<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Groen, Richard W J</style></author><author><style face="normal" font="default" size="100%">Oud, Monique E C M</style></author><author><style face="normal" font="default" size="100%">Schilder-Tol, Esther J M</style></author><author><style face="normal" font="default" size="100%">Overdijk, Marije B</style></author><author><style face="normal" font="default" size="100%">ten Berge, Derk</style></author><author><style face="normal" font="default" size="100%">Nusse, Roel</style></author><author><style face="normal" font="default" size="100%">Spaargaren, Marcel</style></author><author><style face="normal" font="default" size="100%">Pals, Steven T</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Illegitimate WNT pathway activation by beta-catenin mutation or autocrine stimulation in T-cell malignancies.</style></title><secondary-title><style face="normal" font="default" size="100%">Cancer Res</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Sep</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">17</style></number><pub-location><style face="normal" font="default" size="100%">Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.</style></pub-location><volume><style face="normal" font="default" size="100%">68</style></volume><pages><style face="normal" font="default" size="100%">6969–6977</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Recent studies in mice have shown a role for the canonical WNT pathway in lymphocyte development. Because cancers often arise as a result of aberrant activation of signaling cascades that normally promote the self-renewal and expansion of their progenitor cells, we hypothesized that activation of the WNT pathway might contribute to the pathogenesis of lymphoproliferative disease. Therefore, we screened a large panel (n = 162) of non-Hodgkin lymphomas (NHL), including all major WHO categories, for nuclear expression of beta-catenin, a hallmark of &quot;active&quot; WNT signaling. In 16 lymphomas, mostly of T-lineage origin, nuclear localization of beta-catenin was detected. Interestingly, some of these tumors contained established gain-of-function mutations in the gene encoding beta-catenin (CTNNB1); however, in the majority, mutations in either CTNNB1 or APC were not detected. Functional analysis of WNT signaling in precursor T-lymphoblastic lymphomas/leukemias, the NHL subset in which beta-catenin accumulation was most prevalent (33% positive), revealed a constitutively activated, but still responsive, WNT pathway, which controlled T-cell factor-mediated gene transcription and cell growth. Our data indicate that activation of the WNT pathway, either by CTNNB1 mutation or autocrine stimulation, plays a role in the pathogenesis of a subset of NHLs, in particular, those of T-cell origin.</style></abstract></record></records></xml>