Age-related loss of chromosome Y is associated with levels of sex hormone binding globulin and clonal hematopoiesis defined by TET2 TP53 and CBL mutations.
Finding that MYC directly deregulates the expression of TET1 and TET2 in T-ALL provides novel evidence that MYC controls DNA (hydroxy)methylation in a genome-wide fashion. It reveals a coordinated interplay between the components of the DNA (de)methylating machinery that contribute to MYC-driven tumor maintenance.
A functional interplay between TET2 and p53 during anti-cancer therapy establishes the rationale for targeting TET2 to overcome chemotherapy resistance associated with mutant p53 tumors.
Data show that tet methylcytosine dioxygenase 2 TET2 isocitrate dehydrogenases 1/2 IDH1/IDH2 serine/arginine-rich splicing factor 2 SRSF2 splicing factor 3b subunit 1 SF3B1 and ras proteins (KRAS/NRAS) are not conserved in dog mast Cell tumors.
Mutation in TET2 or TP53 predicts poor survival in patients with myelodysplastic syndrome receiving hypomethylating treatment or stem cell transplantation.
Mutations in TET2 occurred with similar frequency in myelodysplastic syndromes and acute myeloid leukemias and associated equally with either ASXL1 or NPM1 mutations; Observational study of gene-disease association. (HuGE Navigator)
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