Premium
Characteristics of translocation (16;16)(p13;q22) acute myeloid leukemia
Author(s) -
Eghtedar Alireza,
Borthakur Gautam,
Ravandi Farhad,
Jabbour Elias,
Cortes Jorge,
Pierce Sherry,
Kantarjian Hagop,
GarciaManero Guillermo
Publication year - 2012
Publication title -
american journal of hematology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.22258
Subject(s) - myeloid leukemia , chromosomal translocation , cytarabine , medicine , fusion gene , myeloid , leukemia , bone marrow , fludarabine , cancer research , immunology , haematopoiesis , oncology , biology , chemotherapy , gene , cyclophosphamide , genetics , stem cell
A subgroup of patients with core binding factor acute myeloid leukemias (AML) is characterized by the presence of the fusion gene CBFb-Myh11. At the cytogenetic level, most of these patients are identified by the presence of an inversion of chromosome 16 [inv(16)(p13q22)] and rarely by a translocation t(16;16)(p13;q22). The aim of this study is to describe the natural history of patients with t(16;16) [N = 6] treated at MD Anderson Cancer Center and compared them with a cohort of patients with inv(16)(p13q22) [n = 61]. In patients with t(16;16) the complete remission rate (CR) was 100% when treated with a combination of fludarabine and high-dose cytarabine. Median overall survival (OS) had not been achieved. There was no difference in response or OS or progression free survival between both groups. Presence of additional chromosomal abnormalities and molecular aberrations had no effect on prognosis. In conclusion, and consistent with previous reports, the natural history of patients with t(16:16)(p13;q22) is similar to that of classic patients with inv16 AML and therefore should be treated similarly.