<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">AVGOUSTIDIS, DIMITRIS</style></author><author><style face="normal" font="default" size="100%">NISYRIOS, THEMISTOKLIS</style></author><author><style face="normal" font="default" size="100%">NKENKE, EMEKA</style></author><author><style face="normal" font="default" size="100%">LIJNEN, ROGER</style></author><author><style face="normal" font="default" size="100%">RAGOS, VASSILIS</style></author><author><style face="normal" font="default" size="100%">PERREA, DESPINA</style></author><author><style face="normal" font="default" size="100%">DONTA, ISMINI</style></author><author><style face="normal" font="default" size="100%">VAENA, APOSTOLIA</style></author><author><style face="normal" font="default" size="100%">YAPIJAKIS, CHRISTOS</style></author><author><style face="normal" font="default" size="100%">VAIRAKTARIS, ELEFTHERIOS</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Oral Carcinogenesis Is not Achieved in Different Carcinogen-treated PAI-1 Transgenic and Wild-type Mouse Models</style></title><secondary-title><style face="normal" font="default" size="100%">In Vivo</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012-11-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">1001-1005</style></pages><volume><style face="normal" font="default" size="100%">26</style></volume><issue><style face="normal" font="default" size="100%">6</style></issue><abstract><style  face="normal" font="default" size="100%">Aim: In an effort to assess the role of plasminogen activator inhibitor-1 (PAI-1) in oral squamous cancer development and progression, two different carcinogen treatment protocols were conducted. Materials and Methods: Protocol I included mice from a PAI-1 transgenic (Tg) breed (n=56) and their wild-type (WT) counterparts (n=56), divided into one control group and two main experimental groups, treated with 7,12-dimethylbenz[a]anthracene (DMBA) for 8 and 16 weeks, respectively. Protocol II included the same number and types of animals and groups, which were similarly treated with 4-Nitroquinoline 1-oxide (4-NQO) in drinking water. Two drugs that affect plasma PAI-1 levels, enalapril and pravastatin, were administered to certain subgroups of animals in both protocols. Results: None of the animals developed macroscopically-visible oral cancer lesions. Eleven animals under Protocol I and 52 animals under Protocol II died. Skin lesions were noted only in DMBA-treated animals (n=9). Almost all animals administered with 4-NQO developed alopecia and lost weight, while two of them developed stomach tumours, and one female mouse developed a large ovarian cyst. Conclusion: Transgenic mice may respond differently when used in well-established carcinogen models and oral carcinogenesis is hard to achieve in these rodents.</style></abstract></record></records></xml>