Changes in 1b5ed2d: Updated CD79B (markdown)

				CD79B.md
			
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           # CD79B

           ## Overview

          -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> 

          +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). 

           ## Relevance tier by entity

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1	1	# CD79B
2	2	## Overview
3		-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>
	3	+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).
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5	5	## Relevance tier by entity
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