormonal therapy including but not limited to aromatase inhibitors, GNRH-agonists, and Zoladex.
10. Patients who have had prior radiation to the pelvis.
11. Patients with psychiatric disorders that would interfere with consent.

Outcome Measures

Primary Outcomes

Prevalence of Endometrial Abnormalities in Obese and Lean Women

Time frame: 6 Years

Locations

University of Texas MD Anderson Cancer Center, Houston, United States

Linked Papers

2020-08-21

Endometrial biomarkers in premenopausal women with obesity: an at-risk cohort

Obesity is a well-known risk factor for endometrial cancer, but the mechanisms of obesity-related carcinogenesis are not well defined, particularly for premenopausal women. With the continuing obesity epidemic, increases in the incidence of endometrial cancer and a younger age of diagnosis are often attributed to a hyperestrogenic state created by hormone production in adipose tissue, but significant knowledge gaps remain. The balance of estrogen-responsive signals has not been defined in the endometrium of premenopausal women with obesity, where obesity may not create hyperestrogenism in the context of ovaries being the primary source of estrogen production. Obesity is associated with a state of low-grade, chronic inflammation that can promote tumorigenesis, and it is also known that hormonal changes alter the immune microenvironment of the endometrium. However, limited research has been conducted on endometrial immune-response changes in women who have an increased risk for cancer due to obesity. Endometrial estrogen-regulated biomarkers, previously shown to be dysregulated in endometrial cancer, were evaluated in a cohort of premenopausal women to determine if obesity is associated with differences in the biomarker expression levels, which might reflect an altered risk of developing cancer. The expression of a multiplexed panel of immune-related genes was also evaluated for expression differences related to obesity. Premenopausal women with a body mass index of ≥30 kg/m In addition to known systemic metabolic differences, histologically normal endometria from women with obesity showed a decrease in gene expression of progesterone receptor (P=.0027) and the estrogen-induced genes retinaldehyde dehydrogenase 2 (P=.008), insulin-like growth factor 1 (P=.016), and survivin (P=.042) when compared with women without obesity. The endometrial biomarkers insulin-like growth factor 1, survivin, and progesterone receptor remained statistically significant in multivariate linear regression models. In contrast, women with obesity and Lynch syndrome had an increased expression of insulin-like growth factor 1 (P=.017). There were no differences in endometrial proliferation, and limited endometrial immune differences were observed. When comparing premenopausal women with and without obesity in the absence of endometrial pathology or an inherited cancer risk, the expression of the endometrial biomarkers does not reflect a local hyperestrogenic environment, but it instead reflects a decreased cancer risk profile that may be indicative of a compensated state. In describing premenopausal endometrial cancer risk, it may be insufficient to attribute a high-risk state to obesity alone; further studies are warranted to evaluate individualized biomarker profiles for differences in the hormone-responsive signals or immune response. In patients with Lynch syndrome, the endometrial biomarker profile suggests that obesity further increases the risk of developing cancer.

Linked Investigators