Changes in 407abd3: add EE

				ATP6V1B2.md
			
          @@ -8,6 +8,10 @@ nocite: |

           [[_TOC_]]

          +## Experimental Evidence

          +

          +Driver mutations affecting this gene in FL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@krysiakRecurrentSomaticMutations2017]

          +

           ## Relevance tier by entity

           [[include:table1_ATP6V1B2.md]]

				BACH2.md
			
          @@ -12,6 +12,10 @@ nocite: |

           Mutations in this gene were first described in BL in 2019 by Grande et al.[@grandeGenomewideDiscoverySomatic2019]

          +## Experimental Evidence

          +

          +Driver mutations affecting this gene in BL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@hunterNFkBSubunitCRel2016]

          +

           ## Relevance tier by entity

           [[include:table1_BACH2]]

				BCL6.md
			
          @@ -13,6 +13,10 @@ BCL6 is one of [a number of genes](https://github.com/morinlab/LLMPP/wiki/ashm) 

           Although common, particularly in DLBCL, the function of many of these mutations remains unclear but some have been shown to affect the regulation of BCL6 expression. The role of BCL6 missense mutations, seen over 9% of patients remains unclear. 

          +## Experimental Evidence

          +

          +Driver mutations affecting this gene in BL/FL/DLBCL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@masclePointMutationsBCL62003]

          +

           ## Relevance tier by entity

           [[include:table1_BCL6]]

				BCL7A.md
			
          @@ -15,6 +15,10 @@ The rate of DLBCLs with biallelic loss of this locus remains unclear.

          +## Experimental Evidence

          +

          +Driver mutations affecting this gene in BL/DLBCL/FL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@balinas-gaviraFrequentMutationsAminoterminal2020]

          +

           ## Relevance tier by entity

           [[include:table1_BCL7A]]

				BRAF.md
			
          @@ -15,6 +15,10 @@ BRAF mutations, particularly the BRAF V600E hot spot mutation, are primarily ass

           Although mutations have also been reported in BL, due to [minimal support](BRAF#representative-mutation) in the original primary data and very few mutations reported in subsequent studies, this gene is very unlikely to be relevant in BL. 

          +## Experimental Evidence

          +

          +Driver mutations affecting this gene in DLBCL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@wanMechanismActivationRAFERK2004]

          +

           ## Relevance tier by entity

           [[include:table1_BRAF.md]]

				BTK.md
			
          @@ -9,6 +9,10 @@ nocite: |

           One study reported BTK mutations in approximately 7% of FL and 11% of transformed FL cases.[@krysiakRecurrentSomaticMutations2017] Another showed these mutations were more common, and typically co-occur in tumours with BCL2 translocations. Despite the known role of certain BTK mutations in acquired resistance to BTK inhibitors, these mutations were found in BTK inhibitor-naïve patients.[@albuquerqueEnhancingKnowledgeDiscovery2017] These mutations often occur in treatment-naive patients and lead to inactivation of the BTK protein through destabilization or by altering key residues involved in enzymatic activity.[@krysiakRecurrentSomaticMutations2017] The mutation pattern in DLBCL and FL implies the preferential accumulation of *inactivating mutations*[@huFollicularLymphomaassociatedBTK2021; @schejbelInactivatingBTKMutations2022]. No notable hot spots have been described in this gene in the context of the cancers listed below. 

          +## Experimental Evidence

          +

          +Driver mutations affecting this gene in FL/DLBCL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@huFollicularLymphomaassociatedBTK2021]

          +

           ## Relevance tier by entity

           [[include:table1_BTK.md]]

				CD70.md
			
          @@ -16,6 +16,10 @@ Genetic perturbation limits the development of an effective CD8+ T-cell immune r

           In mouse models, CD70 loss promoted lymphomagenesis, consistent with its role as a tumor suppressor gene in B-cell lymphomas.[@mandatoAbstractA38Cd702022]

          +## Experimental Evidence

          +

          +Driver mutations affecting this gene in DLBCL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@nieDualRoleCD702022]

          +

           ## Relevance tier by entity

           [[include:table1_CD70.md]]

				ZC3H12A.md
			
          @@ -8,6 +8,10 @@ nocite: |

           [[_TOC_]]

          +## Experimental Evidence

          +

          +Driver mutations affecting this gene in DLBCL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@skalniakRegulatoryFeedbackLoop2009]

          +

           ## Relevance tier by entity

           [[include:table1_ZC3H12A]]

