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Loss of TNFAIP3 enhances MYD88(L265P)-driven signaling in non-Hodgkin lymphoma
MYD88 mutations are one of the most recurrent mutations in hematologic malignancies. However, recent mouse models suggest that MYD88(L265P) alone may not be sufficient to induce tumor formation. Interplay between MYD88(L265P) and other genetic events is further supported by the fact that TNFAIP3 (A2...
Autores principales: | Wenzl, Kerstin, Manske, Michelle K., Sarangi, Vivekananda, Asmann, Yan W., Greipp, Patricia T., Schoon, Hanna R., Braggio, Esteban, Maurer, Matthew J., Feldman, Andrew L., Witzig, Thomas E., Slager, Susan L., Ansell, Stephen M., Cerhan, James R., Novak, Anne J. |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6177394/ https://www.ncbi.nlm.nih.gov/pubmed/30301877 http://dx.doi.org/10.1038/s41408-018-0130-3 |
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