EVALUATION OF BECLIN-1 PROTEIN EXPRESSION IN CHRONIC MYELOID LEUKEMIA PATIENTS ON IMATINIB THERAPY
(Abstract release date: 05/19/16)
EHA Library. Emarah Z. 06/09/16; 134713; PB1813
Dr. Ziad Emarah
Contributions
Contributions
Abstract
Abstract: PB1813
Type: Publication Only
Background
Imatinib is a tyrosine kinase inhibitors that used for the treatment of chronic myeloid leukemia (CML). Recent studies showed imatinib-induced cell death in many types of cancers. Autophagy is the physiological process in which cellular components are broken down by the lysosomal activation. Beclin-1 is a protein that encoded by the BECLN1 gene which sits at the core of autophagy regulation.
Aims
the aim of this study is to evaluate the role of Beclin-1 in regulation of BCR-ABL1 fusion gene in patients with chronic myeloid leukemia.
Methods
Peripheral blood samples collected from 30 patients (16 males and 14 females) diagnosed with CML at Oncology Center Mansoura University. Ages ranged from 18 to 50 (44.7 ± 10.2) years. Diagnosis was based on typical finding in the peripheral blood smear and bone marrow aspiration then confirmed by detection of Philadelphia chromosome by cytogenetics or BCR/ABL1 fusion gene using Quantitative RT-PCR. Further samples collected form 30 apparently healthy individuals (16 males and 14 females) subjected as matched controls. Beclin-1 protein was measured by ELISA technique in serum of controls and patients before starting treatment (Time point A) and after 6 months of Imatinib therapy (Time point B).
Results
there was a significant increase in mean Beclin-1 protein level in CML patients either at initial diagnosis (32.6 ng/dl, p ≤ 0.001) or after 6 month of imatinib therapy (44.3, p ≤ 0.001) compared to matched control (9.5 ng/dl). Although its mean level increased after 6 month of imatinib therapy, this increase was not statistically significant. There was a strong negative correlation between mean Beclin-1 protein and hemoglobin level (r= -0.56, p= 0.001), white blood cells count (r= -0.62, p= 0.008), BCR/ABL1 fusion gene level (r= -0.43, p= 0.03).
Conclusion
there was a statistically significant negative correlation between Beclin-1 protein expression and BCR/ABL1 fusion gene level. Beclin-1 protein expression may be used as a dynamic biomarker to predict response to imatinib therapy. However, larger studies are needed to validate these results.
Session topic: E-poster
Keyword(s): BCR-ABL
Type: Publication Only
Background
Imatinib is a tyrosine kinase inhibitors that used for the treatment of chronic myeloid leukemia (CML). Recent studies showed imatinib-induced cell death in many types of cancers. Autophagy is the physiological process in which cellular components are broken down by the lysosomal activation. Beclin-1 is a protein that encoded by the BECLN1 gene which sits at the core of autophagy regulation.
Aims
the aim of this study is to evaluate the role of Beclin-1 in regulation of BCR-ABL1 fusion gene in patients with chronic myeloid leukemia.
Methods
Peripheral blood samples collected from 30 patients (16 males and 14 females) diagnosed with CML at Oncology Center Mansoura University. Ages ranged from 18 to 50 (44.7 ± 10.2) years. Diagnosis was based on typical finding in the peripheral blood smear and bone marrow aspiration then confirmed by detection of Philadelphia chromosome by cytogenetics or BCR/ABL1 fusion gene using Quantitative RT-PCR. Further samples collected form 30 apparently healthy individuals (16 males and 14 females) subjected as matched controls. Beclin-1 protein was measured by ELISA technique in serum of controls and patients before starting treatment (Time point A) and after 6 months of Imatinib therapy (Time point B).
Results
there was a significant increase in mean Beclin-1 protein level in CML patients either at initial diagnosis (32.6 ng/dl, p ≤ 0.001) or after 6 month of imatinib therapy (44.3, p ≤ 0.001) compared to matched control (9.5 ng/dl). Although its mean level increased after 6 month of imatinib therapy, this increase was not statistically significant. There was a strong negative correlation between mean Beclin-1 protein and hemoglobin level (r= -0.56, p= 0.001), white blood cells count (r= -0.62, p= 0.008), BCR/ABL1 fusion gene level (r= -0.43, p= 0.03).
Conclusion
there was a statistically significant negative correlation between Beclin-1 protein expression and BCR/ABL1 fusion gene level. Beclin-1 protein expression may be used as a dynamic biomarker to predict response to imatinib therapy. However, larger studies are needed to validate these results.