...	...	@@ -8,6 +8,10 @@ nocite: \|
8	8	[[_TOC_]]
9	9
10	10
	11	+## Experimental Evidence
	12	+
	13	+Driver mutations affecting this gene in FL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@krysiakRecurrentSomaticMutations2017]
	14	+
11	15	## Relevance tier by entity
12	16
13	17	[[include:table1_ATP6V1B2.md]]

...	...	@@ -12,6 +12,10 @@ nocite: \|
12	12	Mutations in this gene were first described in BL in 2019 by Grande et al.[@grandeGenomewideDiscoverySomatic2019]
13	13
14	14
	15	+## Experimental Evidence
	16	+
	17	+Driver mutations affecting this gene in BL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@hunterNFkBSubunitCRel2016]
	18	+
15	19	## Relevance tier by entity
16	20
17	21	[[include:table1_BACH2]]

...	...	@@ -13,6 +13,10 @@ BCL6 is one of [a number of genes](https://github.com/morinlab/LLMPP/wiki/ashm)
13	13	Although common, particularly in DLBCL, the function of many of these mutations remains unclear but some have been shown to affect the regulation of BCL6 expression. The role of BCL6 missense mutations, seen over 9% of patients remains unclear.
14	14
15	15
	16	+## Experimental Evidence
	17	+
	18	+Driver mutations affecting this gene in BL/FL/DLBCL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@masclePointMutationsBCL62003]
	19	+
16	20	## Relevance tier by entity
17	21
18	22	[[include:table1_BCL6]]

...	...	@@ -15,6 +15,10 @@ The rate of DLBCLs with biallelic loss of this locus remains unclear.
15	15
16	16
17	17
	18	+## Experimental Evidence
	19	+
	20	+Driver mutations affecting this gene in BL/DLBCL/FL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@balinas-gaviraFrequentMutationsAminoterminal2020]
	21	+
18	22	## Relevance tier by entity
19	23
20	24	[[include:table1_BCL7A]]

...	...	@@ -15,6 +15,10 @@ BRAF mutations, particularly the BRAF V600E hot spot mutation, are primarily ass
15	15	Although mutations have also been reported in BL, due to [minimal support](BRAF#representative-mutation) in the original primary data and very few mutations reported in subsequent studies, this gene is very unlikely to be relevant in BL.
16	16
17	17
	18	+## Experimental Evidence
	19	+
	20	+Driver mutations affecting this gene in DLBCL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@wanMechanismActivationRAFERK2004]
	21	+
18	22	## Relevance tier by entity
19	23
20	24	[[include:table1_BRAF.md]]

...	...	@@ -9,6 +9,10 @@ nocite: \|
9	9	One study reported BTK mutations in approximately 7% of FL and 11% of transformed FL cases.[@krysiakRecurrentSomaticMutations2017] Another showed these mutations were more common, and typically co-occur in tumours with BCL2 translocations. Despite the known role of certain BTK mutations in acquired resistance to BTK inhibitors, these mutations were found in BTK inhibitor-naïve patients.[@albuquerqueEnhancingKnowledgeDiscovery2017] These mutations often occur in treatment-naive patients and lead to inactivation of the BTK protein through destabilization or by altering key residues involved in enzymatic activity.[@krysiakRecurrentSomaticMutations2017] The mutation pattern in DLBCL and FL implies the preferential accumulation of inactivating mutations[@huFollicularLymphomaassociatedBTK2021; @schejbelInactivatingBTKMutations2022]. No notable hot spots have been described in this gene in the context of the cancers listed below.
10	10
11	11
	12	+## Experimental Evidence
	13	+
	14	+Driver mutations affecting this gene in FL/DLBCL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@huFollicularLymphomaassociatedBTK2021]
	15	+
12	16	## Relevance tier by entity
13	17
14	18	[[include:table1_BTK.md]]

...	...	@@ -16,6 +16,10 @@ Genetic perturbation limits the development of an effective CD8+ T-cell immune r
16	16	In mouse models, CD70 loss promoted lymphomagenesis, consistent with its role as a tumor suppressor gene in B-cell lymphomas.[@mandatoAbstractA38Cd702022]
17	17
18	18
	19	+## Experimental Evidence
	20	+
	21	+Driver mutations affecting this gene in DLBCL have been experimentally demonstrated to cause a reduction or loss of function (LOF).[@nieDualRoleCD702022]
	22	+
19	23	## Relevance tier by entity
20	24
21	25	[[include:table1_CD70.md]]