PHD finger protein 19 gene expression pattern and enhancer of zeste homolog 2 gene deletion: laboratory and clinical outcomes in adult patients with acute myeloid leukemia

Abstract

Background
Acute myeloid leukemia (AML) is a heterogeneous clonal disorder with immature myeloid proliferation and epigenetic dysregulation. Enhancer of zeste homolog 2 (EZH2) gene is the catalytic subunit for polycomb repressive complex 2 (PRC2) and essential for epigenetic gene silencing. EZH2 gene deletion is associated with poor outcome in myeloid malignancies. PHD finger protein 19 (PHF19) is PRC2 cofactor which is upregulated in different malignancies.


Aim
This study aimed to detect patterns of PHF19 gene expression and EZH2 gene deletion, detecting their role in AML prognosis and studying the association between them.


Patients and methods
This study was conducted on 40 AML patients and 20 healthy age and sex-matched controls. PHF19 gene expression pattern was detected by real-time PCR. EZH2 gene deletion was conducted by fluorescence in situ hybridization.


Results
There was a significant increase in PHF19 gene expression level in AML patients (7.01 ± 18.89) when compared with control group (0.16 ± 0.22). There was a significant increase in EZH2 gene deletion in AML patients (37.5%) when compared with control group (0%). Patients with both PHF19 overexpression and EZH2 gene deletion show a significant increase in died patients. Expression PHF19 gene had an insignificant relation to EZH2 gene deletion.


Conclusion
PHF19 gene is overexpressed in AML patients, so it may participate in the carcinogenic progression of AML. EZH2 gene deletion was detected in AML patients. This reinforce the idea of EZH2 being a tumor suppressor gene. Patients with both PHF19 overexpression and EZH2 gene deletion have poor predictive outcome.