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Can Apela be a Novel Target in the Treatment of Chronic Lymphocytic Leukaemia?
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Abstract
Background: It has been shown that bcl2, bcl-XL and mcl-1 protein levels are high in chronic lymphocytic leukemia cells, and resultantly, apoptosis does not occur chronic lymphocytic leukemia cells. Apelin and apela are two peptide ligands for a class A G-protein coupled receptor called apelin receptor. Studies have shown that apella inhibits apoptosis by inhibiting apoptotic proteins and activating anti-apoptotic proteins. Proteins and genes involved in apoptosis are valuable for targeted cancer therapy. We hypothesized that serum levels may be increased in patients with chronic lymphocytic leukemia based on the antiapoptotic effect of apelin. We compared serum apelin levels of healthy volunteers and patients with chronic lymphocytic leukemia. We aimed to draw attention to a new molecule worthy of research in targeted cancer treatment.
Methods: 42 untreated CLL patients and 41 healthy volunteers were included in the study. Serum Apela levels were measured by by using enzyme-linked immunosorbent assay (ELISA) kits (Dhanghai Sunred Biological Technology co. Ltd), automated ELISE reader (Thermo Scientific, FİNLAND) and computer program (Scanlt for Multiscan F.C.2.5.1) in accordance with the manufacturer’s instructions. Statistical analysis was made by Statistical Package for Social Sciences (SPSS) for Windows 20 (IBM SPSS Inc., Chicago, IL) ve MedCalc programs. Apela and variables related to CLL were correlated with Spearman correlation anlysis test. ROC analysis and Youden index method were used to determine a cut off point for apela. All p-values were 2-sided with statistical significance at 0.05 alpha levels.
Results: In our study, we found that serum apela levels were significantly higher in patients with CLL.
Conclusions: This study highlights that apela targeting may be a potential therapeutic option for treating CLL.
Keywords: Apela; apelinergic system; chronic lymphocytic leukaemia; apoptosis
Springer Science and Business Media LLC
Title: Can Apela be a Novel Target in the Treatment of Chronic Lymphocytic Leukaemia?
Description:
Abstract
Background: It has been shown that bcl2, bcl-XL and mcl-1 protein levels are high in chronic lymphocytic leukemia cells, and resultantly, apoptosis does not occur chronic lymphocytic leukemia cells.
Apelin and apela are two peptide ligands for a class A G-protein coupled receptor called apelin receptor.
Studies have shown that apella inhibits apoptosis by inhibiting apoptotic proteins and activating anti-apoptotic proteins.
Proteins and genes involved in apoptosis are valuable for targeted cancer therapy.
We hypothesized that serum levels may be increased in patients with chronic lymphocytic leukemia based on the antiapoptotic effect of apelin.
We compared serum apelin levels of healthy volunteers and patients with chronic lymphocytic leukemia.
We aimed to draw attention to a new molecule worthy of research in targeted cancer treatment.
Methods: 42 untreated CLL patients and 41 healthy volunteers were included in the study.
Serum Apela levels were measured by by using enzyme-linked immunosorbent assay (ELISA) kits (Dhanghai Sunred Biological Technology co.
Ltd), automated ELISE reader (Thermo Scientific, FİNLAND) and computer program (Scanlt for Multiscan F.
C.
2.
5.
1) in accordance with the manufacturer’s instructions.
Statistical analysis was made by Statistical Package for Social Sciences (SPSS) for Windows 20 (IBM SPSS Inc.
, Chicago, IL) ve MedCalc programs.
Apela and variables related to CLL were correlated with Spearman correlation anlysis test.
ROC analysis and Youden index method were used to determine a cut off point for apela.
All p-values were 2-sided with statistical significance at 0.
05 alpha levels.
Results: In our study, we found that serum apela levels were significantly higher in patients with CLL.
Conclusions: This study highlights that apela targeting may be a potential therapeutic option for treating CLL.
Keywords: Apela; apelinergic system; chronic lymphocytic leukaemia; apoptosis.
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