Nonpersistent endocrine disrupting chemicals (npEDCs) are exogenous chemicals or mixtures of industrial agents that can interfere with the normal action of hormone with a shorter half-life and lower liposolubility. These are commonly found in plastics, medical equipment, detergents, and cosmetics. Recently, role of npEDCs on the changes of ovary and/or uterus development and alterations in hormonal signaling has been emphasized. However, many controversial results exist on the effects of npEDCs and reproductive health of women. Thus, we have focused to review the scientific evidence of a causal relationship between exposure to npEDCs and representative female reproductive issues such as menstrual cycle, endometriosis, uterine fibroids, polycystic ovarian syndrome and infertility/subfertility. Though not all studies indicated a positive correlation of npEDCs with female reproductive issues, the reviewed data illustrated that the majority of the available data strengthen the evidence of reproductive health-related actions of npEDCs. In future, recommendations should be made in order to reduce human exposure to npEDCs and to protect from steadily increasing reproductive health risks.

The major risk factor for ovarian cancer (OC) is mutation of the BRCA1 or BRCA2 DNA mismatch repair genes, which occurs in approximately 10% of OC cases. Most previous studies have demonstrated that BRCA1- and BRCA2-mutated OCs are associated with better prognosis than sporadic OCs. However, information about the patterns and clinical course of the metastatic spread of BRCA-mutated OCs is limited. Herein, we describe a case of OC with a BRCA1 mutation and skin metastases in a 49-year-old patient, which to the best of our knowledge has not been reported previously.

Triphenyl phosphate (TPHP) is one of the most commonly used organophosphorus flame retardants that may accumulate in the environment. However, its effects on human reproductive organs have not been well studied. We aimed to investigate the in vitro effects of TPHP in human Ishikawa endometrial cancer cells to elucidate how TPHP exposure disrupts intracellular signaling and cell proliferation in reproductive tissues. MethodsHuman Ishikawa endometrial cancer cells were exposed to TPHP. Results Exposureto TPHP elevated the levels of estrogen receptor (ER) α and progesterone receptor-B and reduced ER β in human Ishikawa endometrial cancer cells. TPHP stimulated phosphoinositide 3-kinase/protein kinase B and MAPK/ERK1/2 kinase signaling, which may contribute to the activation of ER function and induce nuclear translocation of nuclear factor kappa-light-chainenhancer of activated B cells (NF-κB) in human Ishikawa endometrial cancer cells. Activated ER and NF-κB stimulate the expression of cyclin D1/cyclin-dependent kinase (CDK) 4/CDK6, indicating cell cycle progression and proliferation. ConclusionThis report may provide new information on the molecular mechanisms underlying how TPHP exposure dysregulates the cellular physiology of the human endometrium.

Epithelioid trophoblastic tumor is a rare malignant lesion of gestational trophoblastic disease, and constitutes an abnormal proliferation of placental trophoblasts. Patients with epithelioid trophoblastic tumor are usually of reproductive age, and have had previous gestations including full-term deliveries, molar pregnancies and abortions. The interval between antecedent gestational events and the diagnosis of epithelioid trophoblastic tumor usually ranges from 0 to 264 months (mean, 84 months). Herein, we report a 42-year-old Korean woman (gravida 2, para 2). At 38 weeks of gestation, she underwent a repeat cesarean section and then hysterectomy due to uterine atony. She was incidentally diagnosed with epithelioid trophoblastic tumor, and postoperatively no metastatic disease was observed. The patient presented no clinical evidence of tumor recurrence for 5 years after surgery. This case is remarkable because epithelioid trophoblastic tumor is a rare disease, and the diagnosis of epithelioid trophoblastic tumor followed immediately after delivery.

Uterine leiomyosarcoma is an uncommon malignancy accounting for approximately 1% of gynecologic oncology cases. Most uterine leiomyosarcomas occur in menopausal women and they are notorious for their aggressive character, early dissemination, and poor prognosis. It is difficult to accurately differentiate uterine leiomyosarcoma from leiomyomas, especially when leiomyomas undergo degenerative changes. We treated two menopausal women with a uterine mass showing cystic change. Clinical work-up included needle aspiration, sonography, computed tomography, and serum tumor markers to differentiate uterine leiomyosarcoma from leiomyoma. All results were negative for malignancy, but uterine leiomyosarcoma was ultimately diagnosed by pathological examination. Until an accurate preoperative diagnostic method is available, menopausal women diagnosed with a degenerating cystic uterine fibroid should be considered to have a malignancy intraoperatively in order to prevent tumor cells from intraperitoneal spreading.