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Changes in expression of apoptosis-related genes are linked to the molecular response to imatinib treatment in chronic-phase chronic myeloid leukemia patients.

Journal article
Authors Yuan Wei
Dick Stockelberg
Sara Hullberg
Anne Ricksten
Hans Wadenvik
Published in Acta haematologica
Volume 117
Issue 2
Pages 83-90
ISSN 1421-9662
Publication year 2007
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Institute of Medicine, Department of Internal Medicine
Pages 83-90
Language en
Links dx.doi.org/10.1159/000096858
Keywords Adult, Aged, Apoptosis, genetics, Benzamides, Female, Fusion Proteins, bcr-abl, Gene Expression Regulation, Leukemic, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, drug therapy, genetics, physiopathology, Leukocytes, Mononuclear, chemistry, Male, Middle Aged, Piperazines, therapeutic use, Protein-Tyrosine Kinases, antagonists & inhibitors, Proto-Oncogene Proteins c-bcl-2, biosynthesis, Pyrimidines, therapeutic use, RNA, Messenger, metabolism, Reverse Transcriptase Polymerase Chain Reaction, bcl-Associated Death Protein, biosynthesis
Subject categories Clinical Medicine

Abstract

Most patients with a chronic phase of chronic myeloid leukemia (CML) treated with imatinib mesylate achieve a cytogenetic remission, but in the majority, residual disease is detectable by RT-PCR. The mechanisms by which residual leukemic cells survive imatinib treatment are unresolved. However, induction of apoptosis in leukemic stem cells and immunotherapy are currently under investigation. We studied the mRNA expression of apoptosis-related genes in peripheral blood mononuclear cells from chronic-phase CML patients before imatinib treatment. It was found that their BCL2 and BAD expression was significantly different compared to the normal controls, and a lower BAD expression was associated with a better molecular response to imatinib treatment at 12 months.

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