No abstract available.
Drug Therapy* ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive*

Splenic irradiation in chronic myelogenous leukemia is reserved for patients who have painful splenomegaly despite chemotherapy and/or inoperable splenomegaly because of huge size. The role of splenic irradiation is diminution of painful splenomegaly and indirect effect of splenic irradiation on unirradiated hematopoietic and lymphoreticular tissue such as reduction of leukocyte count and increase of hemoglobin level. We report on a useful clinical method for splenic irradiation in chronic myelogenous leukemia. We have used sonography as the tool of simulation. The portal size using modified method is smaller than the field size of conventional simulation, and so this method suggests that useful to irradiation of huge splenomegaly, effective shielding of critical organ and the downfall of complication during irradiation of spleen.
Drug Therapy ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Leukocyte Count ; Spleen ; Splenomegaly

No abstract available.
Drug Therapy* ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive* ; Leukocytosis* ; Lymphoma, B-Cell*

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

No abstract available.
Dasatinib ; Drug Therapy ; Humans ; Hypopigmentation ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Protein-Tyrosine Kinases

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

OBJECTIVETo evaluate the safety and efficacy of nilotinib in chronic myelogenous leukemia (CML) patients with resistance or intolerance to imatinib.

METHODSThirty-five CML patients after imatinib failure or intolerance received oral administration of 400 mg nilotinib twice daily. The overall survival, hematologic and cytogenetic responses, as well as adverse events were evaluated.

RESULTSThe median duration of nilotinib therapy was 11 (1 - 23) months, with a median follow-up of 19 months. Nonhematologic adverse events were mostly of grade 1-2. The most common ones possibly related to nilotinib were increase of bilirubin (76%) and rash (46%). Grade 3-4 hematologic adverse events includes thrombocytopenia (37%), neutropenia (26%) and anemia (26%). Nilotinib was proved to be well-tolerated in this study. Grade 3-4 hematologic adverse events happened more frequently in advanced phase CML. The rate of major cytogenetic response in chronic phase (CP) CML was much higher than those in advanced CML (38.5% vs 22.2%). The median time to major cytogenetic response was 3 months. The estimated overall survival at 18 months was (93.5 +/- 1.0)%.

CONCLUSIONNilotinib is a more effective and safe treatment option for imatinib-resistant or -intolerant CML-CP patients.

Benzamides ; Drug Resistance, Neoplasm ; Fusion Proteins, bcr-abl ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; drug therapy ; Piperazines ; therapeutic use ; Treatment Outcome

This study was aimed to investigate the application value of the dual color dual fusion fluorescence in situ hybridization (DCDF-FISH) in BCR/ABL (+) acute lymphoblastic leukemia patients with complex chromosomal translocation. The clinical presentations of a patient with ALL were monitored regularly by bone marrow cell morphology test, chromosome analysis, flow cytometry and DCDF-FISH technique, and the reaction of patients to treatment and disease progression were dynamically observed by DCDF-FISH. The results indicated that the patient showed the typical presentation of B lineage acute lymphoblastic leukemia (B-ALL) with expression of CD10, CD19 and CD34; the chromosome analysis showed 46,XY, i(8), ider(9)t (9; 22) [23]/47, idem, +der(22) t (9;22) [7] karyotype in the bone marrow cells, FISH showed that 83% cells contained BCR/ABL fusion gene in the patient's bone marrow, among which 5% cells showed 1R1G2F signalling model, 14% cells showed 1R1G3F, and 64% cells showed 1R1G4F. The patient got complete remission when the imatinib chemotherapy combined with VTLP was carried out, and the tumor cells decreased to 19%, but the cells with 1R1G2F signal model increased to 18%. The 1R1G2F cell signal model increased up to 38% when patient relapsed. The patient died of the drug-resistance. It is concluded that the BCR/ABL (+) leukemia patient with complex translocation has multiple tumor cell subsets, and the responses of different cell subsets to the treatment are different, therefore the response to therapy and drug resistance of patient can be monitored early by the signal model of DCDF-FISH and the observation of dynamical changes of different cell subset.
Adult ; Drug Resistance, Neoplasm ; genetics ; Fusion Proteins, bcr-abl ; genetics ; Humans ; In Situ Hybridization, Fluorescence ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; drug therapy ; genetics ; Male

OBJECTIVE: To investigate the effect of etoposide (ETO) on elimination of chronic myeloid leukemia (CML) stem cells by imatinib mesylate(IM) in vivo. METHODS: SCL-tTA/BCR-ABL mice were used as CML animal model. Flow cytometry was used to assess the effect of ETO alone or in combination with IM on the number of leukemia stem cell （LSC） in bone marrow and spleen, and peripheral blood neutrophils in CML mice and normal control FVB mice. RESULTS: The results showed that in CML mice, the number and proportion of LSC in bone marrow and the proportion of neutrophils in peripheral blood decreased significantly after ETO and IM combined treatment, and the degree of decrease was more significant than that of both alone. While in wild type FVB mice, the combination of ETO and IM showed no significant effect on the number and proportion of LSK cells in bone marrow and the proportion of neutrophils in spleen. CONCLUSION ETO can selectively enhance elimination of CML LSC by IM in vivo.
Animals ; Drug Resistance, Neoplasm ; Etoposide ; Fusion Proteins, bcr-abl ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy* ; Mice ; Stem Cells

Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; drug therapy ; Protein Kinase Inhibitors ; therapeutic use ; Protein-Tyrosine Kinases ; antagonists & inhibitors