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Co-expression of HoxA9 and bcr-abl genes in chronic myeloid leukemia
Fabián A Tedeschi1, Maria A Cardozo, Rosanna Valentini
1Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Hospital Dr. J. M. Cullen, Avenida Freyre 2150 (S3000EOZ), Santa Fe, Argentina. fzalazar@fbcb.unl.edu.ar
Insights
Researchers studied the co-expression of bcr-abl and HoxA9 genes in chronic myeloid leukemia (CML) patients. Increased expression of both genes was linked to poor prognosis, suggesting a role in CML progression.
Area of Science:
- Hematology
- Molecular Biology
- Oncology
Background:
- Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm.
- The bcr-abl fusion gene is a hallmark of CML.
- HoxA9 gene expression is generally stable in adults.
Purpose of the Study:
- To analyze the co-expression of bcr-abl and HoxA9 genes in CML patients.
- To investigate the correlation between gene expression levels and patient prognosis.
Main Methods:
- Quantitative analysis of bcr-abl and HoxA9 gene expression in sequential patient samples.
- Relating gene expression levels to Sokal's score for prognosis assessment.
Main Results:
- All patients showed detectable levels of both bcr-abl and HoxA9.
- Patients with poor prognosis (intermediate/high Sokal's score) exhibited increased bcr-abl and HoxA9 expression (p < 0.05).
- Clinically stable patients with low Sokal's score showed no significant changes in gene expression.
Conclusions:
- The co-expression of bcr-abl and HoxA9 is associated with disease progression in CML.
- Elevated HoxA9 expression in CML may reflect changes linked to bcr-abl activity.
- These findings suggest a potential role for HoxA9 in CML pathogenesis.
Abstract:
We have analyzed the co-expression of the bcr-abl and HoxA9 genes in the follow-up of patients with chronic myeloid leukemia (CML). In the present work we measured the HoxA9 and bcr-abl gene expression in sequential samples. In all patients, bcr-abl and HoxA9 were expressed at detectable levels in every sample. When the results were expressed in relation to abl, two different situations were found: (a) patients clinically stable at second sampling, with low relative risk at diagnosis (low Sokal's score), did not show significant differences in both bcr-abl and HoxA9 levels in the sequential samples analyzed, and (b) patients with poor prognosis (showing intermediate or high Sokal's score at diagnosis) had increased expression of bcr-abl as well as HoxA9 genes (p < 0.05). Since HoxA9 gene expression remains at relatively constant levels throughout adult life, our results could reflect actual changes in the expression rate of this gene associated with bcr-abl during the progression of CML.
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