Changes in the genetic code (mutations) that reduce TET2 function are found in 10 percent of patients with acute myeloid leukemia (AML), 30 percent of those with a form of pre-leukemia
called myelodysplastic syndrome, and in nearly 50 percent of patients with chronic
myelomonocytic leukemia.
The team has shown that the microenvironment that controls hematopoietic stem cells can be targeted for the treatment of a set of disorders
called myeloproliferative neoplasias, the most prominent of which are chronic
myelomonocytic leukemia (CMML), juvenile
myelomonocytic leukemia (JMML), and atypical chronic myelogenous leukemia (CML).