RESUMEN
PURPOSE: To assess the effectiveness and safety of uterine artery embolization (UAE) using progressively larger calibrated gelatin sponge particles for symptomatic uterine fibroids. MATERIAL AND METHODS: Thirty patients with symptomatic uterine fibroids underwent UAE. Calibrated gelatin sponge particles were used in all patients, beginning with 355-500 µm particles, progressively increasing to 500-710 µm and finally to 710-1000 µm particles. Changes in tumor, uterine volume, and tumor infarction rate were assessed using pelvic magnetic resonance imaging (MRI). The level of complication, improvement of clinical symptoms, and Uterine Fibroid Symptom and Quality of Life (UFS-QOL) score were assessed. RESULTS: MR imaging revealed the mean largest tumor volume reduction was 56.23 ± 16.25% at three months and 72.61 ± 14.47% at 12 months after the procedure. 100% infarction of the dominant fibroids was 91.27 ± 5.02% at three months and 96 ± 5.20% at 12 months after the procedure. Menorrhagia improved markedly in all 23 patients. Bulk-related symptoms improved in 12 (92.30%) of 13 patients. The baseline UFS-QOL score was 43.13 and improved to 11.88 (p < 0.001). No major complications were observed. CONCLUSION: UAE using progressively larger calibrated gelatin sponge particles is an effective and safe treatment for symptomatic uterine fibroids.
Asunto(s)
Gelatina/administración & dosificación , Leiomioma/terapia , Embolización de la Arteria Uterina/métodos , Adenomiosis/epidemiología , Adulto , Femenino , Estudios de Seguimiento , Humanos , Leiomioma/epidemiología , Imagen por Resonancia Magnética , Persona de Mediana Edad , Tamaño de los Órganos , Tamaño de la Partícula , Calidad de VidaRESUMEN
Aberrant promoter methylation of tumor suppressor genes including retinoic acid receptor-ß2 (RAR-ß2) is frequently detected in hepatitis C virus (HCV)-associated hepatocellular carcinoma; however, the mechanism and its significance are relatively unknown. Here, we showed that HCV Core induced promoter hypermethylation of RAR-ß2 to inhibit its expression via up-regulation of DNA methyltransferases 1 and 3b. Under the condition, all-trans retinoic acid (ATRA) failed to activate p16 expression and thus could not inactivate the Rb-E2F pathway. Accordingly, Core-expressing cells exhibited resistance to ATRA-induced growth inhibition. Taken together, HCV Core antagonizes ATRA, a natural anti-cancer compound, to stimulate cell growth via epigenetic down-regulation of RAR-ß2.
Asunto(s)
Metilación de ADN , Antígenos de la Hepatitis C/metabolismo , Receptores de Ácido Retinoico/metabolismo , Tretinoina/farmacología , Proteínas del Núcleo Viral/metabolismo , Carcinoma Hepatocelular , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Inhibidor p16 de la Quinasa Dependiente de Ciclina , Regulación hacia Abajo , Regulación Neoplásica de la Expresión Génica , Células Hep G2 , Hepacivirus , Humanos , Neoplasias Hepáticas , Metiltransferasas/biosíntesis , Proteínas de Neoplasias/biosíntesis , Regiones Promotoras Genéticas , Interferencia de ARN , ARN Interferente Pequeño , Receptores de Ácido Retinoico/genéticaRESUMEN
All-trans retinoic acid (ATRA) inhibits the invasive and metastatic potentials of various cancer cells; however, the underlying mechanism is unclear. Here, we show that ATRA activated E-cadherin expression via promoter hypomethylation to facilitate Sp1 binding on its recognition sites in human colon carcinoma HCT116 cells. This effect was mediated by retinoic acid receptor-ß2, as demonstrated by knock-down experiments using a specific siRNA. As a result, ATRA increased cell-to-cell interactions, reduced cell migration, and downregulated levels of Vimentin and Fibronectin in HCT116 cells. The present study thus provides the mechanism for the beneficial effects of ATRA in the treatment of metastatic human carcinomas.