No abstract available.
B-Lymphocytes ; Blast Crisis ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive

No abstract available.
Blast Crisis* ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive* ; Megakaryocyte Progenitor Cells*

Adult ; Blast Crisis ; Female ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; complications ; diagnosis ; Ulcer ; diagnosis ; etiology

Chronic myeloid leukemia is a myeloproliferative disorder characterized by excessive cloning of bone marrow multipotent stem cells. According to the disease course, the CML may be divided into chronic phase (CP), accelerated phase (AP) and blastic phase (BP). At present, the molecular mechanisms of acute transformation of CML has not been fully understood. The recent studies have shown that the epigenetics is one of mechanisms in blastic transformation of CML, including three molecular mechanisms such as DNA modification, histone modifications and RNA-related dysregulation. The molecular mechanisms for epigenetics leading to the transformation of CML are discussed in this review.
Blast Crisis ; genetics ; Disease Progression ; Epigenesis, Genetic ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; genetics

Chronic myeloid leukemia (CML) is a myeloproliferative disorder, characterized by excessive proliferation of myeloid cells. CML patients in early phase [also known as chronic phase (CP)] usually respond to treatment with tyrosine kinase inhibitors (TKI), some patients respond initially to TKI, but later become resistant, then resulting in the transformation from CP to more advanced phase, which were subclassified as either accelerated phase or blastic phase. At present, the molecular mechanisms of CML have been not yet clear, and acute transformation has been not fully understood, studies have shown that genomic instability promotes the acute conversion of CML. This review discusses the molecular mechanisms leading to the transformation of CML, and some therapeutic approaches.
Blast Crisis ; Drug Resistance, Neoplasm ; Genomic Instability ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive

Atypical chronic myelogenous leukemia (aCML) has dysplastic as well as proliferative features in most instance and rarely evolves to blast crisis, so it is considered as a distinct clinical entity to classical BCR-ABL (+) CML. We experienced a patient who are diagnosed aCML and transformed to myeloid blast crisis after 17 months. Monosomy 7 and deletion of 12p were found on conventional cytogenetics.
Blast Crisis* ; Cytogenetics ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive* ; Monosomy

Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Leukemia, Myeloid, Chronic-Phase ; drug therapy ; Protein-Tyrosine Kinases ; antagonists & inhibitors

OBJECTIVES: To explore the clinical significance of clonal evolution of additional chromosomal 8 in CML progression. METHODS: An unusual case with the clonal evolution from trisomy 8 to tetrasomy 8 accompanied by 2 time of CML blast crisis (BC) was reported. RESULTS: This patient suffered from 2 time of CML blast crisis and the additional chromosome 8 aberrations were accompanied. Trisomy 8 and tetrasomy 8 were detected at first CML blast crisis and second CML blast crisis, respectively. After tetrasomy 8 was developed, the c-Myc was over-expressed and the central nervous system leukemia happened in this case. Only high dose Ara-C and MTX regimen could induce remission for a short period. CONCLUSION These findings suggested that additional chromosome 8 aberrations are important marker for poor prognosis of CML patients and contribute to a poor prognosis.
Blast Crisis ; Chromosome Aberrations ; Chromosomes, Human, Pair 8 ; Clonal Evolution ; Disease Progression ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive

The blast phase in chronic myelogenous leukemia (CML) is associated with mutation of several genes. It is well known that p53 gene mutation plays a key role in the myeloid or lymphoid blast phase of CML. But for the case of the N-ras gene, the association between N-ras mutations and the blast phase of CML is not yet known. We report here on a case of detecting N-ras point mutation without p53 mutation in a 64 year-old man who suffered from the lymphoblastic blast phase of CML.
Blast Crisis ; Genes, p53 ; Genes, ras ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Point Mutation ; Stress, Psychological

BACKGROUND: STI571, a potent and specific inhibitor of the BCR-ABL tyrosine kinase, causes arrest of growth or apoptosis in leukemic cells that express BCR-ABL. We evaluated the therapeutic effects and clinical events after the STI571 treatment in advanced chronic myelogenous leukemia (CML). METHODS: STI571 was administered orally to 24 patients with CML in accelerated phase (AP) (N=17) or blast crisis (BC) (N=7) with a daily dose of 600mg. Adverse events were observed, and hemotologic, cytogenetic, and molecular responses were evaluated on 1 month of STI571 treatment. RESULTS: Hematologic responses were observed in 20 of 24 patients with higher complete hematologic responses in AP (35.3%) compared to BC (14.3%). Partial cytogenetic responses were observed in 2 cases. Fluorescence in situ hybridization showed significant decrease in the percentage of BCR-ABL positive cells, but all still remained above the upper limit of normal range at the time of analysis. No significant changes were observed in BCR-ABL transcripts after treatment by reverse transcription polymerase chain reaction (PCR) and real-time quantitative PCR. Non- hematologic adverse events after STI571 treatment were minimal, whilst hematologic ones were significant with higher frequency in BC rather than AP. CONCLUSION: STI571 induced rapid and significant hematologic responses in patients with advanced CML and adverse events were tolerable. The fact that no responses were achieved in some of these advanced cases underlies the importance of earlier treatment with STI571 to prolong the survival.
Apoptosis ; Blast Crisis ; Cytogenetics ; Fluorescence ; Fusion Proteins, bcr-abl ; Humans ; In Situ Hybridization ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive* ; Polymerase Chain Reaction ; Reference Values ; Reverse Transcription ; Imatinib Mesylate