CD79B.md
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+---
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+bibliography: 'morinlab.bib'
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+csl: 'NLM.csl'
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+link-citations: true
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+---
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# CD79B
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## Overview
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-CD79B mutations significantly contribute to the pathogenesis of DLBCL by enhancing BCR signaling and promoting tumor survival. These mutations, especially when co-occurring with MYD88 mutations, define a unique molecular subtype.<sup>1</sup> This has clinical and therapeutic implications as it may contribute sensitivity to BTK inhibitors. In an inducible mouse model of MYD88-driven DLBCL, CD79B mutations did not accelerate lymphomagenesis but demonstrated an increased sensitivity to pharmacological BTK inhibition.<sup>2</sup> In a retrospective analysis, younger patients with MCD DLBCL that were treated with ibrutinib had significantly better outcomes.<sup>3</sup> The most common hotspot mutation in CD79B is at the tyrosine residue 196 (Y196). This and other common mutations primarily occur in the immunoreceptor tyrosine-based activation motif (ITAM) domain and prevent the negative regulatory feedback provided by Lyn kinase thereby enhancing BCR signaling.
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+CD79B mutations significantly contribute to the pathogenesis of DLBCL by enhancing BCR signaling and promoting tumor survival. These mutations, especially when co-occurring with MYD88 mutations, define a unique molecular subtype.<sup>1</sup> This has clinical and therapeutic implications as it may contribute sensitivity to BTK inhibitors. In an inducible mouse model of MYD88-driven DLBCL, CD79B mutations did not accelerate lymphomagenesis but demonstrated an increased sensitivity to pharmacological BTK inhibition.<sup>2</sup> In a retrospective analysis, younger patients with MCD DLBCL that were treated with ibrutinib had significantly better outcomes.<sup>3</sup> The most common hotspot mutation in CD79B is at the tyrosine residue 196 (Y196). This and other common mutations primarily occur in the immunoreceptor tyrosine-based activation motif (ITAM) domain and prevent the negative regulatory feedback provided by Lyn kinase thereby enhancing BCR signaling.
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## History
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```mermaid
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%%{init: { 'logLevel': 'debug', 'theme': 'dark' } }%%
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|Entity|Tier|Description |
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|:------:|:----:|--------------------------------------|
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-|![BL](images/icons/BL_tier2.png) |2 |relevance in BL not firmly established|
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-|![DLBCL](images/icons/DLBCL_tier1.png) |1 |high-confidence DLBCL gene |
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+|![BL](images/icons/BL_tier2.png) |2 |relevance in BL not firmly established[@paneaWholeGenomeLandscape2019]|
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+|![DLBCL](images/icons/DLBCL_tier1.png) |1 |high-confidence DLBCL gene [@morinFrequentMutationHistonemodifying2011]|
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|![FL](images/icons/FL_tier2.png) |2 |relevance in FL not firmly established|
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## Mutation incidence in large patient cohorts (GAMBL reanalysis)