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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Bibliographic Details
Published in:Blood Cancer J
Main Authors: 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.
Format: Artigo
Language:Inglês
Published: Nature Publishing Group UK 2018
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Online Access:https://ncbi.nlm.nih.gov/pmc/articles/PMC6177394/
https://ncbi.nlm.nih.gov/pubmed/30301877
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/s41408-018-0130-3
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