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MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia
MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia
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MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia
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MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia
MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia

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MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia
MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia
Journal Article

MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia

2015
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Overview
Patients with Waldenström's macroglobulinemia without mutations in MYD88 tend to have a shorter median survival and a lower probability of response to ibrutinib than do those with MYD88 mutations. To the Editor: Whole-genome sequencing identified the MYD88 L265P variant as the most prevalent mutation in patients with Waldenström's macroglobulinemia (WM), a type of non-Hodgkin's lymphoma. 1 In 93 to 97% of patients with this disorder, allele-specific polymerase-chain-reaction (AS-PCR) assays identified MYD88 L265P, which results from a T→C transversion at position 38182641 on chromosome 3p22.2. Signaling studies showed that the mutant protein that is encoded by MYD88 L265P triggers tumor growth through the activation of nuclear factor kappa light-chain enhancer of activated B cells (NF-κB) by Bruton's tyrosine kinase. This kinase is targeted by ibrutinib, a drug that is widely used . . .