Re-activation of mitochondrial apoptosis inhibits T-cell lymphoma survival and treatment resistance View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2016-07

AUTHORS

S Spinner, G Crispatzu, J-H Yi, E Munkhbaatar, P Mayer, U Höckendorf, N Müller, Z Li, T Schader, H Bendz, S Hartmann, M Yabal, K Pechloff, M Heikenwalder, G L Kelly, A Strasser, C Peschel, M-L Hansmann, J Ruland, U Keller, S Newrzela, M Herling, P J Jost

ABSTRACT

T lymphocyte non-Hodgkin's lymphoma (T-NHL) represents an aggressive and largely therapy-resistant subtype of lymphoid malignancies. As deregulated apoptosis is a frequent hallmark of lymphomagenesis, we analyzed gene expression profiles and protein levels of primary human T-NHL samples for various apoptotic regulators. We identified the apoptotic regulator MCL-1 as the only pro-survival BCL-2 family member to be highly expressed throughout all human T-NHL subtypes. Functional validation of pro-survival protein members of the BCL-2 family in two independent T-NHL mouse models identified that the partial loss of Mcl-1 significantly delayed T-NHL development in vivo. Moreover, the inducible reduction of MCL-1 protein levels in lymphoma-burdened mice severely impaired the continued survival of T-NHL cells, increased their susceptibility to chemotherapeutics and delayed lymphoma progression. Lymphoma viability remained unaffected by the genetic deletion or pharmacological inhibition of all alternative BCL-2 family members. Consistent with a therapeutic window for MCL-1 treatment within the context of the whole organism, we observed an only minimal toxicity after systemic heterozygous loss of Mcl-1 in vivo. We conclude that re-activation of mitochondrial apoptosis by blockade of MCL-1 represents a promising therapeutic strategy to treat T-cell lymphoma. More... »

PAGES

1520

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/leu.2016.49

    DOI

    http://dx.doi.org/10.1038/leu.2016.49

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1010157990

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27055871


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