<?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%">Tornese, Gianluca</style></author><author><style face="normal" font="default" size="100%">Faleschini, Elena</style></author><author><style face="normal" font="default" size="100%">Matarazzo, Lorenza</style></author><author><style face="normal" font="default" size="100%">Bibalo, Cristina</style></author><author><style face="normal" font="default" size="100%">Zanazzo, Giulio Andrea</style></author><author><style face="normal" font="default" size="100%">Rabusin, Marco</style></author><author><style face="normal" font="default" size="100%">Tonini, Giorgio</style></author><author><style face="normal" font="default" size="100%">Zennaro, Floriana</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Relapse and metastasis of atypical teratoid/rhabdoid tumor in a boy with neurofibromatosis type 1 treated with recombinant human growth hormone.</style></title><secondary-title><style face="normal" font="default" size="100%">Neuropediatrics</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Neuropediatrics</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Brain Stem Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Cerebellar Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Human Growth Hormone</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Magnetic Resonance Imaging</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Neurofibromatosis 1</style></keyword><keyword><style  face="normal" font="default" size="100%">Recombinant Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword><keyword><style  face="normal" font="default" size="100%">Rhabdoid Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Teratoma</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">46</style></volume><pages><style face="normal" font="default" size="100%">126-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Even though no increased recurrence rate seems to be reported in patients with brain tumors receiving recombinant human growth hormone (rhGH) replacement, in some patients multiple risk factors could put at higher risk for recurrence. In such cases, the decision to start rhGH therapy should be very cautious. A boy with neurofibromatosis type 1 developed an atypical teratoid/rhabdoid tumor (AT/RT) of right cerebellum, treated with surgery, radiotherapy, and chemotherapy. After 3 years of remission, he started rhGH for growth hormone deficiency, having a negative magnetic resonance imaging (MRI) scan. Ten weeks after starting therapy, the boy became symptomatic and MRI showed relapse of AT/RT in the right cerebellum and a new lesion in the brainstem. The boy died of progressive disease. In this case, the connection between AT/RT recurrence and the beginning of rhGH therapy, with a negative pretreatment MRI, cannot be excluded. Additional caution should be used for rhGH in patients with multiple risk factors.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25625887?dopt=Abstract</style></custom1></record><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%">Franca, Raffaella</style></author><author><style face="normal" font="default" size="100%">Stocco, Gabriele</style></author><author><style face="normal" font="default" size="100%">Favretto, Diego</style></author><author><style face="normal" font="default" size="100%">Giurici, Nagua</style></author><author><style face="normal" font="default" size="100%">Decorti, Giuliana</style></author><author><style face="normal" font="default" size="100%">Rabusin, Marco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Role of Pharmacogenetics in Hematopoietic Stem Cell Transplantation Outcome in Children.</style></title><secondary-title><style face="normal" font="default" size="100%">Int J Mol Sci</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Int J Mol Sci</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">18601-27</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Hematopoietic stem cell transplantation (HSCT) is an established therapeutic procedure for several congenital and acquired disorders, both malignant and nonmalignant. Despite the great improvements in HSCT clinical practices over the last few decades, complications, such as graft vs. host disease (GVHD) and sinusoidal obstructive syndrome (SOS), are still largely unpredictable and remain the major causes of morbidity and mortality. Both donor and patient genetic background might influence the success of bone marrow transplantation and could at least partially explain the inter-individual variability in HSCT outcome. This review summarizes some of the recent studies on candidate gene polymorphisms in HSCT, with particular reference to pediatric cohorts. The interest is especially focused on pharmacogenetic variants affecting myeloablative and immunosuppressive drugs, although genetic traits involved in SOS susceptibility and transplant-related mortality are also reviewed.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">8</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26266406?dopt=Abstract</style></custom1></record></records></xml>