Session topic: E-poster
Keyword(s): BCR-ABL
Abstract: PB1813
Type: Publication Only
Background
Imatinib is a tyrosine kinase inhibitors that used for the treatment of chronic myeloid leukemia (CML). Recent studies showed imatinib-induced cell death in many types of cancers. Autophagy is the physiological process in which cellular components are broken down by the lysosomal activation. Beclin-1 is a protein that encoded by the BECLN1 gene which sits at the core of autophagy regulation.
Aims
the aim of this study is to evaluate the role of Beclin-1 in regulation of BCR-ABL1 fusion gene in patients with chronic myeloid leukemia.
Methods
Peripheral blood samples collected from 30 patients (16 males and 14 females) diagnosed with CML at Oncology Center Mansoura University. Ages ranged from 18 to 50 (44.7 ± 10.2) years. Diagnosis was based on typical finding in the peripheral blood smear and bone marrow aspiration then confirmed by detection of Philadelphia chromosome by cytogenetics or BCR/ABL1 fusion gene using Quantitative RT-PCR. Further samples collected form 30 apparently healthy individuals (16 males and 14 females) subjected as matched controls. Beclin-1 protein was measured by ELISA technique in serum of controls and patients before starting treatment (Time point A) and after 6 months of Imatinib therapy (Time point B).
Results
there was a significant increase in mean Beclin-1 protein level in CML patients either at initial diagnosis (32.6 ng/dl, p ≤ 0.001) or after 6 month of imatinib therapy (44.3, p ≤ 0.001) compared to matched control (9.5 ng/dl). Although its mean level increased after 6 month of imatinib therapy, this increase was not statistically significant. There was a strong negative correlation between mean Beclin-1 protein and hemoglobin level (r= -0.56, p= 0.001), white blood cells count (r= -0.62, p= 0.008), BCR/ABL1 fusion gene level (r= -0.43, p= 0.03).
Conclusion
there was a statistically significant negative correlation between Beclin-1 protein expression and BCR/ABL1 fusion gene level. Beclin-1 protein expression may be used as a dynamic biomarker to predict response to imatinib therapy. However, larger studies are needed to validate these results.
Session topic: E-poster
Keyword(s): BCR-ABL
Type: Publication Only
Background
Imatinib is a tyrosine kinase inhibitors that used for the treatment of chronic myeloid leukemia (CML). Recent studies showed imatinib-induced cell death in many types of cancers. Autophagy is the physiological process in which cellular components are broken down by the lysosomal activation. Beclin-1 is a protein that encoded by the BECLN1 gene which sits at the core of autophagy regulation.
Aims
the aim of this study is to evaluate the role of Beclin-1 in regulation of BCR-ABL1 fusion gene in patients with chronic myeloid leukemia.
Methods
Peripheral blood samples collected from 30 patients (16 males and 14 females) diagnosed with CML at Oncology Center Mansoura University. Ages ranged from 18 to 50 (44.7 ± 10.2) years. Diagnosis was based on typical finding in the peripheral blood smear and bone marrow aspiration then confirmed by detection of Philadelphia chromosome by cytogenetics or BCR/ABL1 fusion gene using Quantitative RT-PCR. Further samples collected form 30 apparently healthy individuals (16 males and 14 females) subjected as matched controls. Beclin-1 protein was measured by ELISA technique in serum of controls and patients before starting treatment (Time point A) and after 6 months of Imatinib therapy (Time point B).
Results
there was a significant increase in mean Beclin-1 protein level in CML patients either at initial diagnosis (32.6 ng/dl, p ≤ 0.001) or after 6 month of imatinib therapy (44.3, p ≤ 0.001) compared to matched control (9.5 ng/dl). Although its mean level increased after 6 month of imatinib therapy, this increase was not statistically significant. There was a strong negative correlation between mean Beclin-1 protein and hemoglobin level (r= -0.56, p= 0.001), white blood cells count (r= -0.62, p= 0.008), BCR/ABL1 fusion gene level (r= -0.43, p= 0.03).
Conclusion
there was a statistically significant negative correlation between Beclin-1 protein expression and BCR/ABL1 fusion gene level. Beclin-1 protein expression may be used as a dynamic biomarker to predict response to imatinib therapy. However, larger studies are needed to validate these results.
Session topic: E-poster
Keyword(s): BCR-ABL
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