@article {cite-key,
	title = {Illegitimate WNT pathway activation by beta-catenin mutation or autocrine stimulation in T-cell malignancies.},
	journal = {Cancer Res},
	volume = {68},
	number = {17},
	year = {2008},
	month = {Sep},
	pages = {6969{\textendash}6977},
	address = {Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.},
	abstract = {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 "active" 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.},
	issn = {1538-7445 (Electronic); 0008-5472 (Linking)},
	doi = {10.1158/0008-5472.CAN-08-1322},
	author = {Groen, Richard W J and Oud, Monique E C M and Schilder-Tol, Esther J M and Overdijk, Marije B and ten Berge, Derk and Nusse, Roel and Spaargaren, Marcel and Pals, Steven T}
}
