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Association of Bcl-xL Expression with Blast Count, CD 34 and CD 7 Expression in Adult Acute Myeloid Leukemia Patients.
- Source :
- Pharmacognosy Journal; Mar/Apr2024, Vol. 16 Issue 2, p460-465, 6p
- Publication Year :
- 2024
-
Abstract
- Background: Acute myeloid leukemia (AML) is a hematological malignancy generally marked by the unregulated proliferation of myeloid series blast cells. The condition of hematologic malignancy is often associated with increased anti-apoptotic activity. One of the Bcl-2 protein families, Bcl-xL, has an important role in controlling apoptosis / programmed cell death in hematologic malignancies. This study, determined the correlations between anti-apoptotic activity from Bcl-xL expression analysis with the number of bone marrow blasts, CD34 activity as a marker of blast cells, and CD7 as an aberration marker are often found in AML patients. Aim: Analysis of the correlation between blast number, and expression of Bcl-xL, CD34, and CD7 in adult Acute Myeloid Leukemia patients. Method: An observational cross-sectional study was performed on 30 adult patients who have recently been diagnosed with Acute Myeloid Leukemia using bone marrow aspiration for examination of the number of blasts by a microscope. Examination of the expression of Bcl-xL, CD34, and CD7 was performed by BD FACSCalibur based on the measured Mean Fluorescence Intensity (MFI). Results: A total of 30 AML patients had a range of blast count 20 - 82%, Bcl-xL expression with MFI 93.06 - 441.09, CD34 expression with MFI 1.06 - 1,452.48, CD7 expression with MFI 9.31 - 90.58. In this study, there was no significant correlation between Bcl-xL expression as an indicator of anti-apoptotic properties with blast count r = 0.118 (p = 0.534), CD34 expression r 0.225 (p = 0.231) and CD7 expression r = 0.148 (p = 0.435). Conclusion: Bcl-xL expression as an indicator of anti-apoptotic properties in adult AML patients had no correlations with the proliferation of blast cells in AML. This suggests that increased anti-apoptotic activity is not the primary mechanism in the pathogenesis of AML. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 09753575
- Volume :
- 16
- Issue :
- 2
- Database :
- Complementary Index
- Journal :
- Pharmacognosy Journal
- Publication Type :
- Academic Journal
- Accession number :
- 177385206
- Full Text :
- https://doi.org/10.5530/pj.2024.16.73