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RNA-Seq revealed a hyperactive\n                    <jats:italic>c-Myc<\/jats:italic>\n                    signature in\n                    <jats:italic>\n                      Tet2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    cells, which is normalized by inhibiting PI3K signaling. Loss of TET2 impairs the maturation of myeloid lineage\u2013derived mast cells by dysregulating the expression of\n                    <jats:italic>Mitf<\/jats:italic>\n                    and\n                    <jats:italic>Cebpa<\/jats:italic>\n                    , which is restored by low-dose ascorbic acid and 5-azacytidine. Utilizing a mouse model in which the loss of TET2 precedes the expression of oncogenic\n                    <jats:italic>Kit<\/jats:italic>\n                    , similar to the human disease, results in the development of a non\u2013mast cell lineage neoplasm (AHNMD), which is responsive to PI3K inhibition. Thus, therapeutic approaches involving hypomethylating agents, ascorbic acid, and isoform-specific PI3K inhibitors are likely to be useful for treating patients with\n                    <jats:italic>TET2<\/jats:italic>\n                    and\n                    <jats:italic>KIT<\/jats:italic>\n                    mutations.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.94679","type":"journal-article","created":{"date-parts":[[2018,2,21]],"date-time":"2018-02-21T11:00:58Z","timestamp":1519210858000},"source":"Crossref","is-referenced-by-count":26,"title":["Loss of epigenetic regulator TET2 and oncogenic KIT regulate myeloid cell transformation via PI3K pathway"],"prefix":"10.1172","volume":"3","author":[{"given":"Lakshmi Reddy","family":"Palam","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, 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