Racial and ethnic disparities in women's health have existed for decades, despite efforts to strengthen women's reproductive health access and utilization. Recent guidance by the American College of Obstetricians and Gynecologists (ACOG) underscores the often unacknowledged and unmeasured role of racial bias and systemic racial injustice in reproductive health disparities and highlights a renewed commitment to eliminating them. Reaching health equity requires an understanding of current racial–ethnic gaps in reproductive health and a concerted effort to develop and implement strategies to close gaps. We summarized national data for several reproductive health measures, such as contraceptive use, Pap tests, mammograms, maternal mortality, and unintended pregnancies, by race–ethnicity to inform health-equity strategies. Studies were retrieved by systematically searching the PubMed (2010–2020) electronic database to identify most recently published national estimates by race–ethnicity (non-Hispanic Black or African American, Hispanic or Latinx, and non-Hispanic White women). Disparities were found in each reproductive health category. We describe relevant components of the Affordable Care Act (ACA) and the Preventing Maternal Deaths Act, which can help to further strengthen reproductive health care, close gaps in services and outcomes, and decrease racial–ethnic reproductive health disparities. Owing to continued diminishment of certain components of the ACA, to optimally reach reproductive health equity, comprehensive health insurance coverage is vital. Strengthening policy-level strategies, along with ACOG's heightened commitment to eliminating racial disparities in women's health by confronting bias and racism, can strengthen actions toward reproductive health equity.

Tumor markers are important tools for early diagnosis, prognosis, therapy response and endometrial cancer monitoring. A large number of molecular and pathologic markers have been described in types I and II endometrial cancers, which has served to define the main oncogenic, epidemiological, genetic, clinical and histopathological features. Ongoing attempts to stratify biological markers of endometrial cancer are presented. However, data on changes in tumor marker profiles in obesity-related endometrial cancer are scarce. Obesity is a pandemic in Western countries that has an important impact on endometrial cancers, albeit through not very well-defined mechanisms. Although endometrial cancer is more common in Caucasian women, higher mortality is found in African Americans who also show higher incidence of obesity. Here, we describe how obesity signals (estrogen, leptin, leptin induced-molecules, Notch; cytokines and growth factors) could affect endometrial cancer. Leptin signaling and its crosstalk may be associated to the more aggressive and poor prognosis type II endometrial cancer, which affects more postmenopausal and African-American women. In this regard, studies on expression of novel molecular markers (Notch, interleukin-1 and leptin crosstalk outcome) may provide essential clues for detection, prevention, treatment and prognosis.

Objective The expression of NILCO molecules (Notch, IL-1, and leptin crosstalk outcome) and the association with obesity were investigated in types I and II endometrial cancer (EmCa). Additionally, the involvement of NILCO in leptin-induced invasiveness of EmCa cells was investigated. Methods The expression of NILCO mRNAs and proteins were analyzed in EmCa from African-American (n = 29) and Chinese patients (tissue array, n = 120 cases). The role of NILCO in leptin-induced invasion of Ishikawa and An3ca EmCa cells was investigated using Notch, IL-1, and leptin signaling inhibitors. Results NILCO molecules were expressed higher in type II EmCa, regardless of ethnic background or obesity status of patients. NILCO proteins were mainly localized in the cellular membrane and cytoplasm of type II EmCa. Additionally, EmCa from obese African-American patients showed higher levels of NILCO molecules than EmCa from lean patients. Notably, leptin-induced EmCa cell invasion was abrogated by NILCO inhibitors. Conclusion Type II EmCa expressed higher NILCO molecules, which may suggest it is involved in the progression of the more aggressive EmCa phenotype. Obesity was associated with higher expression of NILCO molecules in EmCa. Leptin-induced cell invasion was dependent on NILCO. Hence, NILCO might be involved in tumor progression and could represent a new target/biomarker for type II EmCa.

HighlightsAggressive course and treatment resistance characterize ectopic human chorionic gonadotropin.Recurrence of endometrial cancer with ectopic hCG was treated with brachytherapy and EMACO.The serum hCG level can serve as a marker in tumors with ectopic hCG expression.