Ronald L. Chandler

Chromatin remodeling plays an integral part in endometrial homeostasis through its roles in the maintenance of cell identity, epithelial integrity, and prevention of endometrial disease. Chromodomain-helicase-DNA-binding protein 4 (CHD4) is…

Endometriosis, defined as the growth of endometrial-like tissues outside the uterus, is a common disease among women. Numerous in vivo rodent models of endometriosis have been developed to explore multiple aspects of this poorly understood …

In vivo models of endometriosis enable the discovery and preclinical testing of new therapies. Several rodent models of endometriosis exist, but a lack of harmonization impedes reproducibility and comparability of results among investigator…

The aetiology of endometriosis remains poorly understood. In vitro model systems provide the opportunity to identify the mechanisms driving disease pathogenesis using human cells. Three-dimensional models, particularly organoid systems, hav…

Pain is a debilitating symptom of endometriosis, and its mechanisms are often explored using rodent models. However, a lack of harmonization amongst models and behavioural measures, in addition to inconsistent reporting, might limit the ove…

Supplementary Material 1

Supplementary Material 1

Endometrial epithelia are known to harbor cancer driver mutations in the absence of any pathologies, including mutations in PIK3CA. Insulin plays an important role in regulating uterine metabolism during pregnancy, and hyperinsulinemia is a…

Endometriosis is a disease defined by the presence of abnormal endometrium at ectopic sites, causing pain and infertility in 10% of women. Mutations in the chromatin remodeling protein ARID1A (AT-rich interactive domain-containing protein 1…

BACKGROUND: SWI/SNF (BAF) chromatin remodeling complexes regulate lineage-specific enhancer activity by promoting accessibility for diverse DNA-binding factors and chromatin regulators. Additionally, they are known to modulate the function …

A growing body of work suggests epigenetic dysregulation contributes to endometriosis pathophysiology and female infertility. The chromatin remodeling complex subunit AT-rich interaction domain 1A (ARID1A) must be properly expressed to main…

Obesity impacts fertility and is positively correlated with endometrial hyperplasia and endometrial cancer occurrence. Endometrial epithelia often harbor disease driver-mutations, while endometrial stroma are highly regulative of neighborin…

Endometrial cancer (EC) is characterized by high estrogen levels unopposed by progesterone. Treatment with progestins is standard for early EC, but the response to progestins is dependent on progesterone receptor (PGR) expression. Here, we …

Endometriosis affects 1 in 10 women and is characterized by the presence of abnormal endometrium at ectopic sites. ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. To identify epigene…

Although ARID1A mutations are a hallmark feature, mutations in other SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling subunits are also observed in endometrial neoplasms. Here, we interrogated the roles of Brahma/SWI2-related g…

STUDY QUESTION: Is it possible to establish a genetically engineered mouse model (GEMM) of endometriosis that mimics the natural spread of invasive endometrium? SUMMARY ANSWER: Endometriosis occurs in an ARID1A (AT-rich interactive domain-…

ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium. Here we show that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleeding when comb…

Abstract Despite being a deadly disease, debates over the origins of ovarian cancer have persisted for many decades. There is evidence that some tumors may not originate from the ovary, but are the result of cells that have moved to the ova…

Ovarian clear-cell carcinoma (OCCC) is an aggressive form of ovarian cancer with high ARID1A mutation rates. Here we present a mutant mouse model of OCCC. We find that ARID1A inactivation is not sufficient for tumour formation, but requires…