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The Allis lab has also investigated mutations in histone H3 that are highly enriched in pediatric gliomas (including the substitution of H3 lysine 27 for methionine, or H3K27M). The team has shown that these so-called oncohistone mutations can alter the recruitment and activity of histone-modifying complexes, and therefore change the epigenetic landscape and gene expression. Given the restricted distribution of these mutations to pediatric gliomas, the Allis lab further hypothesizes that a cell-lineage specific cellular context is crucial for the ability of these mutations to mediate oncogenesis. In support of this idea, current findings have documented that the substitution of H3 lysine 36 for methionine (H3K36M) impairs the differentiation of mesenchymal progenitor cells and generates a type of tumor called undifferentiated sarcoma in vivo. H3K36M mutations have also been documented in a subset of head and neck squamous cell carcinomas. Studies in the lab are now expanding the landscape of oncohistones to a wide range of diverse tumor types and developmental syndromes.
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