Multidrug resistance (MDR) remains a major obstacle in the treatment of acute myeloid leukemia (AML) and is frequently associated with the overexpression of the MDR1 gene and its protein product, P-glycoprotein (P-gp). The present study aimed to evaluate MDR1 gene expression and P-glycoprotein levels in AML patients and to investigate their relationships with selected clinical and molecular parameters. This study was conducted in Diyarbakır, Türkiye, and included 45 newly diagnosed AML patients and 20 healthy controls. MDR1 mRNA expression was analyzed using real-time PCR, while P-glycoprotein expression was evaluated by flow cytometry before and after chemotherapy. Both MDR1 gene expression and P-gp levels were higher in AML patients compared with healthy controls. P-glycoprotein positivity was detected in approximately 60–65% of the patients, and MDR1 expression was observed in the majority of AML cases. Comparison of MDR1 expression before and after chemotherapy demonstrated that MDR1 levels increased in 30 of 45 patients (67.5%), whereas decreased expression was observed in 15 patients (32.5%). Higher MDR1 and P-glycoprotein levels were also observed in patients who died during the follow-up period compared with surviving patients. In addition, gender-based analysis showed that MDR1 gene expression and P-glycoprotein levels tended to be higher in male patients, whereas FLT3-ITD mutation frequency appeared to be higher among female patients. Because AML-M3 patients received a distinct treatment regimen, a separate descriptive subgroup analysis was performed. The AML-M3 subgroup (n = 6) demonstrated heterogeneous changes in MDR1 gene expression and P-glycoprotein expression following treatment. No significant correlations were identified between MDR1/P-gp expression and blast percentage, white blood cell count, or FLT3-ITD mutation status. These findings suggest that MDR1 expression and P-glycoprotein are commonly observed in AML and may be associated with multidrug resistance. When interpreted together with established clinical and molecular parameters, these biomarkers may provide complementary information regarding treatment resistance in AML. However, these findings should be interpreted in light of the relatively small AML-M3 subgroup and require validation in larger, prospective studies.
Science
