<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Sioulas, V.D.</style></author><author><style face="normal" font="default" size="100%">Politi, E.</style></author><author><style face="normal" font="default" size="100%">Rizos, D.</style></author><author><style face="normal" font="default" size="100%">Augoulea, A.</style></author><author><style face="normal" font="default" size="100%">Kyroudi, A.</style></author><author><style face="normal" font="default" size="100%">Sergentanis, T.N.</style></author><author><style face="normal" font="default" size="100%">Panoulis, C.</style></author><author><style face="normal" font="default" size="100%">Aravantinos, L.</style></author><author><style face="normal" font="default" size="100%">Creatsa, M.</style></author><author><style face="normal" font="default" size="100%">Lambrinoudaki, I.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Does hormone therapy, tibolone or raloxifene modify VEGF expression in cervical epithelial cells?</style></title><secondary-title><style face="normal" font="default" size="100%">Climacteric</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">cervical</style></keyword><keyword><style  face="normal" font="default" size="100%">hormone therapy</style></keyword><keyword><style  face="normal" font="default" size="100%">raloxifene</style></keyword><keyword><style  face="normal" font="default" size="100%">Tibolone</style></keyword><keyword><style  face="normal" font="default" size="100%">VEGF</style></keyword><keyword><style  face="normal" font="default" size="100%">Δ4-androstenedione</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012///</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">15</style></volume><pages><style face="normal" font="default" size="100%">181 - 185</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Aim Vascular endothelial growth factor (VEGF) seems to be a critical molecule in cervical carcinogenesis. We aimed to investigate the possible associations between hormonal factors and VEGF expression in cervical epithelial cells from postmenopausal women. Method A total of 105 healthy postmenopausal women (aged 4568 years old) attending a university menopause clinic were enrolled in this cross-sectional study. Pap smears were derived from current users of 17β-estradiol 1 mg + norethisterone acetate 0.5 mg (n = 28), tibolone 2.5 mg (n = 23), raloxifene HCl 60 mg (n = 21) and women not receiving treatment (n = 33). VEGF immunostaining was evaluated in squamous, glandular and metaplastic cells, using a semiquantitative method (rating scale: 03). Results Concerning endogenous hormones, higher Δ4-androstenedione levels were associated with more intense VEGF immunostaining in glandular (p = 0.041) and metaplastic cells (p = 0.004). Hormone therapy and raloxifene did not induce any changes in VEGF immunoreactivity in the examined cells. In contrast, tibolone administration was accompanied by diminished VEGF presence in metaplastic cells (p = 0.016 vs. controls). Conclusion Our findings may in part reflect the molecular processes contributing to the safe profile of hormone therapy, tibolone and raloxifene in cervical carcinogenesis. © 2012 International Menopause Society.</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue></record></records></xml>