TRANSCRIPTIONAL LEVELS OF
- 1Universidade Federal do Triângulo Mineiro, Uberaba, MG, Brazil
Abstract
Background: Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm associated with the BCR-ABL1 fusion gene, resulting from the translocation between chromosomes 9 and 22 and is characterized by proliferative dysregulation of cell expansion in the myeloid compartment. Although tyrosine kinase inhibitors have revolutionized treatment, cases of resistance and therapeutic failure still occur. MicroRNAs that regulate granulocytic differentiation, such as miR-223-3p, frequently repressed by BCR-ABL1 signaling, and surveillance genes such as TP53, emerge as potential molecular biomarkers. Aim: To evaluate the transcriptional levels of miR-223-3p and TP53 as potential biomarkers of severity and therapeutic response in patients with CML, as well as to correlate the expression of these targets with parameters of myeloid differentiation and maturation. Material and methods: A prospective study was conducted with 17 CML patients treated at the Hospital de Clínicas of the Universidade Federal do Triângulo Mineiro and a group of 8 healthy individuals. Target levels were quantified by RT-qPCR in peripheral blood samples using the comparative 2-ΔΔCt method, with normalization by endogenous controls (miR-16-5p and miR-191-5p for miR-223-3p; ACTB and GAPDH for TP53). Data were correlated with clinical and laboratory variables and analyzed using t-tests, Mann-Whitney tests, Pearson/Spearman correlation, and Fisher's exact test (p<0.05). Results: There was no significant difference in miR-223-3p and TP53 expression between patients and controls, nor between patients with and without therapeutic failure or between regular and irregular treatment adherence (p>0.05 for all comparisons). However, miR-223-3p expression correlated positively with absolute leukocyte count (r=0.50; p=0.04), immature cell count (r=0.67; p<0.01), and mature granulocyte count (r=0.56; p=0.02), being higher in patients with a left shift up to promyelocytes (p=0.01). A positive correlation was also observed between TP53 and miR-223-3p levels (r=0.62; p=0.03). Discussion: The findings suggest that, although the markers evaluated do not independently discriminate prognostic groups or therapeutic response, miR-223-3p tracks the intensity of granulopoiesis in CML, possibly reflecting activation of the C/EBPα axis, its main transcriptional inducer and a target of repression by BCR-ABL1. This pattern is consistent with studies demonstrating expansion of the granulocytic compartment in the absence of this miRNA, reinforcing its role in regulating myeloid differentiation. The correlation with TP53 points to a possible coordination between myeloid differentiation and genomic surveillance pathways, suggesting that miR-223-3p expression in peripheral blood reflects both circulating cellular composition and broader regulatory mechanisms of hematopoiesis in CML. Given the number of comparisons performed and the small sample size, the findings should be considered exploratory. Conclusion: The results reinforce the role of miR-223-3p in the dynamics of hematopoiesis in CML, particularly in its association with myeloid maturation parameters and TP53, highlighting relationships between cell expansion and genomic regulation. Studies with larger sample sizes are important to validate its potential as a complementary biomarker.
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BibTeX
@article{egilio2026transcriptional,
title = {{TRANSCRIPTIONAL LEVELS OF}},
author = {Thauani Isabelle EGILIO and Lucas Fernandes ANANIAS and Fernando Lopes SOUZA and Helio MORAES-SOUZA and Sarah Cristina Sato Vaz TANAKA and Fernanda Bernadelli DE VITO},
journal = {Hematology, Transfusion and Cell Therapy},
year = {2026},
month = oct,
doi = {10.1016/j.htct.2026.107541},
url = {https://doi.org/10.1016/j.htct.2026.107541},
note = {CC BY},
}
RIS
TY - JOUR
TI - TRANSCRIPTIONAL LEVELS OF
AU - Thauani Isabelle EGILIO
AU - Lucas Fernandes ANANIAS
AU - Fernando Lopes SOUZA
AU - Helio MORAES-SOUZA
AU - Sarah Cristina Sato Vaz TANAKA
AU - Fernanda Bernadelli DE VITO
PY - 2026
DA - 2026/10/23
JO - Hematology, Transfusion and Cell Therapy
DO - 10.1016/j.htct.2026.107541
UR - https://doi.org/10.1016/j.htct.2026.107541
AB - Background: Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm associated with the BCR-ABL1 fusion gene, resulting from the translocation between chromosomes 9 and 22 and is characterized by proliferative dysregulation of cell expansion in the myeloid compartment. Although tyrosine kinase inhibitors have revolutionized treatment, cases of resistance and therapeutic failure still occur. MicroRNAs that regulate granulocytic differentiation, such as miR-223-3p, frequently repressed by BCR-ABL1 signaling, and surveillance genes such as TP53, emerge as potential molecular biomarkers. Aim: To evaluate the transcriptional levels of miR-223-3p and TP53 as potential biomarkers of severity and therapeutic response in patients with CML, as well as to correlate the expression of these targets with parameters of myeloid differentiation and maturation. Material and methods: A prospective study was conducted with 17 CML patients treated at the Hospital de Clínicas of the Universidade Federal do Triângulo Mineiro and a group of 8 healthy individuals. Target levels were quantified by RT-qPCR in peripheral blood samples using the comparative 2-ΔΔCt method, with normalization by endogenous controls (miR-16-5p and miR-191-5p for miR-223-3p; ACTB and GAPDH for TP53). Data were correlated with clinical and laboratory variables and analyzed using t-tests, Mann-Whitney tests, Pearson/Spearman correlation, and Fisher's exact test (p<0.05). Results: There was no significant difference in miR-223-3p and TP53 expression between patients and controls, nor between patients with and without therapeutic failure or between regular and irregular treatment adherence (p>0.05 for all comparisons). However, miR-223-3p expression correlated positively with absolute leukocyte count (r=0.50; p=0.04), immature cell count (r=0.67; p<0.01), and mature granulocyte count (r=0.56; p=0.02), being higher in patients with a left shift up to promyelocytes (p=0.01). A positive correlation was also observed between TP53 and miR-223-3p levels (r=0.62; p=0.03). Discussion: The findings suggest that, although the markers evaluated do not independently discriminate prognostic groups or therapeutic response, miR-223-3p tracks the intensity of granulopoiesis in CML, possibly reflecting activation of the C/EBPα axis, its main transcriptional inducer and a target of repression by BCR-ABL1. This pattern is consistent with studies demonstrating expansion of the granulocytic compartment in the absence of this miRNA, reinforcing its role in regulating myeloid differentiation. The correlation with TP53 points to a possible coordination between myeloid differentiation and genomic surveillance pathways, suggesting that miR-223-3p expression in peripheral blood reflects both circulating cellular composition and broader regulatory mechanisms of hematopoiesis in CML. Given the number of comparisons performed and the small sample size, the findings should be considered exploratory. Conclusion: The results reinforce the role of miR-223-3p in the dynamics of hematopoiesis in CML, particularly in its association with myeloid maturation parameters and TP53, highlighting relationships between cell expansion and genomic regulation. Studies with larger sample sizes are important to validate its potential as a complementary biomarker.
SN - 2531-1379
SN - 2531-1387
ER -