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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...

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Detalles Bibliográficos
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.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
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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