Field cancerization in endometrial carcinoma

As increasing amounts of data highlighting the importance of the cancer "field" in regard to tumorigenesis begin to surface, efforts to understand the interchanges between tumors and their microenvironments have amplified. It is well documented that interactions between epithelial and stromal components are critical for normal tissue function as well as malignant transformation. Through paracrine/autocrine mechanisms, stromal cells affect epithelial gene expression and proliferation. The uterine endometrium is subject to tight hormonal control, and the synchronized action of glandular epithelial and stromal cells is required for menstrual cycling, fertility, and menopausal adaptation. Endometrial carcinoma (EC) is the most prevalent gynecologic malignancy, and the fourth most common cancer in women. Several studies on EC pathogenesis have concentrated on the stromal milieu surrounding hyperplastic/malignant cells. Here, we describe the cancer field associated with endometrial carcinoma and discuss the nature and role of major field factors involved in EC tumorigenesis and metastasis, including inflammation, angiogenesis, hormonal regulation, obesity/diabetes, and epigenetics. Knowledge of EC fields and their cancerizing alterations will help our understanding of EC pathogenesis, which may lead to improved management of endometrial cancer patients.