Changes in c9af66d: add clinical section

				CD79B.md
			
          @@ -14,7 +14,7 @@ This has clinical and therapeutic implications as it may contribute sensitivity 

           In an inducible mouse model of MYD88-driven DLBCL, CD79B mutations did not accelerate lymphomagenesis but demonstrated an increased sensitivity to pharmacological BTK inhibition.[@flumannInducibleCd79bMutation2024] 

           In a retrospective analysis, younger patients with MCD DLBCL that were treated with ibrutinib had significantly better outcomes.[@wilsonEffectIbrutinibRCHOP2021]

           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.[@kimCD79BMYD88Mutations2014; @davisChronicActiveBcellreceptor2010]

          +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.[@kimCD79BMYD88Mutations2014; @davisChronicActiveBcellreceptor2010] CD79B is both a recurrent oncogenic signalling node in ABC-DLBCL and an ideal lineage-restricted, rapidly internalizing surface antigen. The antibody–drug conjugate polatuzumab vedotin exploits CD79B surface expression to deliver a cytotoxic payload to malignant B cells, independent of CD79B mutation status[@assiPolatuzumabVedotinCurrent2021].

...	...	@@ -14,7 +14,7 @@ This has clinical and therapeutic implications as it may contribute sensitivity
14	14	In an inducible mouse model of MYD88-driven DLBCL, CD79B mutations did not accelerate lymphomagenesis but demonstrated an increased sensitivity to pharmacological BTK inhibition.[@flumannInducibleCd79bMutation2024]
15	15	In a retrospective analysis, younger patients with MCD DLBCL that were treated with ibrutinib had significantly better outcomes.[@wilsonEffectIbrutinibRCHOP2021]
16	16	The most common hotspot mutation in CD79B is at the tyrosine residue 196 (Y196).
17		-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.[@kimCD79BMYD88Mutations2014; @davisChronicActiveBcellreceptor2010]
	17	+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.[@kimCD79BMYD88Mutations2014; @davisChronicActiveBcellreceptor2010] CD79B is both a recurrent oncogenic signalling node in ABC-DLBCL and an ideal lineage-restricted, rapidly internalizing surface antigen. The antibody–drug conjugate polatuzumab vedotin exploits CD79B surface expression to deliver a cytotoxic payload to malignant B cells, independent of CD79B mutation status[@assiPolatuzumabVedotinCurrent2021].
18	18
19	19
20	20