scholarly journals Programmed cell death 4 and BCR-ABL fusion gene expression are negatively correlated in chronic myeloid leukemia

2016 ◽  
Vol 12 (4) ◽  
pp. 2976-2981 ◽  
Author(s):  
Xia Zhang ◽  
Riming Liu ◽  
Baohua Huang ◽  
Xiaolu Zhang ◽  
Weijuan Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Chronic Myeloid Leukemia ◽  
Programmed Cell Death ◽  
Myeloid Leukemia ◽  
Fusion Gene ◽  
Programmed Cell Death 4

Abnormal expression of the programmed cell death 5 gene in acute and chronic myeloid leukemia

2006 ◽  
Vol 30 (9) ◽  
pp. 1159-1165 ◽  
Author(s):  
Guo-Rui Ruan ◽  
Ya-Zhen Qin ◽  
Shan-Shan Chen ◽  
Jin-Lan Li ◽  
Xi Ma ◽  
...  
Keyword(s):  
Cell Death ◽  
Chronic Myeloid Leukemia ◽  
Programmed Cell Death ◽  
Myeloid Leukemia ◽  
Abnormal Expression ◽  
Programmed Cell Death 5

hOCT1 Gene Expression Might Predict Molecular Response In Patients with Chronic Myeloid Leukemia

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4838-4838
Author(s):  
Lurdes Zamora ◽  
Marta Cabezon ◽  
Concha Boqué ◽  
Silvia Marce ◽  
Jordi Ribera ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Conflicts Of Interest ◽  
Fusion Gene ◽  
Chronic Phase ◽  
Organic Cation Transporter ◽  
Initial Response ◽  
Molecular Response ◽  
Hematopoietic Malignancy

Abstract Abstract 4838 Introduction: Chronic myeloid leukemia (CML) is a clonal hematopoietic malignancy characterized by the presence of BCR/ABL fusion gene. The resulting protein has a high tyrosine kinase (TK) activity. The first-line treatment for CML is Imatinib, which allow the achievement of cytogenetic and molecular response in most of patients with CML in chronic phase. However, some patients do not respond to this treatment or lose their initial response. Imatinib has been reported to be incorporated into the cell through hOCT1 transporter (human organic cation transporter). The aim of this study was to determine whether the expression of hOCT1 at diagnosis of CML influenced the achievement of molecular response. Patients and Methods: We analyzed hOCT1 gene expression by quantitative PCR in 42 patients at diagnosis and 18 months after treatment with Imatinib. We compared the expression with the presence of compleat molecular response (CMR) at 18 months. We consider CMR when the Ratio (BCR-ABL/ABL)×100 was <0.1% (after International Scale correction). For statistical analysis methods we have used Kolmogorov-Smirnov and Mann-Whitney nonparametric methods. Results: Of the 42 patients, 2 were in hematological response, 22 were in cytogenetic response and 18 in CMR at 18 months. We found a higher hOCT1 gene expression at 18 month than at diagnosis (53.3 versus 29.6, p<0.001) in all patients (Figure 1). We have found some tendency of higher hOCT1 expression at diagnosis in patients with CMR at 18 months than in those who did not had (25.5 versus 18.8, p = 0.07) (Figure 2). Conclusions: Partially funded by FICJ-P-EF-09, RD06/0020/1056 de RTICC and Novartis. We want to thank Dr. David Marin for providing us plasmid for quantitative analysis. Disclosures: No relevant conflicts of interest to declare.

Coordination of Intrinsic, Extrinsic and Endoplasmic Reticulum-Mediated Apoptosis by Imatinib Mesylate Combined with Arsenic Trioxide in Chronic Myeloid Leukemia.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4841-4841
Author(s):  
Ji Zhang ◽  
Yanzhi Du ◽  
Kankan Wang ◽  
Hai Fang ◽  
Junmin Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Chronic Myeloid Leukemia ◽  
Programmed Cell Death ◽  
Er Stress ◽  
Arsenic Trioxide ◽  
Imatinib Mesylate ◽  
Cell Apoptosis ◽  
Myeloid Leukemia ◽  
Molecular Networks ◽  
Two Agents

Abstract A treatment strategy that combines arsenic trioxide (ATO) with the tyrosine kinase inhibitor imatinib mesylate (STI571, Gleevec) appears to induce more cell apoptosis than STI571 alone in chronic myeloid leukemia (CML). To understand the mechanisms underlying the synergistic action of these agents, we applied cDNA microarrays, component plane presentation integrated self-organizing maps (CPP-SOM) and methods of protein biochemistry to study proapoptotic and apoptotic activities in programmed cell death induced by STI571, ATO and the combination of the two agents in detail. Numerous features with temporospatial relationship were revealed, indicating the coordinated regulation of molecular networks from various aspects of proapoptotic and apoptotic activities in CML. In consequence, STI571 induces the intrinsic pathway of cell apoptosis, whereas ATO induces the ER stress-mediated pathway of cell apoptosis, and the combination of the two agents induces the intrinsic, extrinsic and ER stress mediated pathways of cell apoptosis, which results in a more effective and efficient induction of programmed cell death in CML. The potential impact of this study on the development of more sophisticated therapy in human malignancy can be substantial.

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