Cytogenetic and FMS-like tyrosine kinase 3 mutation analyses in acute promyelocytic leukemia patients
IBJ-Iranian Biomedical Journal. 2012; 16 (1): 10-17
in English
| IMEMR
| ID: emr-124805
ABSTRACT
The secondary genetic changes other than the promyelocytic leukemia-retinoic acid receptor [PML-RARA] fusion gene may contribute to the acute promyelocytic leukemogenesis. Chromosomal alterations and mutation of FLT3 [FMS-like tyrosine kinase 3] tyrosine kinase receptor are the frequent genetic alterations in acute myeloid leukemia. However, the prognostic significance of FLT3 mutations in acute promyelocytic leukemia [APL] is not firmly established. In this study, the chromosomal abnormalities were analyzed by bone marrow cytogenetic in 45 APL patients and FLT3 internal tandem duplications [ITD] screening by fragment length analysis and FLT3 D835 mutation by melting curve analysis were screened in 23 APL samples. Cytogenetic study showed 14.3% trisomy 8 and 17.1% chromosomal abnormalities other than t[15;17]. About 13% of the patients had FLT3 ITD, and 26% had D835 point mutation. FLT3 ITD mutation was associated with higher white blood cell count at presentation and poor prognosis. The PML-RARA translocation alone may not be sufficient to induce leukemia. Therefore, we assume that FLT3 mutations and the other genetic and chromosomal alterations may cooperate with PML-RARA in the development of APL disease
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Index:
IMEMR (Eastern Mediterranean)
Main subject:
Oncogene Proteins, Fusion
/
Receptor Protein-Tyrosine Kinases
/
Gene Duplication
/
Fms-Like Tyrosine Kinase 3
/
Mutation
Limits:
Humans
Language:
English
Journal:
Iran. Biomed. J.
Year:
2012
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