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Title: | Association of Bcl-xL Expression with Blast Count, CD 34 and CD 7 Expression in Adult Acute Myeloid Leukemia Patients |
Authors: | Puspitasari, Febriani Notopuro, Paulus B. |
Keywords: | AML Bcl-x CD34 CD7 |
Issue Date: | Mar-2024 |
Publisher: | Pharmacognosy Journal |
Citation: | Research Article |
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. |
URI: | http://localhost:8080/xmlui/handle/123456789/8567 |
Appears in Collections: | VOL 16 NO 2 2024 |
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File | Description | Size | Format | |
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460-465.pdf | 628.41 kB | Adobe PDF | View/Open |
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