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MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia
by
Treon, Steven P
, Hunter, Zachary
, Xu, Lian
in
Humans
/ Lymphoma
/ Macroglobulinemia
/ Mutation
/ MyD88 protein
/ Myeloid Differentiation Factor 88 - genetics
/ Patients
/ Pyrazoles - therapeutic use
/ Pyrimidines - therapeutic use
/ Waldenstrom Macroglobulinemia - drug therapy
/ Waldenstrom Macroglobulinemia - genetics
/ Waldenstrom Macroglobulinemia - mortality
2015
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MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia
by
Treon, Steven P
, Hunter, Zachary
, Xu, Lian
in
Humans
/ Lymphoma
/ Macroglobulinemia
/ Mutation
/ MyD88 protein
/ Myeloid Differentiation Factor 88 - genetics
/ Patients
/ Pyrazoles - therapeutic use
/ Pyrimidines - therapeutic use
/ Waldenstrom Macroglobulinemia - drug therapy
/ Waldenstrom Macroglobulinemia - genetics
/ Waldenstrom Macroglobulinemia - mortality
2015
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Do you wish to request the book?
MYD88 Mutations and Response to Ibrutinib in Waldenström's Macroglobulinemia
by
Treon, Steven P
, Hunter, Zachary
, Xu, Lian
in
Humans
/ Lymphoma
/ Macroglobulinemia
/ Mutation
/ MyD88 protein
/ Myeloid Differentiation Factor 88 - genetics
/ Patients
/ Pyrazoles - therapeutic use
/ Pyrimidines - therapeutic use
/ Waldenstrom Macroglobulinemia - drug therapy
/ Waldenstrom Macroglobulinemia - genetics
/ Waldenstrom Macroglobulinemia - mortality
2015
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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 . . .
Publisher
Massachusetts Medical Society
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