Human Papillomavirus E6 Knockdown Restores Adenovirus Mediated-estrogen Response Element Linked p53 Gene Transfer in HeLa Cells.

The p53 gene is inactivated by the human papillomavirus (HPV) E6 protein in the majority of cervical cancers. Treatment of HeLa S3 cells with siRNA for HPV E6 permitted adenovirus-mediated transduction of a p53 gene linked to an upstream estrogen response element (ERE). Our previous study in non-siRNA treated HHUA cells, which are derived from an endometrial cancer and express estrogen receptor β, showed enhancing effects of an upstream ERE on adenovirus-mediated p53 gene transduction.

An upstream estrogen response element linked to exogenous p53 tumor suppressor gene expression differentiates effects of the codon 72 polymorphism.

The objective of this study was to assess the effects of an upstream estrogen response element (ERE) on exogenous p53 tumor suppressor gene with a codon 72 polymorphism about which there have been controversial reports in relation to cancer risk. The p53 gene (bases 166-1143 from start codon) with the codon 72 polymorphism, inserted into the pIRES-hrGFP II plasmid with or without upstream ERE, were transfected into HHUA endometrial cancer cells expressing the estrogen receptor. The ERE-linked p53 gene with the proline variant at codon 72 showed lower transfection rates than the gene without ERE or with the arginine variant at codon 72.

Transcervical microwave myolysis for uterine myomas assisted by transvaginal ultrasonic guidance.

Aim: The effects of transcervical microwave myolysis at 2.45 GHz after microwave endometrial ablation for menorrhagia were examined in patients with myomas.

Methods: A transcervical microwave irradiation system assisted by transvaginal ultrasonic guidance was developed.

Endometrial thickness in Japanese women with hypertension or/and type 2 diabetes mellitus.

Objectives: The purpose of this study was: (a) to examine whether the endometrium of postmenopausal women with hypertension (HT) and/or type 2 diabetes mellitus (DM) was thicker than that of healthy controls (HC) and (b) whether endometrial thickness (ET) was associated with endometrial cancer risk factors.

Study Design: A total of 242 postmenopausal women were included in this study. Thirty women with type 2 DM, 49 women with HT, 23 women with DM and HT and 140 HCs were studied.