Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies
Copyright policy )Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies
Abstract Disease alleles that activate signal transduction are common in myeloid malignancies; however, there are additional unidentified mutations that contribute to myeloid transformation. Based on the recent identification of TET2 mutations, we evaluated the mutational status of TET1, TET2, and TET3 in myeloproliferative neoplasms (MPNs), chronic myelomonocytic leukemia (CMML), and acute myeloid leukemia (AML). Sequencing of TET2 in 408 paired tumor/normal samples distinguished between 68 somatic mutations and 6 novel single nucleotide polymorphisms and identified TET2 mutations in MPN (27 of 354, 7.6%), CMML (29 of 69, 42%), AML (11 of 91, 12%), and M7 AML (1 of 28, 3.6%) samples. We did not identify somatic TET1 or TET3 mutations or TET2 promoter hypermethylation in MPNs. TET2 mutations did not cluster in genetically defined MPN, CMML, or AML subsets but were associated with decreased overall survival in AML (P = .029). These data indicate that TET2 mutations are observed in different myeloid malignancies and may be important in AML prognosis.
- Northwestern University United States
- Massachusetts Institute of Technology United States
- Broad Institute United States
- University of Chicago United States
- New York Medical College United States
Myeloproliferative Disorders, Mutation, Missense, Leukemia, Myelomonocytic, Chronic, Exons, Prognosis, Polymorphism, Single Nucleotide, Dioxygenases, Mixed Function Oxygenases, DNA-Binding Proteins, Survival Rate, Leukemia, Myeloid, Acute, Codon, Nonsense, Case-Control Studies, Proto-Oncogene Proteins, Mutation, Humans, Frameshift Mutation, Sequence Deletion
Myeloproliferative Disorders, Mutation, Missense, Leukemia, Myelomonocytic, Chronic, Exons, Prognosis, Polymorphism, Single Nucleotide, Dioxygenases, Mixed Function Oxygenases, DNA-Binding Proteins, Survival Rate, Leukemia, Myeloid, Acute, Codon, Nonsense, Case-Control Studies, Proto-Oncogene Proteins, Mutation, Humans, Frameshift Mutation, Sequence Deletion
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