American Association for Cancer Research
Browse
00085472can081322-sup-stable_3.pdf (7.42 kB)

Supplementary Table 3 from Illegitimate WNT Pathway Activation by β-Catenin Mutation or Autocrine Stimulation in T-Cell Malignancies

Download (7.42 kB)
journal contribution
posted on 2023-03-30, 18:31 authored by Richard W.J. Groen, Monique E.C.M. Oud, Esther J.M. Schilder-Tol, Marije B. Overdijk, Derk ten Berge, Roel Nusse, Marcel Spaargaren, Steven T. Pals
Supplementary Table 3 from Illegitimate WNT Pathway Activation by β-Catenin Mutation or Autocrine Stimulation in T-Cell Malignancies

History

ARTICLE 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 β-catenin, a hallmark of “active” WNT signaling. In 16 lymphomas, mostly of T-lineage origin, nuclear localization of β-catenin was detected. Interestingly, some of these tumors contained established gain-of-function mutations in the gene encoding β-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 β-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. [Cancer Res 2008;68(17):6969–77]

Usage metrics

    Cancer Research

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC