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OCT-1 Expression in Patients with Chronic Myeloid Leukemia: A Comparative Analysis with Respect to Response to
Betul Bozkurt Bulakcı1, Aynur Daglar Aday2, Basak Gurtekin3
1Department of Family Medicine, Cemil Tascıoglu City Hospital, University of Health Sciences, Istanbul, Turkey.
Abstract:
The introduction of tyrosine kinase inhibitors (TKI) has resulted in a significant improvement in the treatment of CML patients. However, some CML patients are resistant to imatinib therapy, the initial TKI therapy in the CML. Therefore, it is important to find prognostic markers for resistance. The OCT-1 gene involved in imatinib uptake is also suspected to cause imatinib resistance. The aim of this study was to investigate the role of OCT-1 in imatinib resistance by comparing OCT-1 expression levels in imatinib resistant and imatinib sensitive patients with chronic myeloid leukemia (CML). This study was conducted on 101 patients with CML [imatinib sensitive (n = 51) and imatinib resistant (n = 50)] who were treated with imatinib. Gene expression analysis was done using QRT-PCR. The relative expression levels of OCT-1 were calculated using 2(-ΔΔCT) method. OCT1 mRNA expression levels were 0.149 (0.011-2.532) and 0.119 (0.008-2.868) in imatinib-sensitive group and imatinib-resistant group, respectively. OCT-1 expression levels were not significantly different in the imatinib-sensitive group when compared to imatinib resistant group (p > 0.05). OCT-1 expression was also similar in BCR-ABL1 kinase domain mutation positive and negative cases (p > 0.05). The imatinib-resistant group had a higher rate of hydroxyurea or interferon-alpha treatment prior to imatinib therapy and a lower rate for first-line imatinib as the only treatment than the imatinib-sensitive group (p = 0.002 and p = 0.002, respectively). According to the results of our study, OCT-1 does not have a biomarker feature in the evaluation of imatinib response. In addition, the study should be performed in larger patient groups.
Insights
This study found that OCT-1 gene expression is not a reliable biomarker for predicting imatinib resistance in chronic myeloid leukemia (CML) patients. Further research with larger patient cohorts is recommended to confirm these findings for CML treatment.
Area of Science:
- Oncology
- Pharmacogenomics
Background:
- Tyrosine kinase inhibitors (TKIs) have improved chronic myeloid leukemia (CML) treatment.
- Imatinib resistance presents a challenge in CML management.
- The OCT-1 gene's role in imatinib uptake suggests it may influence resistance.
Purpose of the Study:
- To investigate the role of OCT-1 gene expression as a prognostic marker for imatinib resistance in CML patients.
- To compare OCT-1 expression levels between imatinib-sensitive and imatinib-resistant CML patient groups.
Main Methods:
- Quantitative reverse transcription PCR (QRT-PCR) was used to analyze OCT-1 gene expression.
- The 2(-ΔΔCT) method was employed to calculate relative OCT-1 mRNA expression levels.
- The study included 101 CML patients stratified into imatinib-sensitive (n=51) and imatinib-resistant (n=50) groups.
Main Results:
- No significant difference in OCT-1 expression was observed between imatinib-sensitive and imatinib-resistant CML groups (p > 0.05).
- OCT-1 expression levels were similar in patients with and without BCR-ABL1 kinase domain mutations (p > 0.05).
- Imatinib-resistant patients showed a higher prior use of hydroxyurea or interferon-alpha and less frequent use of imatinib as a sole first-line treatment.
Conclusions:
- OCT-1 expression does not appear to be a useful biomarker for predicting imatinib response in CML.
- The findings suggest that OCT-1 is unlikely to be a key factor in imatinib resistance mechanisms.
- Larger-scale studies are warranted to further validate these results and explore other resistance markers.
