Abstract
Background: AML is a multifactorial disease and different factors play a role in its occurrenc, timely diagnosis and appropriate treatment. On the other hand, due to the importance of PLOD family genes (PLOD1, PLOD2, PLOD3) that lysine hydroxylase enzyme is directly involved in collagen synthesis and extracellular matrix regeneration and their vital role in migration, invasion and angiogenesis in many cancers. Aims: Since the expression of PLOD family genes in AML patients have not been studied so far, also due to the importance of these two risk factors, namely invasion and angiogenesis and the relationship between the expression of these genes and the prognosis of patients, the expression status of PLOD family genes were studied in patients with acute myeloid leukemia. Methods: In this study, the expression of PLOD family genes (PLOD1, PLOD2, PLOD3) in 54 newly identified AML patients and 53 healthy controls was evaluated by qRT-PCR. Then, the obtained results were interpreted using statistical analysis. Results: In this study, 54 patients with AML were studied. 35% of the patients were female and 65% were male. The mean age of patients was 42.05 years. Hematological findings showed that the number of white blood cells and platelets as well as hemoglobin in patients was significantly different from healthy individuals (P <0.05). Classification of patients based on FAB subgroups showed that most patients (50%) belong to M4 subgroup. Gene expression studies showed that PLOD1 and PLOD3 gene expression was significantly increased in AML patients compared to healthy controls (P value = 0.0002 and P value = <0.0001, respectively). But there was no significant difference in PLOD2 gene expression in AML patients compared to normal control group (P value = 0.3). Summary/Conclusion: Expression of PLOD1 and PLOD3 genes in patients with acute myeloid leukemia has significantly increased compared to the healthy control group and may be used as a prognostic factor in AML patients. There was no significant difference in PLOD2 gene expression in AML patients compared to the normal control group. However, due to the heterogeneity of AML, further studies are needed in different AML subgroups based on FAB and cytogenetic classification.
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