WRAP53 is Downregulated in Acute Myeloid Leukemia Patients and Positively Correlates With HTERT Expression.

BACKGROUND

Acute myeloid leukemia (AML) is a prevalent hematologic malignancy in adults, marked by clonal disorders in hematopoietic cells, rapid progression, and genetic heterogeneity. The WRAP53 gene, which is associated with genomic stability due to its involvement in activities, such as DNA repair, TP53 regulation, and association with telomerase (hTERT), was the focus of this study.

AIMS: This study aimed to identify new potential molecular markers with prognostic value, based on specific targets, in order to contribute to a more accurate stratification of patients.

METHODS AND

RESULTS

We assessed WRAP53 and hTERT expression in 110 AML patients classified according to World Health Organization (WHO) guidelines. Using real-time quantitative PCR, we investigated their expression and correlation with clinical outcome variables. WRAP53 expression was significantly decreased in AML patients compared to controls, whereas we did not detect differences in hTERT expression. Correlation analysis revealed a moderate positive relationship between WRAP53 and hTERT expression. Concerning the clinical parameters analyzed, significant differences were observed for WRAP53 in terms of sex and age, whereas for hTERT, no differences in the parameters analyzed were observed. Overall survival analysis did not reveal a significant difference for either WRAP53 or hTERT. The results presented demonstrate a downregulation of WRAP53 in the studied sample and that, furthermore, the expression of the WRAP53 and hTERT genes was correlated. In addition, the expression of hTERT, which is already indicated as a biomarker in AML, could not be correlated with the clinical characteristics analyzed in this study.

CONCLUSION

We also suggest that the low expression of WRAP53 may be associated with other mechanisms in AML, such as DNA repair, thus becoming a possible new promising molecular biomarker related to genomic stability in AML.