The Relationships between the Alteration of MAP۱LC۳B, and BECN۱ Gene Expression with Minimal Residual Disease in Acute Lymphoblastic Leukemia Patients
Publish place: Middle East Journal of Cancer، Vol: 12، Issue: 3
Publish Year: 1400
نوع سند: مقاله ژورنالی
زبان: English
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شناسه ملی سند علمی:
JR_MISJ-12-3_004
تاریخ نمایه سازی: 25 آبان 1402
Abstract:
Background: Acute lymphoblastic leukemia (ALL) is known as a sort of malignancy in the blood lymphoid progenitors, specifically in B and T precursors of the lymphocyte. Autophagy is a protected hemostatic and catabolic process during evolution, through which lysosomes degrade the cytoplasmic components, such as redundant or dysfunctional organelles and misfolded proteins. We conducted the present study to investigate the link between gene expression changes of BECN۱, MAP۱LC۳B, and P۶۲ as the main regulators of remission and response to chemotherapy in ALL patients with minimal/measurable residual disease in ALL. Method: In this case-control study, BECN۱, MAP۱LC۳B, and P۶۲ gene expression were assessed in ۳۰ ALL patients at the diagnosis phase, ۱۸ patients on day ۱۵ of the therapy, and ۱۱ controls employing qRT-PCR. Results: The results revealed that BECN۱and MAP۱LC۳B gene expression levels were significantly lower in ALL patients; whereas, P۶۲ gene expression levels were significantly higher than the controls (P < ۰.۰۵). We found that the expression level of the BECN۱ and P۶۲ genes increased and decreased respectively in patients on day ۱۵ of the therapy compared with newly diagnosed ALL patients. Nevertheless, neither BECN۱ nor P۶۲ genes were significantly different at the rate of ۰.۷۳-fold (P > ۰.۰۵). Conclusion: Our study demonstrated the relationship between autophagy-related markers, such as BECN۱, MAP۱LC۳B, and P۶۲ with pathogenesis in Iranian children with ALL. We found that BECN۱and MAP۱LC۳B genes significantly decreased in newly diagnosed ALL patients and may play a part in ALL pathogenesis.
Keywords:
Precursor B-Cell Lymphoblastic Leukemia , Autophagy , BECN۱ protein , MAP۱LC۳B protein , Sqstm۱ protein
Authors
Mozhgan Hayatmanesh
Department of Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
Gholamhossein Tamaddon
Department of Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
Alieh Fazeli
Department of Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
Tahereh Kalantari
Department of Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran