Gallery
See also
Intranodal palisaded myofibroblastoma
List of inclusion bodies that aid in diagnosis of cutaneous conditions
Neurofibroma
Palisaded encapsulated neuroma

References


== External links ==
While fatal in up to 20% of cases, ~80 of infants with TMD fully recover from the diseases within 4 months. However, ~10% of individuals with a history of symptomatic or silent TMD develop DS-AMKL within 4 years. During this interval, these individuals may acquire somatic mutations in those of their megakaryoblasts that bear the original truncating GATA1 mutation. These newly acquired mutations appear to result from the interactions of GATAT1 truncating mutations with excessive copies of chromosome 21 genes. The genes with these mutations include TP53, FLT3, ERG, DYRK1A, CHAF1B, HLCS, RUNX1, MIR125B2 (which is the gene for microRNA MiR125B2CTCF, STAG2, RAD21, SMC3, SMC1A, NIPBL, SUZ12, PRC2, JAK1, JAK2, JAK3, MPL, KRAS, NRAS, and SH2B3. At least one but probably several of these mutations, whether occurring in individuals with silent or symptomatic TMD, are presumed responsible for or to contribute to the development of DS-AMKL.Rare cases of transient myeloproliferative disease and DS-AMKL occur in individuals who do not have Down syndrome. These individuals usually have a history of TMD and invariably have megakaryoblasts which bear extra copies of key chromosome 21 genes, truncating mutations in GATA1, and somatic mutations in one or more of the genes listed in the previous section. These individuals have extra copies of only a portion of the genes on chromosome 21.