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As mentioned previously, it is postulated that certain levels of functional loss, based on the presence of compound heterozygosity, the type and site of variants, the interaction of other proteins and residual wild-type expression levels contribute to the development of myeloid versus lymphoid malignancies. Biallelic variants are more common in the absence of an Arg882 variant. ''FLT3''-ITD, ''NPM1'' and ''IDH1'' cooperating mutations are seen in the context of AML; ''SF3B1'' and ''U2AF1'' cooperating mutations in the context of MDS; ''IDH1'' and ''IDH2'' variants in isolation are associated with MPN; ''TET2'', ''IDH2'' and ''RHOA'' are associated with PTCL.  See Figure 2 in [1]. Cooperating variants are not usually seen in the context of ''DNMT3A''-mutated T-ALL, but ''DNMT3A'' biallelic variants are more commonly seen in T-ALL. Biallelic ''DNMT3A'' variants are rare in PTCL [1].

As mentioned previously, it is postulated that certain levels of functional loss, based on the presence of compound heterozygosity, the type and site of variants, the interaction of other proteins and residual wild-type expression levels contribute to the development of myeloid versus lymphoid malignancies. Biallelic variants are more common in the absence of an Arg882 variant. ''FLT3''-ITD, ''NPM1'' and ''IDH1'' cooperating mutations are seen in the context of AML; ''SF3B1'' and ''U2AF1'' cooperating mutations in the context of MDS; ''IDH1'' and ''IDH2'' variants in isolation are associated with MPN; ''TET2'', ''IDH2'' and ''RHOA'' are associated with PTCL.  See Figure 2 in [1]. Cooperating variants are not usually seen in the context of ''DNMT3A''-mutated T-ALL, but ''DNMT3A'' biallelic variants are more commonly seen in T-ALL. Biallelic ''DNMT3A'' variants are rare in PTCL [1].

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