Approximately 30% of individuals with myeloid malignancy diseases have a mutation in a certain gene called tet methylcytosine dioxygenase 2 (TET2). This gene is responsible for providing instructions on creating certain proteins and is known to have a tumor-suppressive function. A study published Oct.
2 in Nature is the first to explain the pathway of TET2's enzymatic activity that is essential for its tumor-suppressing function. Mingjiang Xu, PhD, a molecular medicine professor at the Joe R. and Teresa Lozano Long School of Medicine, The University of Texas Health Science Center at San Antonio (UT Health San Antonio), is the co-primary investigator for the study.
The work is a collaborative effort between UT Health San Antonio scientists and University of Chicago scientists led by co-primary investigator Chuan He, PhD. There currently is no specific, targeted treatment or therapy for these TET2-mutated cancers. This pathway opens a door for targeted therapeutics and targeted prevention.
" Mingjiang Xu, PhD, molecular medicine professor at the Joe R. and Teresa Lozano Long School of Medicine, UT Health San Antonio When TET2 is mutated and not working properly, malignant cells can grow out of control. Mutation of this gene was pinpointed years ago as a culprit in blood cancers such as chronic myelomonocytic leukemia, acute myeloid leukemia and myelodysplastic syndromes, but the mechanisms behind how TET2 genetic changes led to disease remained a mystery -; until now.
About 15 y.
