Populational equilibrium through exosome-mediated Wnt signaling in tumor 
progression of diffuse large B-cell lymphoma.

Koch, R.; Demant, M.; Aung, T.; Diersing, N.; Cicholas, A.; Chapuy, B.; Wenzel, D.; Lahmann, M.; Güntsch, A.; Kiecke, C.; Becker, S.; Hupfeld, T.; Venkataramani, V.; Ziepert, M.; Opitz, L.; Klapper, W.; Trümper, L.; Wulf, G. G.

doi:10.1182/blood-2013-08-523886

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Journal Article

Populational equilibrium through exosome-mediated Wnt signaling in tumor progression of diffuse large B-cell lymphoma.

MPS-Authors

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Wenzel, D.
Facility for Electron Microscopy, MPI for biophysical chemistry, Max Planck Society;

External Ressource

http://bloodjournal.hematologylibrary.org/content/123/14/2189.full-text.pdf+html
(Publisher version)

Fulltext (public)

2033364.pdf
(Publisher version), 2MB

Supplementary Material (public)

2033364-Suppl-1.pdf
(Supplementary material), 877KB

2033364-Suppl-2.xlsx
(Supplementary material), 19KB

Citation

Koch, R., Demant, M., Aung, T., Diersing, N., Cicholas, A., Chapuy, B., et al. (2014). Populational equilibrium through exosome-mediated Wnt signaling in tumor progression of diffuse large B-cell lymphoma. Blood, 123(14), 2189-2198. doi:10.1182/blood-2013-08-523886.

Cite as: http://hdl.handle.net/11858/00-001M-0000-0019-BD1F-E

Abstract

Tumors are composed of phenotypically heterogeneous cell populations. The non-genomic mechanisms underlying transitions and interactions between cell populations are largely unknown. Here, we show that diffuse large B-cell lymphomas possess a self-organized infrastructure comprising side population (SP) and non-SP cells, where transitions between clonogenic states are modulated by exosome-mediated Wnt signaling. DNA methylation modulated SP-non-SP transitions and was correlated with the reciprocal expressions of Wnt signaling pathway agonist Wnt3a in SP cells and the antagonist secreted frizzled-related protein 4 in non-SP cells. Lymphoma SP cells exhibited autonomous clonogenicity and exported Wnt3a via exosomes to neighboring cells, thus modulating population equilibrium in the tumor.